I initially was going to write on a different topic in this Editor’s Note until I opened an email message that completely changed my direction. A just-released white paper from the American Dental Hygienists’ Association titled, “Dental Hygiene Self-Governance: An Ethical and Economic Imperative” appeared in my inbox.¹ My initial thought was that the paper was likely a rehashing of the self-regulation concept that we’ve focused on for so long. Yes, that’s an important topic, but then I noticed the word “self-governance” in the title. I was intrigued … what’s the difference? I read the paper and immediately knew it was a game changer.

Why self-governance instead of self-regulation? There are important differences between the two concepts, and both are necessary to have a viable, relevant, legitimate profession. Simply put, self-regulation connotes oversight while self-governance grants authority. Self-regulation is important for overseeing the conduct within the profession, self-governance defines the profession itself. You can see how using the appropriate term is significant when we consider what we want to accomplish. As stated in the paper, “Each profession must be supported by structures that reflect its distinct roles, responsibilities, and competencies.” If we want to achieve a profession that better aligns our authority, education, and public need, then self-governance is the goal. And as described in the paper, this is the overall premise of the Dental Hygiene Modernization Act. This act provides a framework for how to attain self-governance.

The white paper comes at a crucial time, with the many challenges facing our profession, including dilution of our education and skills. The author of the paper, Derik J. Sven, DHSc, MBA, MPH, RDH, CDT, FADHA, FAADH, notes, “The Dental Hygiene Modernization Act is not about independence for its own sake, nor is it about disrupting the current workforce. It provides states with a framework to expand authority through a clearly defined pathway based on education, experience, and demonstrated competence while preserving collaboration and respecting the many ways dental hygienists practice today.”

In August, the Dimensions’ Discovery EXPO included a legislative forum, along with a panel focused on the registered dental hygienist advanced practice designation. One word that resonated throughout both discussions was autonomy. If we had the autonomy to work in nontraditional settings, we could have a greater impact. If we had the autonomy to regulate ourselves, we could ensure a more cohesive standard of practice across the country. If we had the autonomy of separate dental and dental hygiene governing boards, we wouldn’t face many of the ethical dilemmas imposed on us now.

It’s time to stop saying “if” and start saying “when.” Self-governance is the way.

Jill Rethman, RDH, BA, FADHA
Editor in Chief
jrethman@belmontbusinessmedia.com

Reference

1. Sven DJ. Dental hygiene self-governance: an ethical and economic imperative. Available at adha.org/advocacy/adha-white-papers/. Accessed August 22, 2026.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):6

While advancements in oncologic therapy significantly improve survival rates for patients with colorectal cancer (CRC), the collateral damage to the oral cavity remains a formidable challenge. The oral cavity maintains a delicate homeostatic balance between the host’s immune system and a complex microbial community of more than 700 species.^1,2 Under normal conditions, commensal bacteria provide essential benefits, such as pathogen exclusion and immune modulation. However, CRC interventions, including 5-fluorouracil chemotherapy regimens and complex surgical stressors, serve as profound physiological insults that precipitate severe oral dysbiosis.³

For the dental hygienist, managing oral complications in patients with CRC has historically been reactive and palliative. A paradigm shift is occurring: protocols are moving away from palliative care toward proactive microbiome modulation.⁴ This is particularly critical in the CRC population, as specific oral pathogens, such as Fusobacterium nucleatum, can translocate to the lower gastrointestinal tract, where they exacerbate inflammation and potentially influence tumor chemoresistance.^5,6 By using intrinsically native commensal probiotics, clinicians can stabilize the oral ecosystem via competitive exclusion and reduce the reservoir of translocating pathogens before the harsh symptoms secondary to the treatment complications.^7,8

The Simultaneous Burden of Mucositis

Microbial ecology provides an ideal lens for understanding complications during CRC therapy. These patients frequently experience a simultaneous burden of inflammation of both the oral and intestinal mucosa. This is driven by the nontargeted cytotoxicity of systemic chemotherapy on rapidly dividing epithelial cells throughout the gastrointestinal tract.^9,10

As these healthy epithelial layers are damaged, the structural integrity of the mucosal barrier collapses. This physical attack exposes underlying tissues, creates a sudden influx of cellular debris, and radically alters the local microenvironment, effectively allowing opportunistic pathogens to overgrow.^3,10 This treatment-induced dysbiosis does not sit quietly; it acts as a secondary biological modifier that actively fuels local tissue damage. Consequently, oral mucositis (OM) manifests as a five-stage biological cascade, comprising initiation, signaling, amplification, ulceration, and healing, driven by the host’s inflammatory response to this shifting microbial dysbiosis.^3,11 As pathogenic bacteria proliferate within the altered biofilm, they accelerate the inflammatory response by releasing pro-inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6, creating a reservoir of pathogens and inflammatory markers that can ultimately impact the lower gastrointestinal tract (Table 1).

Simultaneously, CRC chemotherapy often triggers intestinal mucositis, resulting in a systemic breakdown of the mucosal barrier and altered intestinal permeability.¹² Within the oral cavity, chemotherapeutic toxicity to the salivary glands induces severe salivary hypofunction, depleting the mouth of its natural flushing mechanism and bicarbonate buffering capacity. Consequently, acids introduced through chemotherapy-induced nausea and vomiting or common patient coping mechanisms, such as consuming fruit juices or sucking on hard candies to combat a chemotherapy-induced metallic taste, become physically trapped. This prolonged acid retention drops the local oral pH below the critical thresholds, creating an environment that favors acidogenic species and rapidly increases the risk for cervical caries.^3,13,14

Furthermore, the loss of healthy bacteria creates an empty ecological space that allows Candida albicans to transform into a harmful invader. This shift leads to secondary infections, such as oral candidiasis, which further compromise the patient’s nutritional status, induce severe oral pain, and disrupt oncology recovery timelines.¹⁴

The Probiotic Shield

Oral-specific probiotics use three primary mechanisms to maintain health: competitive exclusion, antimicrobial production, and immunological stabilization. Unlike transient gut-derived probiotics that cannot effectively colonize oral structures, these indigenous strains specifically target the oral-gut axis by adhering directly to oral mucosa and dental hard tissues (Table 2).^1,2

Clinicians can mitigate the loss of healthy microbes traditionally seen during chemotherapy-induced dysbiosis through early biofilm saturation.³ Streptococcus rattus (JH145) serves as a primary replacement therapy strain. As a nonacidogenic variant, S. rattus lacks the genetic capacity to synthesize lactic acid, yet it actively outcompetes cariogenic S. mutans for binding sites on the salivary pellicle.¹⁵

By occupying these hard-tissue niches prior to the onset of chemotherapy-induced xerostomia, S. rattus effectively crowds out pathogens before stagnant dietary and regurgitated gastric acids become physically trapped in the oral microenvironment. This targeted colonization prevents the rapid, aggressive development of cervical decay patterns common to patients undergoing active cancer treatment.^13,14 Furthermore, addressing this dysbiosis early matches the supportive care goals outlined by international mucositis management protocols, which emphasize mitigating local tissue insults to prevent secondary microbial complications.⁴

Healthy biofilms contain high concentrations of peroxide-producing streptococci, such as S. uberis (KJ2) and S. oralis (KJ3). Originally isolated from healthy subgingival plaque, these strains naturally synthesize low levels of hydrogen peroxide, creating a localized biochemical barrier that inhibits anaerobic pathogens such as F. nucleatum and Porphyromonas gingivalis.¹⁶ In patients with CRC, using this natural biological barrier to reduce the oral load of F. nucleatum is a protective strategy. Minimizing this oral reservoir directly limits the volume of bacteria capable of traveling through the oral-gut translocation pathway to colorectal lesions.⁵ Upon arrival at the gut mucosa, F. nucleatum utilizes specialized surface adhesins to attach to overexpressed tumor cell sugar residues, actively promoting cell proliferation, driving chronic inflammation, and compromising gut barrier permeability.^12,17 Intercepting this pathogenic migration at its oral origin represents a potent preventive strategy in oncology care (Table 3).¹⁸

Probiotics also influence the host’s inflammatory response by downregulating destructive pro-inflammatory pathways. Strains, such as Lactobacillus brevis CD2, produce specific enzymes, such as arginine deiminase. The enzymes break down local L-arginine in the mouth, which directly starves the host pathways that would otherwise use that arginine to produce nitric oxide, a primary chemical driver of tissue damage, swelling, and severe pain in the oral lining.¹⁹

By calming this inflammatory chain reaction at the cellular level, L. brevis CD2 helps shield the delicate lining of the mouth, protects the barrier integrity of the tissue, and reduces the severity of painful mucosal sores. Research in cancer patients undergoing intensive treatments show that this protective enzyme pathway significantly limits the progression of severe, high-grade ulcers, allowing patients to continue eating and avoiding costly delays in their primary cancer treatment (Table 3).²⁰

The Role of the Dental Hygienist

Within the dental hygiene “assessment, diagnosis, planning,implementation, evaluation, and documentation” process of care, clinicians must possess the knowledge to manage oral complications and infection risks across pre-, intra-, and post-treatment oncology phases. During the medical history review, clinicians must collect pertinent information to provide informed care and promote a collaborative relationship with the patient and the interprofessional care team.

Conducting interviews or a questionnaire needs to encourage open communication while allowing for further expansion of details with the patient^.21 For example, asking questions such as:

• Are you currently being treated for any type of cancer?
• If you are currently being treated for a type of cancer, what kind of cancer is it?
• What kind of treatment are you undergoing? Is it surgery, radiation, chemotherapy, or some other kind?
• Has your oncology care team planned out any medication, vitamin, or supplement regimens for you for treatment or management of symptoms?
• Have you noticed any issues/symptoms from treatment so far with your mouth, such as dry mouth, ropey saliva, ulcers/sores, or any other issues?
• So that we can support you on this healthcare journey, can we have the name and phone number of the physician/oncologist you are working with so we can coordinate any dental or overall oral care needs?

Comprehensive data information collection enables quality communication with the interprofessional care team and supports necessary medical consultation during pretreatment and active oncologic care.²² It also allows patients to preliminarily tell the dental hygienist about what they may be experiencing before the extraoral and intraoral examination begins. Once initial information about the patient’s cancer status and phase of treatment is obtained, the oncology care team should be contacted to establish a line of communication between the dental home and the oncologist. The dental hygienist can request medical clearance and establish necessary protocols for elective, nonelective, or emergency procedures before initiating in-office care.²²

When completing the extraoral and intraoral examination, make sure to note salivary flow, tongue texture, mucosal integrity, and any signs of ulcers, sores, or abnormal lesions. Documentation is key during this stage to managing patients’ needs and concerns throughout their treatment and establishes baseline data.²¹

Along with a comprehensive extraoral and intraoral examination, radiographs are essential for evaluating caries, osseous defects, and developmental anomalies. These should be completed in consultation with the dentist and the oncology care team depending on whether the patient is undergoing radiation treatment.²² Additionally, the dental hygiene care plan needs to include evidence-based recommendations for at-home oral hygiene therapies and specialized delivery techniques. The dental hygiene team is responsible for adjusting preventive strategies throughout treatment as needed based on changing symptoms or product intolerance.²¹

Educational Integration and Patient Counseling

While dental hygiene curricula comprehensively address nutritional counseling and medically complex care, there remains a need for stronger integration of continuing education content focused on managing oral and systemic side effects in patients undergoing cancer treatment. One of the current methodologies being explored is the synbiotic, or “seed, feed and protect” counseling strategy that incorporates the use of pre- and probiotics.^23,24 This counseling strategy emphasizes the utilization of both pre- and probiotic products to be more successful than probiotics alone in management of oral pain, ulcers, and other side effects that arise during cancer treatments such as chemotherapy and radiation.²³

The prebiotic provides nutrients that selectively support the growth of beneficial bacteria already living in the gastrointestinal tract. Prebiotics act as a “seed” for a healthy microbiome. In contrast, a probiotic contains live microorganisms that are introduced directly to the body to help “feed” and balance the existing microbiome. Collectively, these interventions are formulated to preserve long-term function and maintenance and mitigate the severity of side effects.^23,24

While natural dietary sources have been shown to provide some of these resources, in patients undergoing cancer treatment, severe depletion within their gut and oral microbiome requires additional assistance. Educating dental hygiene students, faculty, and clinicians to effectively discuss structured dietary counseling with patients is fundamental, especially as many patients experience malnutrition and difficulty maintaining routines due to taste aversions or oral pain.

Collaboration with the patient’s oncologist remains mandatory to select appropriate pre- and probiotic products, and delivery methods that support the oral and gut microbiome and help reduce symptoms.²² A large variety of products, such as toothpastes, lozenges, mouthrinses, pills, capsules, gummies, powders, tablets, gels, and liquids, are available.²⁵ Finding a product that the patient will be most compliant with and is most accessible is important, but monitoring and documenting patient success are also essential.

Coordination with the patient’s oncological team is critical. The patient’s absolute neutrophil count should be closely monitored when it comes to treatment with pre- and probiotics. The immune system is already in a compromised state through anticancer treatments and if the white cell count (neutrophils) decreases too rapidly then the patient’s immune system is less likely to fight off infection.²²

Conclusion

Long term maintenance of dental hygiene patients undergoing chemotherapeutic and radiation therapies for CRC who experience oral manifestations can facilitate stability or even resolution in some cases through use of a multistrain probiotic. The most successful probiotic strains identified as S. rattus, S. uberis, S. oralis, and L. brevis combat three of the more common oral bacteria directly related to oral symptoms and a potential progression of CRC effects. Through comprehensive medical history reviews, structured in-office preventive care, collaboration with the interprofessional care team, and patient-specific product selection recommendations, dental hygienists can significantly assist patients by managing and minimizing the oral and systemic side effects throughout treatment.

Acknowledgment

The authors wish to acknowledge the inspiration for this work: the memory of Heather M. Tuthill’s father, who passed away from cancer in 2020, and the ongoing strength of Emilie B. Ellis’s father in recently overcoming his battle with colon cancer.

References

1. Deo PN, Deshmukh R. Oral microbiome: Unveiling the fundamentals. J Oral Maxillofac Pathol. 2019;23:122–128.
2. Dewhirst FE, Chen T, Izard J, et al. The human oral microbiome. J Bacteriol. 2010;192:5002–5017.
3. Hong BY, Sobue T, Choquette L, et al. Chemotherapy-induced oral mucositis is associated with detrimental bacterial dysbiosis. Microbiome. 2019;7:66.
4. Elad S, Cheng KKF, Lalla RV, et al. MASCC/ISOO clinical practice guidelines for the management of mucositis secondary to cancer therapy. Cancer. 2020;126:4423–4431.
5. Komiya Y, Shimomura Y, Higurashi T, et al. Patients with colorectal cancer have identical strains of Fusobacterium nucleatum in their colorectal cancer and oral cavity. Gut. 2019;68:1335–1337.
6. Abed J, Emgård JEM, Zamir G, et al. Fap2 mediates fusobacterium nucleatum colorectal adenocarcinoma enrichment by binding to tumor-expressed gal-galnac. Cell Host Microbe. 2016;20:215–25.
7. Peng X, Li Z, Pei Y, Zheng S, et al. Streptococcus salivarius K12 alleviates oral mucositis in patients undergoing radiotherapy for malignant head and neck tumors: a randomized controlled trial. J Clin Oncol Off J Am Soc Clin Oncol. 2024;42:1426–1435.
8. Wescombe PA, Hale JDF, Heng NCK, Tagg JR. Developing oral probiotics from Streptococcus salivarius. Future Microbiol. 2012;7:1355–1371.
9. Aprile G, Rihawi K, De Carlo E, Sonis ST. Treatment-related gastrointestinal toxicities and advanced colorectal or pancreatic cancer: A critical update. World J Gastroenterol. 2015;21:11793–1803.
10. Sonis ST. Oral mucositis in cancer therapy. J Support Oncol. 2004;2(6 Suppl 3):3–8.
11. Villa A, Sonis ST. Mucositis: pathobiology and management. Curr Opin Oncol. 2015;27:159–164.
12. Hamouda N, Sano T, Oikawa Y, et al. Apoptosis, dysbiosis and expression of inflammatory cytokines are sequential events in the development of 5-fluorouracil-induced intestinal mucositis in mice. Basic Clin Pharmacol Toxicol. 2017;121:159–168.
13. Bomfin LE, Braga CM, Oliveira TA, et al. 5-Fluorouracil induces inflammation and oxidative stress in the major salivary glands affecting salivary flow and saliva composition. Biochem Pharmacol. 2017;145:34–45.
14. Sroussi HY, Epstein JB, Bensadoun RJ, et al. Common oral complications of head and neck cancer radiation therapy: mucositis, infections, saliva change, fibrosis, sensory dysfunctions, dental caries, periodontal disease, and osteoradionecrosis. Cancer Med. 2017;6:2918–2931.
15. Hillman JD, McDonell E, Cramm T, Hillman CH, Zahradnik RT. A spontaneous lactate dehydrogenase deficient mutant of Streptococcus rattus for use as a probiotic in the prevention of dental caries. J Appl Microbiol. 2009;107:1551–1558.
16. Beattie RE. Probiotics for oral health: a critical evaluation of bacterial strains. Front Microbiol. 2024;15:1430810.
17. Rubinstein MR, Wang X, Liu W, Hao Y, Cai G, Han YW. Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β-catenin signaling via its FadA adhesin. Cell Host Microbe. 2013;14:195–206.
18. Wang S, Liu Y, Li J, et al. Fusobacterium nucleatum acts as a pro-carcinogenic bacterium in colorectal cancer: from association to causality. Front Cell Dev Biol. 2021;9:710165.
19. Riccia DND, Bizzini F, Perilli MG, et al. Anti-inflammatory effects of Lactobacillus brevis (CD2) on periodontal disease. Oral Dis. 2007;13:376–385.
20. Sharma A, Rath GK, Chaudhary SP, Thakar A, Mohanti BK, Bahadur S. Lactobacillus brevis CD2 lozenges reduce radiation- and chemotherapy-induced mucositis in patients with head and neck cancer: a randomized double-blind placebo-controlled study. Eur J Cancer. 2012;48:875–881.
21. Boyd L, Mallonnee L, Wyche C. Wilkins’ Clinical Practice of the Dental Hygienist. 13th ed. Burlington, Massachusetts: Jones and Bartlett Learning; 2020.
22. Kerr A, Miller C, Rhodus N, Stoopler E, Tresiter N. Little and Falace’s Dental Management of the Medically Compromised Patient. 10th ed. St. Louis: Elsevier; 2024.
23. Singh NK, Beckett JM, Kalpurath K, Ishaq M, Ahmad T, Eri RD. Synbiotics as supplemental therapy for the alleviation of chemotherapy-associated symptoms in patients with solid tumours. Nutrients. 2023;15:1759.
24. Dietert RR, Dietert JM. The microbiome and sustainable healthcare. Healthcare. 2015;3:100–129.
25. Bruhn A, Suedbeck J, Eusner L. Probiotic supplements and oral health. Dimensions of Dental Hygiene. 2024;22(3):14–17.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):9-13

For decades, dental unit waterline (DUWL) management has existed in a space between recommendation and enforcement, contributing to variability in implementation across dental practices. Concerns regarding biofilm formation and microbial contamination in DUWLs have been documented extensively in dental literature, and organizations, such as the United States Centers for Disease Control and Prevention (CDC) and American Dental Association (ADA), have issued guidance aimed at reducing exposure risks for patients and oral health professionals alike.¹ Despite longstanding recommendations for waterline treatment and monitoring, adherence to preventive protocols has not been uniform across clinical settings.² This ambiguity is now diminishing. Emerging state-level regulations requiring documented testing, remediation, and verification are transforming DUWL oversight from an advisory infection-prevention recommendation into a verifiable compliance expectation. Recent regulatory actions in Georgia and Washington state illustrate this shift toward enforceable accountability. In both states, dental practices are required to perform routine DUWL testing, initiate corrective action when microbial thresholds are exceeded, and maintain records for inspection purposes.^3,4

Although currently limited to a small number of states, including California, these regulations are likely to serve as a model for broader national adoption. These developments coincide with heightened awareness of waterborne pathogen outbreaks, increased scrutiny of infection prevention programs, and growing expectations for documentation-based verification. The Association for Dental Safety (ADS; formerly OSAP) reinforced these priorities in its 2018 white paper, emphasizing that water quality monitoring, documentation, and verification are essential components of an effective DUWL management program.⁵

Why Dental Unit Waterlines Require Oversight

DUWLs are uniquely susceptible to microbial contamination due to narrow tubing, low flow rates, and frequent periods of water stagnation. These conditions promote the formation of biofilm, a structured microbial community encased within a protective extracellular matrix that adheres to moist surfaces and resists routine flushing.⁶

Water clarity is not a reliable indicator of microbial safety. DUWL biofilm may harbor opportunistic pathogens, such as Legionella spp., Pseudomonas aeruginosa, and nontuberculous mycobacterium, organisms associated with healthcare-related infections.⁶ Importantly, DUWL contamination is often not visible; water that appears clear and odorless may still exceed recommended microbial thresholds.⁷

The CDC recommends that water used for nonsurgical dental procedures meet the Environmental Protection Agency (EPA) drinking water standard of ≤ 500 CFU/mL of heterotrophic water bacteria.⁷ Current ADA guidance similarly emphasizes maintaining dental treatment water at or below the EPA drinking water standard through routine treatment, monitoring, and documentation.⁸

Despite longstanding guidance, maintaining compliant DUWL water quality remains challenging. Research has demonstrated that established biofilms can persist despite intermittent flushing and periodic shock treatments, creating the potential for rapid recolonization when continuous maintenance protocols are not consistently implemented.^5,8

The gap between guidance and regulatory oversight became increasingly untenable following several highly publicized outbreaks linked to contaminated dental water systems. In 2022, the CDC issued a Health Alert Network advisory following pediatric infections associated with contaminated dental treatment water during pulpotomy procedures.^9-11 This alert reinforced the importance of routine waterline disinfection, continuous monitoring and documentation, and strict adherence to manufacturer instructions for use as foundational components of a comprehensive DUWL management program.^9,12

In response, state dental boards have begun codifying DUWL requirements into enforceable regulations. Georgia’s Rule 150-8-.05 mandates quarterly testing and retention of records for 5 years, while Washington state’s WAC 246-817-660 requires routine testing and remediation to confirm acceptable water quality.^3,4 Together, these regulations signal a transition from recommendation to enforceable expectation.

Testing Does Not Eliminate Biofilm, It Verifies Control

A critical distinction in DUWL management is recognizing that testing is not the intervention, but rather the mechanism used to verify whether maintenance protocols effectively control biofilm.⁶ Reliance on testing alone, without continuous antimicrobial maintenance, may create a false sense of safety.

Historically, many dental practices relied on independent water bottle systems combined with periodic shock treatments, sometimes with limited monitoring. However, CDC guidance and the ADS White Paper emphasize that independent reservoirs alone do not ensure acceptable water quality and must be combined with validated treatment methods, routine monitoring, documentation, and adherence to manufacturer instructions to achieve sustained biofilm control.^5,7

DUWL management requires a clear distinction between maintenance and remediation. Maintenance involves continuous low-level antimicrobial treatment designed to suppress biofilm development during routine clinical use. Remediation refers to implementation of a shock-treatment protocol following unacceptable microbial test results. Without continuous maintenance and verification testing, biofilm can rapidly recolonize the system following remediation. ^5,8

As regulatory expectations evolve, DUWL oversight is best understood as a quality assurance model comparable to sterilization monitoring. Effective compliance requires integration of multiple interdependent components (Figure 1).

Effective DUWL compliance follows a continuous cycle of antimicrobial maintenance, routine monitoring, documentation, corrective action when indicated, and verification testing before returning units to service.

Verification, defined as documented confirmation that microbial counts have returned to acceptable levels, is the essential final step before clinical use resumes.^6,8 This model emphasizes that remediation alone is insufficient; verification is required to align DUWL management with established healthcare quality assurance frameworks.

Table 1 illustrates what is needed to meet current and emerging regulatory expectations.^5,12 Together, these elements transform DUWL management from a task-oriented activity into a defensible, inspection-ready quality assurance system.

Dental Hygienist’s Role

Human factors including workflow pressures, insufficient training, unclear delegation, and inconsistent documentation have been identified as barriers to effective DUWL infection-control implementation. Recent survey data demonstrated substantial knowledge and practice gaps regarding testing requirements, documentation procedures, and corrective actions following failed water-quality tests, despite widespread recognition of the importance of DUWL infection prevention.²

Dental hygienists are particularly well positioned to lead DUWL quality assurance efforts because accredited dental hygiene curricula include extensive education in microbiology, infection prevention, patient safety, and quality assurance principles. Commission on Dental Accreditation standards require programs to prepare graduates who are competent in infection prevention and control practices, providing a strong foundation for leadership in DUWL compliance initiatives.¹³

Conclusion

The trajectory of DUWL oversight is clear: what was once a recommendation is rapidly becoming a regulated standard of care. Mandates for testing, documentation, remediation, and verification reflect a broader shift toward measurable infection-prevention outcomes. For oral health professionals, particularly dental hygienists, this transition presents both a responsibility and an opportunity. As practices adapt to increasing regulatory expectations, dental hygienists are well suited to assume expanded leadership roles in infection prevention, quality assurance, staff training, and compliance oversight.

Practices that adopt structured quality assurance programs will be better positioned to meet evolving expectations while strengthening patient trust. Biofilm management is no longer limited to flushing lines; it now requires systems that are measurable, defensible, and verifiable.

References

1. United States Centers for Disease Control and Prevention. Guidelines for Infection Control in Dental Health-Care Settings—2003. MMWR Recomm Rep. 2003;52(RR-17):1-6.
2. Vinh R, Azzolin KA, Stream SE, et al. Dental unit waterline infection control practice and knowledge gaps. J Am Dent Assoc. 2024;155:515-525.
3. Georgia Board of Dentistry. Dental Unit Water Quality. Rule 150-8-.05. Available at: https://rules.sos.georgia.gov/gac/150-8-.05. Accessed August 22, 2026.
4. Washington State Dental Quality Assurance Commission. Dental Unit Water Quality. WAC 246-817-660. Available at: https://app.leg.wa.gov/wac/default.aspx?cite=246-817-660 Accessed August 22, 2026.
5. Mills SE, Porteous N, Zawada J, eds. Dental unit water quality: Organization for Safety, Asepsis and Prevention white paper and recommendations—2018. Available at https://osapjdics.scholasticahq.com/article/5075-dental-unit-water-quality-organization-for-safety-asepsis-and-prevention-white-paper-and-recommendations-2018. Accessed August 22, 2026.
6. Spagnolo AM, Sartini M, Cristina ML. Microbial contamination of dental unit waterlines and potential risk of infection: a narrative review. Pathogens. 2020;9:651.
7. US Centers for Disease Control and Prevention. Dental Unit Water Quality. Available at cdc.gov/dental-infection-control/hcp/summary/dental-unit-water-quality.html Accessed August 22, 2026.
8. American Dental Association. Dental Unit Waterlines. Available at ada.org/resources/ada-library/oral-health-topics/dental-unit-waterlines. Accessed August 22, 2026.
9. US Centers for Disease Control and Prevention. Health Alert Network (HAN) No. 00478: Dental Infections Associated with Contaminated Water Systems. Available at https://emergency.cdc.gov/han/2022/han00478.asp. Accessed August 22, 2026.
10. Peralta G, Tobin-D’Angelo M, Parham A, et al. Notes from the field: Mycobacterium abscessus infections among patients of a pediatric dentistry practice—Georgia, 2015. MMWR Morb Mortal Wkly Rep. 2016;65(13):355–356.
11. Castellano Realpe OJ, Gutiérrez JC, Sierra DA, et al. Dental unit waterlines contaminated with nontuberculous mycobacteria: a potential health risk. Int J Environ Res Public Health. 2020;17:2348.
12. US Centers for Disease Control and Prevention. Best Practices for Dental Unit Water Quality. Available at cdc.gov/dental-infection-control/hcp/dental-ipc-faqs/best-practices-dental-unit-water-quality.html Accessed August 22, 2026.
13. Commission on Dental Accreditation. Accreditation Standards for Dental Hygiene Education Programs. Available at https://coda.ada.org. Accessed August 22, 2026.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):16-18

Dental implants are an effective option for replacing missing teeth, with long-term success rates exceeding 90% and millions placed worldwide each year.^1,2 Despite favorable outcomes in implant placement and long-term preservation of alveolar bone, maintenance is essential for preserving peri-implant tissues and osseointegration, and preventing biological complications. A majority of peri-implant mucositis and peri-implantitis cases are plaque-induced inflammatory conditions that may compromise implant success if left untreated.³ Systematic reviews report the prevalence of peri-implant mucositis at 43% to 46.8% and peri-implantitis at 19.8% to 22%, underscoring the importance of vigilant implant maintenance as a key component of successful implant therapy.²

Implant maintenance requires routine clinical evaluations, patient education, self-care education and reinforcement, professional biofilm and calculus removal to support peri-implant tissue health, and ongoing management of risk factors. Routine clinical evaluations include visual inspection of peri-implant tissues; periodontal probing to assess pocket depths, suppuration, and bleeding; and radiographic evaluation of crestal bone levels and osseointegration.⁴ In addition, implant maintenance visits involve reviewing self-care routines of patients, the effectiveness of oral hygiene tools recommended, counseling on modifiable risk factors, and performing professional debridement using implant-safe instruments.

While the importance of professional care is well-established, variability exists in clinical approaches and mechanical plaque control techniques for the prevention and management of peri-implant mucositis. The inconsistency in clinical implant maintenance standards highlights the need to identify and validate evidence-based professional approaches to implant care.⁵ Subgingival air polishing has emerged as a promising adjunctive technique for managing biofilm around implants with minimal surface alteration.⁶

Benefits of Subgingival Air Polishing with Mechanical Instrumentation

Oral biofilm is widely recognized as the primary etiologic factor in the development of gingivitis, periodontitis, peri-implant mucositis, and peri-implantitis.^7,8 Effective disruption of biofilm is essential for preventing disease, controlling inflammation, and maintaining periodontal and peri-implant health.^4,7 In addition to its role in oral disease, biofilm management has implications for systemic health; growing evidence links poor biofilm control to chronic conditions such as cardiovascular disease, diabetes mellitus, chronic kidney disease, cancers, adverse pregnancy outcomes, and autoimmune disorders.⁹

Proper oral hygiene practices combined with routine professional care enable early detection and management of inflammatory conditions benefiting peri-implant tissues. Inadequate maintenance significantly increases the risk of progression from peri-implant mucositis to peri-implantitis, which can progress to implant failure.¹⁰ The primary objective of professional implant maintenance therapy is effective biofilm disruption; however, commonly used mechanical instruments, including curets and ultrasonic scalers, may have limited efficacy in completely removing biofilm from exposed titanium implant surfaces, particularly in areas with complex implant geometry.¹¹

In a randomized controlled trial by Flemming et al,¹² subgingival glycine air polishing resulted in significantly lower total viable bacterial counts in moderate-to-deep pockets compared with scaling and root planing immediately after treatment and at 10 days, and demonstrated a greater reduction in Porphyromonas gingivalis at 90 days. These findings underscore the need for adjunctive approaches to supplement conventional mechanical instrumentation.

By delivering minimally abrasive powder streams, air polishing can more effectively access challenging areas, achieving more uniform biofilm disruption while enhancing patient comfort.^13-15 Current evidence also indicates that air polishing performs comparably to conventional instrumentation for many maintenance outcomes, with distinct advantages in patient comfort, treatment efficiency, and biofilm disruption.^14,16-19 Zhu et al¹⁴ reported that glycine powder air polishing was associated with greater bleeding reduction than hand instrumentation and lower patient discomfort than ultrasonic scaling.

The limitations of conventional mechanical instrumentation for implant maintenance highlight the need for adjunctive approaches that can supplement biofilm removal by delivering minimally abrasive powder streams capable of penetrating challenging areas. These approaches can disrupt biofilm more uniformly and efficiently, while supporting patient comfort.^12-14

Subgingival air-polishing powders have antimicrobial properties that reduce periopathogenic bacteria.¹³ Glycine- and erythritol-based powders have shown to disrupt biofilm architecture and inhibit the growth of key pathogens associated with peri-implant mucositis, including P. gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans, Fusobacteriaum nucleatum, Actinomyces naeslundii, Veillonella parvula, and Streptococcus oralis.^9,20 These powders create an environment less-conducive to biofilm formation and recolonization, thereby enhancing overall decontamination of the implant and promoting health of peri-implant tissues.

Effectiveness may decrease in deeper pockets where access is limited or calculus deposits are present, necessitating integrated treatment approaches.¹⁴ In early peri-implant disease management, combination therapies, such as ultrasonic scaling followed by air polishing or adjunctive antimicrobial rinses, have been shown to produce favorable outcomes comparable to conventional nonsurgical therapies.¹⁶ In 2017, a randomized clinical trial compared glycine air-abrasive debridement to manual debridement with chlorhexidine over 6 months for maintaining peri-implant health. Both groups showed improvements, but the air-abrasive approach was equally effective and provided consistent control of plaque, bleeding, and probing depth around implants compared to conventional instrumentation. Additionally, adding air-abrasive debridement-maintained peri-implant tissues without causing damage, supporting its use as a safe and efficient alternative to traditional manual methods for routine maintenance.²¹

Types of Subgingival Air Polishing Powder

Subgingival air-polishing powders must meet specific clinical requirements, including biocompatibility with hard and soft tissues, low abrasivity, and the ability to effectively disrupt biofilm. Early air-polishing powders, such as sodium bicarbonate, were not recommended for subgingival use due to their larger particle size and increased abrasiveness, which posed a risk to root surfaces and soft tissues.^14,22

Advances in air-polishing technology have led to the development of low-abrasive powders designed for safe subgingival application.^13,16 Air-polishing devices function by delivering a pressurized slurry composed of air, water, and an abrasive powder. The powder component is essential to the effectiveness of the system, as biofilm removal is significantly reduced in the absence of the abrasive particles. Biocompatible powders allow for effective decontamination while minimizing surface alteration of oral appliances.²²

Powder characteristics, including particle size, hardness, and solubility, play a critical role in determining their suitability for use around natural teeth and implant surfaces. Table 1 summarizes key physical characteristics and clinical considerations associated with commonly used subgingival air-polishing powders, supporting their safe use on titanium implant surfaces when used according to manufacturer guidelines. Currently, glycine and erythritol powders are the most extensively studied and commonly used for subgingival air polishing. Both powders exhibit low abrasivity, small particle size, and have antimicrobial properties, making them appropriate for use in periodontal and peri-implant maintenance.^15,22,23 Trehalose powder has more recently been introduced as an alternative low-abrasive option; however, its clinical application remains less established, with existing evidence primarily derived from in vitro and limited clinical studies.^22-25

Clinical Implications

Effective and ongoing maintenance of dental implants requires individualized clinical decision-making based on peri-implant tissue health, implant surface characteristics, and patient-specific risk factors such as history of periodontitis and oral hygiene practices.^4,8 Mechanical instrumentation remains essential for removal of calculus deposits and for management of advanced peri-implant disease, particularly in sites with hard deposits or deep, inaccessible defects.^8,10,16

Subgingival air polishing with low-abrasive powders such as glycine, erythritol, or trehalose is an effective adjunct for biofilm disruption during supportive implant maintenance.^13,25 Subgingival air polishing has demonstrated clinical outcomes comparable to conventional debridement in residual periodontal pockets, while improving patient comfort and reducing treatment time.^12,15,23-24 In 2015, a randomized clinical trial compared glycine air-polishing to conventional mechanical debridement for peri-implant mucositis; the study demonstrated significantly greater reductions in bleeding on probing and inflammation, along with improved patient comfort, and was also more effective at disrupting biofilm on implant surfaces without causing damage, making it a preferred approach for peri-implant maintenance.²⁶

A 2025 review emphasized the reversible nature of peri-implant mucositis and represents a critical intervention point to prevent peri-implantitis. The article found that early detection, consistent maintenance, and the use of adjunctive therapies such as air polishing improve clinical outcomes, while patient-specific risk factors must be managed to ensure long-term peri-implant health.¹⁰

The use of low-abrasive air-polishing powders may enhance patient comfort and reduce the risk of implant surface alteration compared with more aggressive instrumentation techniques.²¹ Patients also frequently report lower pain perception and less gingival irritation with these powders than with hand or ultrasonic instruments.^12,15 Selection of powder type should be guided by particle size, hardness, and available clinical and in vitro evidence, with particular consideration of biocompatibility and the limited long‑term data for newer powders.^6,14,16,25

Experimental evidence demonstrates that glycine-, erythritol-, and trehalose-based powders effectively reduce subgingival biofilm and inflammatory parameters while maintaining acceptable cellular responses and preserving implant surface characteristics when used according to manufacturer guidelines.^{13,14,16,20,25} Accordingly, incorporating subgingival air polishing into comprehensive, evidence-based implant maintenance protocols may support peri-implant health while helping preserve implant and abutment surface integrity over time.^4,11

Despite its clinical advantages, practical barriers may limit the routine adoption of subgingival air polishing. The initial investment in air-polishing units, along with the ongoing cost of low-abrasive powders can pose financial challenges. Clinicians must also account for the time required for device preparation, disassembly, cleaning, sterilization, and routine maintenance, including waterline flushing and powder chamber care, to ensure proper function and compliance with infection control standards. These steps may increase chairside turnover time compared with traditional instrumentation. In addition, successful implementation requires adequate training to ensure proper powder selection, angulation, and application time to optimize outcomes while minimizing tissue trauma and adverse effects. Although limited research specifically addresses barriers to implementation, careful consideration of these financial, logistical, and educational factors is essential when integrating subgingival air polishing into comprehensive implant maintenance protocols.

References

1. Moraschini V, Da C Poubel L, Ferreira V, Barboza EDS. Evaluation of survival and success rates of dental implants reported in longitudinal studies with a follow-up period of at least 10 years: a systematic review. Int J Oral Maxillofac Surg. 2015;44:377–388.
2. Cheung MC, Hopcraft MS, Darby BI. Dentists’ preferences in implant maintenance and hygiene instruction. Aust Dent J. 2021;66:278-288.
3. Jayachandran S, Walmsley AD, Hill K. Challenges in dental implant provision and its management in general dental practice. J Dent. 2020:99:103414.
4. Perussolo J, Donos N. Maintenance of peri-implant health in general dental practice. Br Dent J. 2024;236:781–789.
5. Jepsen S, Berglundh T, Genco R, et al. Primary prevention of peri‐implantitis: Managing peri‐implant mucositis. J Clin Periodontol. 2015;42:S16.
6. Tastepe CS, Lin X, Donnet M, Wismeijer D, Liu Y. Parameters that improve cleaning efficiency of subgingival air polishing on titanium implant surfaces: an in vitro study. J Periodontol. 2016;88:407–414.
7. Toshniwal SH, Reche A, Bajaj P, Maloo LM. Status quo in mechanical plaque control then and now: a review. Cureus. 2022;14: e28613.
8. Kwon T, Lamster IB, Levin L. Current concepts in the management of periodontitis. Int Dent J. 2020;71:462–476.
9. Kurtzman GM, Horowitz RA, Johnson R, Prestiano RA, Klein BI. The systemic oral health connection: biofilms. Medicine (Baltimore). 2022;101:e30517.
10. Pereira R, Sabri H, Nava P, Alrmali A, Wang HL. Treatment strategies for peri-implant mucositis: the final stop for preventing peri-implantitis. Int J Dent. 2025;2025:6901156.
11. Araújo TG, Moreira CS, Neme RA, Luan H, Bertolini M. Long-term implant maintenance: a systematic review of home and professional care strategies in supportive implant therapy. Braz Dent J. 2024:35:e246178.
12. Flemmig TF, Arushanov D, Daubert D, Rothen M, Mueller G, Leroux BG. Randomized controlled trial assessing efficacy and safety of glycine powder air polishing in moderate-to-deep periodontal pockets. J Periodontol. 2012;83:444-452.
13. Wenzler JS, Krause F, Böcher S, et al. Antimicrobial impact of different air-polishing powders in a subgingival biofilm model. Antibiotics (Basel). 2021;10:1464.
14. Weusmann J, Deschner J, Imber J, et al. Impact of glycine and erythritol/chlorhexidine air-polishing powders on human gingival fibroblasts: An in vitro study. Ann Anat. 2022;243:151949.
15. Zhu M, Zhao M, Hu B, Wang Y, Li Y, Song J. Efficacy of glycine powder air-polishing in supportive periodontal therapy: a systematic review and meta-analysis. J Periodontal Implant Sci. 2021;51:147-162.
16. Gheorghe DN, Bennardo F, Silaghi M, et al. Subgingival use of air-polishing powders: status of knowledge: a systematic review. J Clin Med. 2023;12:6936.
17. Cosgarea R, Roccuzzo A, Jepsen K, Sculean A, Jepsen S, Salvi GE. Efficacy of mechanical/physical approaches for implant surface decontamination in non-surgical submarginal instrumentation of peri-implantitis. A systematic review. J Clin Periodontol. 2023;50(Suppl. 26):188–211.
18. Liu CC, Dixit N, Hatz CR, et al. Air powder waterjet technology using erythritol or glycine powders in periodontal or peri-implant prophylaxis and therapy: A consensus report of an expert meeting. Clin Exp Dent Res. 2024;10:e855.
19. Tan SL, Grewal GK, Mohamed Nazari NS, Mohd-Dom TN, Baharuddin NA. Efficacy of air polishing in comparison with hand instruments and/or power-driven instruments in supportive periodontal therapy and implant maintenance: a systematic review and meta-analysis. BMC Oral Health. 2022;22:85.
20. Amate-Fernández P, Figueiredo R, Blanc V, Àlvarez G, León R, Valmaseda-Castellón E. Erythritol-enriched powder and oral biofilm regrowth on dental implants: an in vitro study. Med Oral Patol Oral Cir Bucal. 2021;26:e602-e610.
21. Lupi SM, Granati M, Butera A, Collesano V, Rodriguez Y, Baena R. Air-abrasive debridement with glycine powder versus manual debridement and chlorhexidine administration for the maintenance of peri-implant health status: a six-month randomized clinical trial. Int J Dent Hyg. 2017;15:287–294.
22. Janaphan K, Hill RG, Gillam D. Air-polishing in subgingival root debridement during supportive periodontal care: a review. J Orthod Craniofac Res. 2020;2:113.
23. Kruse AB, Maamar R, Akakpo DL, et al. Effects of subgingival air-polishing with trehalose powder on oral biofilm during periodontal maintenance therapy: a randomized-controlled pilot study. BMC Oral Health. 2020;20:123.
24. Jentsch HFR, Flechsig C, Kette B, Eick S. Adjunctive air-polishing with erythritol in nonsurgical periodontal therapy: a randomized clinical trial. BMC Oral Health. 2020;20:364.
25. Weusmann J, Deschner J, Imber JC, Damanaki A, Leguizamón NDP, Nogueira AVB. Cellular effects of glycine and trehalose air-polishing powders on human gingival fibroblasts in vitro. Clin Oral Investig. 2022;26:1569-1578.
26. Sahm N, Becker J, Santel T, Schwarz F. Non-surgical treatment of peri-implantitis using an air-abrasive device or mechanical debridement and local application of chlorhexidine: a prospective, randomized, controlled clinical study. J Clin Periodontol. 2011;38:872-878.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):20-22,24

Venous thromboembolism (VTE), and its clinical manifestations deep vein thrombosis (DVT) and pulmonary embolism (PE), are uniquely dangerous conditions due to the range of their presentation: from no symptoms at all to sudden death. Due to the prevalence of VTE, and the associated morbidity and mortality, as well as the bleeding risks associated with anticoagulant therapies, accurate diagnostic/prognostic and treatment strategies are essential to confirm these conditions.

The role of the oral health professional may be limited in the diagnosis of VTE and its clinical manifestations, but is critical in identifying risk factors based on patients’ medical/medication history. Moreover, knowledge of these conditions, their etiology and risk factors, prevention and treatment strategies as well as potential treatment complications, will lead to appropriate patient management and successful outcomes.

As many as 900,000 Americans are affected by VTE, with 25% experiencing sudden death as their first symptom.¹ This statistic is likely an underestimate due to underdiagnosis of these conditions.² Death from all causes of VTE is estimated at 60,000 to 100,000 annually. Risk factors include recent hospitalization, surgical procedures, cancer and cancer treatment, pregnancy, childbirth, and post-partum complications within 3 months of giving birth.

PE is among the most common causes of pregnancy-related death. Hospital-acquired VTE, defined as occurring during or within 3 months of a hospital stay, accounts for more than half of all VTE in the US population and globally.³ Additionally, VTE can recur within 10 years, and long-term complications of DVT can occur in the affected limb. Heritability of VTE estimated from family studies is 40% to 60%, with many confirmed genes related to coagulation/anticoagulation, platelets, immune system cells, erythrocytes, and yet unknown cells/pathways.⁴ Additionally, there is a risk for a repeated VTE following the initial occurrence once the anticoagulant treatment is stopped, which depends on whether the initial incident was due to identified risk factors or was without identified risk factors.⁵ A recent systematic review found that the highest risk of recurrence was in patients with unprovoked VTE (7.4% over 0 to 24 months after stopping anticoagulant therapy).⁶ This risk is approximately 2.5 times higher than for patients with VTE provoked by surgery or a nonsurgical trigger.

Pathophysiology

In 1856, German physician Rudolf Virchow described three factors that contribute to the formation of venous blood clots: slow or stagnant blood flow (venous stasis), damage to the blood vessel lining, and increased blood clotting (hypercoagulability). This concept, known as Virchow’s Triad, remains the foundation for understanding VTE. Virchow also demonstrated that clots typically form in the peripheral veins and can then travel to the lungs, rather than forming in the pulmonary arteries themselves.⁷

Venous stasis is an important risk factor, but stasis alone generally is not enough to cause a clot; at least two of the three factors in Virchow’s Triad are typically involved.^7,8 Clots often begin near venous valves, where blood moves more slowly. This can promote fibrin buildup, low oxygen levels, and an environment that favors clotting. A protein called tissue factor helps activate the blood-clotting process, ultimately leading to clot formation and possible blockage of the vessel.⁹ Inflammation can further increase this risk because inflammatory substances can promote both blood clotting and damage to the vessel lining.¹⁰

DVT and PE are the two manifestations of VTE: DVT, ranging from asymptomatic to life-threatening venous obstruction of the deep veins of the limbs/abdomen, and PE, an occlusion of one or more of the pulmonary arteries by the embolus (dislodged thrombus) are both nonspecific, and therefore often underdiagnosed and dangerous conditions.² An estimated 25% of patients with clinical symptoms of DVT and only 5% of patients with suspected PE actually have the condition. This very low specificity can be explained by the challenges of the differential diagnosis, ranging from chronic venous insufficiency and thrombophlebitis to heart failure, lymphedema, and cellulitis.²

Signs and symptoms of DVT include pain, swelling, warmth, discoloration/cyanosis of the lower extremity, which is usually unilateral and can be distal, involving the calf, or proximal involving calf or whole leg. Although lower-extremity DVT is most common, it may happen in other sites leading to upper-extremity DVT (most commonly catheter-associated, which composes approximately 5% to 10% of all DVT); splanchnic vein thrombosis (portal, mesenteric, and splenic veins); cerebral venous sinus thrombosis; and retinal vein occlusion associated with sudden unilateral vision loss, the most common retinal vascular disease after diabetic retinopathy.¹¹

Dyspnea (about 70% of cases) is the most common symptom of a PE, usually with a rapid onset. Pleuritic chest pain is also common (~66%), often presenting with a cough. Patients may experience unexplained syncope, which, particularly in the presence of sudden dyspnea, is indicative of PE. A massive PE may lead to hemodynamic instability, right heart failure, and obstructive shock.¹¹ If PE leads to chronic pulmonary hypertension, the condition can prevent blood from reaching the lungs, resulting in death.¹

Risk Factors

Several medical conditions are responsible for the majority of all VTE cases: undergoing a surgical procedure, hospitalization, the presence of cancer in the body and cancer treatment itself, and pregnancy and post-partum. Numerous preventive protocols, or thromboprophylaxis, have been developed to address these risks based on patient characteristics, genetic history, and disease characteristics. Implementation of routine comprehensive risk assessments have been encouraged by stakeholders, such as the American Heart Association, to reduce the burden of VTE for hospitalized patients.³

Hospital-acquired VTE is the leading cause of preventable hospital-associated death, despite conclusive evidence of the efficacy, safety, and cost-effectiveness of thromboprophylaxis for high-risk hospitalized medical and surgical patients.³ Thromboprophylaxis regimens for presurgical procedures and hospitalized patients as well as routine VTE risk assessments are still underutilized.^3,11

The necessity, method, and duration of VTE prophylaxis are determined by patient characteristics, risk assessments for both VTE and potential bleeding, and, if applicable, planned surgical procedure. Orthopedic surgical procedures present the highest risk for VTE events, with total hip and knee arthroplasty and hip or pelvic fractures on the high end, and procedures below the knee or upper extremities and arthroscopic procedures on the lower end of the risk continuum.¹¹ Thromboprophylaxis may include pharmacological and/or mechanical methods. Patients at low-risk who are not undergoing surgery may only require early ambulation or walking and use of mechanical compression or compression stockings. Conversely, patients deemed at high risk for bleeding events may also be prescribed mechanical prophylaxis, even if VTE risk is moderate to high.¹¹

Pharmacologic VTE prophylaxis for patients evaluated as moderate to high risk for VTE includes low-molecular-weight heparin (LMWH) or unfractionated heparin, and in some cases, direct oral anticoagulants (DOACs) such as dabigatran, apixaban, or rivaroxaban.^3,11 Patients generally discontinue pharmacologic prophylaxis upon discharge unless immobilized. Surgical patients may be required to extend this practice up to 2 weeks post-surgically, and those at highest risk, such as after abdominal or pelvic surgery for cancer and major orthopedic patients, may continue for as long as 35 days.¹¹

A variety of physiological processes involved in the invasion of cancer cells in the human body contribute to a prothrombotic state, which may directly and indirectly cause life-threatening thromboses. Patients with cancer have a six-fold risk of VTE compared to those without malignancies; cancer-associated thrombosis (CAT) is the second-leading cause of death after the cancer itself.¹² Among cancer patients, those who develop VTE have a mortality rate more than twice of those without this complication. For those with cancer, arterial embolism is an additional risk, potentially leading to stroke and myocardial infarction.¹³

Relative risk of VTE is highest among those with primary cancer sites in the brain, pancreas, stomach, and lungs as well as hematologic cancers. The risk is low in breast and prostate cancers.¹⁴ Risk of VTE actually increases dramatically among children and adolescents with cancer, and CAT among all age groups mostly occurs within the first 6 months of diagnosis.¹³ While VTE risk is also elevated among hospitalized patients receiving systemic chemotherapy, risk assessments and prophylactic anticoagulation therapies may be recommended based on patient-associated characteristics, and extended to post-surgical and outpatient treatment.¹²

Cancer can increase the risk of VTE in several ways, including when cancer cells enter the bloodstream and spread to other parts of the body. Cancer cells can also attach to blood vessel walls and release substances that activate platelets and fibrin, creating a hypercoagulable state that promotes blood clot formation.¹² This injury to the vessels, which may also include compression from a tumor mass, combined with hemostasis due to bed rest, and various systemic chemotherapies, recreate the classic triad of VTE risk in many cases.

Treatment of CAT includes the use of LMWH, while DOACs may be used for VTE prophylaxis or extended therapy.¹⁴ As the nature and duration of cancer treatment is highly variable, oral health professionals may encounter ambulatory patients seeking treatment for noncancer-related and routine dental care. Evaluation of treatment risks, especially bleeding and immune status, should be considered.

The risk of VTE during pregnancy is approximately five times higher than in the nonpregnant state and increases as delivery approaches.¹⁵ Additionally, this risk increases to nearly 60 times during the post-partum period, with a total worldwide incidence rate of 0.5 to two per 1,000 pregnancies and a mortality rate of one per 100,000 deliveries.¹⁵ These phenomena are attributed to what is known as the maternal hemostatic shift, a natural protective physiologic adaptation, which includes hypercoagulability and reduced fibrinolysis to prevent excessive hemorrhaging during delivery.¹⁵

During pregnancy, the growing fetus exerts pressure on the iliac veins, contributing to hemostasis, and late in gestation when maternal immobility is common, the situation meets the third risk factor of Virchow’s Triad. Endothelial trauma during delivery may add an additional risk, and VTE occurrence after a Caesarean birth is understandably greater. Individual factors that contribute to risk include maternal age, obesity, diabetes, thrombophilia, and family history of VTE. In recent years, clinical guidelines have added risk assessments for women with these predisposing factors. This has contributed to thromboprophylaxis strategies for pregnant women identified as high-risk.¹⁵ Anticoagulants used either for thromboprophylaxis during pregnancy and breastfeeding, or for women who develop VTE post-partum, include UFH and LMWH preferentially over warfarin and DOACs.¹⁵

Treatment

Risk evaluation, thromboprophylaxis, and treatment strategies are highly dependent on patient characteristics and history, followed by formalized predictive assessments and diagnostic testing for DVT and PE. Diagnostic testing may include blood assays, such as the D-dimer, which measures protein fragments from clot dissolution; ultrasonography; contrast venography to locate thrombi for DVT; and magnetic resonance pulmonary angiography, a nonradiation MRI with contrast dye for PE. Anticoagulant therapy is the mainstay of VTE treatment, and utilizes many of the same agents used for thromboprophylaxis: warfarin, DOACs, UFH, LMWH, and fondaparinux.^3,12,14–16 The duration of anticoagulant therapy following a VTE event is usually a minimum of 3 months, and 6 to 12 months for those with increased thrombosis burden, long-lasting risk factors, or significant PE events, and may be indefinite for unprovoked or recurrent VTE.¹¹

For all patients exhibiting symptoms, assessment and treatment become urgent. Diagnostic testing includes assessment of hemodynamic stability. If deemed hemodynamically unstable, anticoagulation therapy may be initiated before definitive diagnosis.³ Additionally, treatment for those with confirmed VTE in the highest risk categories or for whom drug therapy is ineffective, may go beyond standard anticoagulants and include pharmacological fibrinolysis to break down the clot, catheter-led or surgical embolectomy for clot removal, or more invasive treatment, such as intravascular filters.

In some situations, patients with VTE may benefit from a percutaneous insertion of inferior vena cava (IVC) filters, which are permanent or temporary medical devices.^17,18 The safety of IVC filters placement and removal has been continually improving, and currently, biocompatible and absorbable filters are being investigated. Nevertheless, this treatment is reserved only for specific situations where anticoagulation is absolutely contraindicated due to the type or trauma or very high bleeding risk.¹⁸ The current recommendation is to have the device removed when the risk of PE has subsided to prevent the adverse events associated with the IVC filters, including device migration, fracture, embolization, and perforation, as well as adverse outcomes of lower extremity DVT and IVC occlusion.¹⁹

In some instances, both DVT and PE may result in chronic complications. Post-DVT syndrome may produce ongoing pain and swelling primarily in the lower leg, managed by medications, therapy and exercise, but with symptoms that mimic recurrent DVT. PE may lead to chronic dyspnea or more serious pulmonary hypertension, where the damage to the pulmonary arteries interferes with effective transfer of oxygen and carbon dioxide, along with increased risk of heart failure.¹¹ For those who experience long-term complications, increased vigilance for VTE symptoms and anxiety over recurring thrombotic events has been shown to reduce quality of life measures in addition to the physical symptoms and limitations.²⁰

Dental Treatment Implications

The prevalence and severity of VTE events warrants the attention of all oral health professionals in examining patients’ medical and drug histories and determining and mitigating any risks while undergoing dental care. In most cases, these risks would primarily involve concerns for perioperative bleeding for those on continued anticoagulant agents for thromboprophylaxis as well as other cardiovascular concerns. Risks of discontinuation of anticoagulants most often outweighs the risk of bleeding events, except in cases of extensive oral maxillofacial procedures, multiple extractions, or surgery for head and neck cancers.²¹

Routine prophylaxis, scaling and root planing, and simple extractions would normally not require drug discontinuation, and a recent review suggests bleeding risk for dental implant surgery for patients on warfarin or DOACs does not result in significant bleeding when local hemostatic measures are used.²² In any case where discontinuation may be warranted, medical clearance from the prescribing physicians must be sought, and appropriate testing obtained. For heparin, medically supervised, short-term discontinuation may be advised for invasive procedures, and local hemostatic measures used for bleeding. For DOACs, consideration for dosage and peak blood level periods, or discontinuation should be coordinated with the advice of the prescribing physician.²¹

Oral health professionals’ awareness of the symptomatology of VTE, as well as treatment and associated risks and best practices, will ensure patients’ safety and successful outcomes of dental/dental hygiene treatment.

References

1. United States Centers for Disease Control and Prevention. Data and Statistics on Venous Thromboembolism. Venous Thromboembolism (Blood Clots). Available at cdc.gov/blood-clots/data-research/facts-stats/index.html. Accessed August 18, 2026.
2. Wenger N, Sebastian T, Engelberger RP, Kucher N, Spirk D. Pulmonary embolism and deep vein thrombosis: Similar but different. Thromb Res. 2021;206:88-98.
3. Henke PK, Kahn SR, Pannucci CJ, et al. Call to action to prevent venous thromboembolism in hospitalized patients: a policy statement from the American Heart Association. Circulation. 2020;141:e914-e931.
4. Zöller B, Svensson PJ, Dahlbäck B, Lind-Hallden C, Hallden C, Elf J. Genetic risk factors for venous thromboembolism. Expert Rev Hematol. 2020;13:971-981.
5. Áinle FN, Kevane B. Which patients are at high risk of recurrent venous thromboembolism (deep vein thrombosis and pulmonary embolism)? Blood Adv. 2020;4:5595-5606.
6. Iorio A, Kearon C, Filippucci E, et al. Risk of recurrence after a first episode of symptomatic venous thromboembolism provoked by a transient risk factor: a systematic review. Arch Intern Med. 2010;170:1710-1716.
7. Kumar DR, Hanlin E, Glurich I, Mazza JJ, Yale SH. Virchow’s contribution to the understanding of thrombosis and cellular biology. Clin Med Res. 2010;8:168-172.
8. Behravesh S, Hoang P, Nanda A, et al. Pathogenesis of thromboembolism and endovascular management. Thrombosis. 2017;2017:3039713.
9. Butenas S, Orfeo T, Mann KG. Tissue factor in coagulation: which? where? when? Arterioscler Thromb Vasc Biol. 2009;29:1989-1996.
10. Branchford BR, Carpenter SL. The role of inflammation in venous thromboembolism. Front Pediatr. 2018;6:142.
11. Stop the Clot. What Every Healthcare Professional Should Know. Available at stoptheclot.org/stop-the-clot-what-every-healthcare-professional-should-know-modules-1-6. Accessed August 18, 2026.
12. Donnellan E, Khorana AA. Cancer and venous thromboembolic disease: a review. Oncologist. 2017;22:199-207.
13. Khorana AA, Mackman N, Falanga A, et al. Cancer-associated venous thromboembolism. Nat Rev Dis Primer. 2022;8:11.
14. Fernandes CJ, Morinaga LTK, Alves JL, et al. Cancer-associated thrombosis: the when, how and why. Eur Respir Rev Off J Eur Respir Soc. 2019;28:180119.
15. Didembourg M, Morimont L, De Gottal E, Douxfils J. The maternal hemostatic shift: Understanding VTE risk in pregnancy and postpartum. Thromb Res. 2026;257:109561.
16. Khorana Risk Score for Venous Thromboembolism in Cancer Patients. MDCalc. Available at mdcalc.com/calc/3315/khorana-risk-score-venous-thromboembolism-cancer-patients. August 18, 2026.
17. Duffett L, Carrier M. Inferior vena cava filters. J Thromb Haemost. 2017;15:3-12.
18. Visconti L, Celi A, Carrozzi L, et al. Inferior vena cava filters: Concept review and summary of current guidelines. Vascul Pharmacol. 2024;155:107375.
19. FDA Updates Safety Communication on IVC Filter Retrieval. Endovascular Today. Available at evtoday.com/news/fda-updates-safety-communication-on-ivc-filter-retrieval. Accessed August 18, 2026.
20. Ghanima W, Wik HS, Tavoly M, Enden T, Jelsness-Jørgensen LP. Late consequences of venous thromboembolism: Measuring quality of life after deep vein thrombosis and pulmonary embolism. Thromb Res. 2018;164:170-176.
21. Boccatonda A, Frisone A, Lorusso F, et al. Perioperative management of antithrombotic therapy in patients who undergo dental procedures: a systematic review of the literature and network meta-analysis. Int J Environ Res Public Health. 2023;20:5293.
22. Zou L, Hua L. Risk of bleeding with dental implant surgery in patients on anticoagulant or antiplatelet drugs: a systematic review and meta-analysis. Acta Odontol Scand. 2023;81:98-104.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):28-31

Part two of a two-part series. Part one appears in the July/August 2026 issue.

Dentistry has long played a central role in facial esthetics. From full-mouth reconstruction, whitening, smile makeovers, to the integration of cosmetic procedures, such as neuromodulators and dermal fillers, oral health professionals routinely influence facial form, balance, and function. Despite the natural alignment of dentistry and esthetics, the incorporation of dermal fillers into dental practice is sometimes viewed as unconventional or even outside traditional boundaries. However, with their extensive knowledge of facial anatomy, oral health professionals are ideal providers to administer dermal fillers.

As fillers continue to evolve, particularly in tissue regeneration and collagen stimulation, their applicability in dentistry may increase both in cosmetic and periodontal procedures. The integration of dermal fillers may represent not a departure from dentistry, rather an extension of its long-standing commitment to comprehensive, patient-centered care.¹

Mechanism of Action for Dermal Fillers

Second only to botulinum toxin type A neuromodulators, dermal fillers rank among the most requested treatments in the esthetic industry, offering the ability to restore lost volume, enhance contours, and support overall facial harmony.² Unlike botulinum toxin type A neuromodulators that reduce wrinkles by inhibiting muscle contraction, dermal fillers can reduce wrinkles and improve skin texture by restoring volume loss.

Dermal fillers, like neuromodulators, are also injected, but not directly into muscle. Instead, dermal fillers are injected into or beneath the skin to add volume and enhance facial structures. By restoring volume to select areas, they can create the appearance of fuller, smoother, and more supple skin.²

Dermal fillers vary in viscosity and clinical purpose. Common components include hyaluronic acid (HA), calcium hydroxylapatite, and biostimulatory polymers such as poly-L-lactic acid (PLLA) and polycaprolactone (PCL).³ Hyaluronic fillers are hydrophilic and restore volume by attracting and binding to water molecules, increasing water retention, tissue hydration, and structural support. These fillers are widely used to enhance facial contours, such as cheeks, lips, and chin, providing both immediate volumizing effects and subtle lifting while smoothing lines and wrinkles.³

Beyond simple volume augmentation, PLLA and PCL fillers demonstrate biostimulatory effects, promoting neocollagenesis and longer-term tissue regeneration in soft tissues. This regenerative potential has expanded their clinical relevance beyond esthetic enhancement into applications aimed at facial form and function.⁴

Applications of Dermal Fillers

Dermal fillers with biostimulant properties promote collagen production and influence tissue quality at a cellular level. Gingival recession is a challenging condition due to limited restorative treatment options. In addition to esthetic concerns, recession frequently results in dentinal hypersensitivity, which may make routine dental hygiene care uncomfortable for patients. Even with topical remineralizing or desensitizing agents, many patients continue to experience sensitivity issues that impact their overall oral care experience.³

Evidence in periodontal literature suggests that HA plays an active role in wound healing and regeneration, enhancing periodontal parameters when used adjunctively with traditional periodontal therapy.⁵ Moreover, some clinical data indicate potential benefits of HA in reducing probing depths and improving clinical attachment levels in recession and periodontal defects.⁶

The regenerative properties of specific dermal fillers, particularly those designed to stimulate collagen synthesis, offer a promising adjunctive approach in managing tissue volume loss. Injecting such fillers into the gingiva where recession is present may restore tissue contour, improve the gingival margin profile, and support underlying periodontal structures.³ While formal clinical trials specifically investigating filler injections for the purpose of reversing gingival recession are emerging, the biologic rationale parallels how HA supports extracellular matrix modulation that guides tissue cell growth and healing.⁶

Dermal fillers are also being explored for interdental use by injecting filler directly into the interdental papilla to correct flattened or blunted papillae following periodontal therapy. By restoring tissue height and volume, dental hygienists can address both esthetic and functional outcomes, promoting improved gingival architecture without compromising tissue appearance. This approach offers a unique opportunity to complement traditional periodontal therapy, enhancing patient satisfaction and supporting comprehensive treatment goals that prioritize both tissue health and facial esthetics.³

Esthetic Enhancements

Beyond gingival applications, dermal fillers play a critical role in comprehensive facial esthetics that support intraoral restorative and cosmetic procedures. Dermal fillers complement esthetic and restorative dentistry by restoring extraoral tissue volume and supporting facial structures that directly influence the appearance and balance of a patient’s smile.

Patients who invest in veneers, orthodontics, or comprehensive smile makeovers may still be dissatisfied with subtle age-related changes, such as thinning lips, hollowed cheeks, or downward-turning smile lines caused by loss of soft tissue volume and collagen.² Addressing these extraoral factors allows clinicians to offer a truly comprehensive smile restoration that considers the teeth, soft tissues, and surrounding facial framework as interconnected elements of esthetics.

These fillers are not only used to restore volume but also to enhance overall facial balance and proportion. Strategic placement can subtly adjust facial contours, supporting esthetic outcomes that complement restorative or cosmetic dental procedures. For example, adding volume to the chin can help elongate the jawline and soften the appearance of a Class II occlusion profile, improving lower-face balance. Conversely, carefully augmenting the nasal area can create visual harmony for patients with a Class III occlusion profile, softening concavities and enhancing midface proportion. By thoughtfully applying dermal fillers in this way, clinicians can provide a more balanced and youthful facial contour, ultimately supporting the esthetic results of restorative and cosmetic treatments.²

Beyond volume and proportion, dermal fillers can also improve lip hydration, enhance midface fullness, and subtly lift areas affected by age-related soft tissue loss. These enhancements not only contribute to facial harmony but also reinforce the esthetic outcomes of intraoral procedures, ensuring that the patient’s smile appears natural and integrated with the surrounding facial tissues. When incorporated thoughtfully into dental practice, dermal fillers allow clinicians to deliver a patient-centered approach that treats the face holistically improving appearance while supporting patient confidence and satisfaction.²

Adverse Reactions and Medical Emergencies

While dermal fillers offer significant esthetic and functional benefits, their administration carries an inherent risk that demands heightened clinical vigilance. Because fillers are typically delivered using larger-gauge needles and placed into deeper tissue planes than neuromodulators or when administering local anesthetics, the potential for serious adverse events, including vascular compromise, is increased.²

Clinicians must possess a comprehensive understanding of facial anatomy, appropriate injection depth, product selection, volume control, aspiration techniques, and expected diffusion profiles. Additionally, safe administration of dermal fillers also requires a strong foundation in pathophysiology and pharmacology, along with careful review of the patient’s medical history, to identify contraindications and prevent adverse reactions or allergic responses. Failure to account for these factors can jeopardize patient safety and outcomes.² Although many complications, such as bruising, resolve over time, others can lead to permanent tissue damage due to vascular occlusion.

Bruising and Vascular Occlusion

Bruising (ecchymosis) at the injection site is a common and expected outcome of dermal filler procedures, but its severity and duration can vary significantly depending on the patient’s anatomy, the injection technique, and product type. Skilled clinicians can minimize bruising by carefully selecting injection sites that avoid dense vascular regions, using appropriate needle or cannula sizes, controlling injection depth, and moderating the volume and speed of product delivery. Pre- and post-procedure measures also play a key role: patients should avoid anticoagulant or antiplatelet medications when medically safe, limit alcohol and certain supplements that increase bleeding risk, and apply cold compresses immediately after treatment to reduce capillary damage and inflammation.²

Additionally, patient-specific factors, such as age, skin thickness, and vascular fragility, should be considered during treatment planning. Gentle handling of soft tissues, precise anatomical knowledge, and real-time assessment during injection can help further reduce the risk of significant bruising.

Vascular occlusion is a rare but serious complication, potentially leading to tissue ischemia, necrosis, or vision loss without prompt treatment. A systematic review of vascular occlusion following filler injections confirms that anatomical regions with complex vasculature, such as the glabella, nose, and nasolabial folds, are most frequently implicated.⁷

Clinicians must differentiate between routine bruising and signs of occlusion, which often present with disproportionate pain, pallor, and delayed capillary refill.^7,8 Vascular occlusion is very serious and immediate treatment is necessary to avoid permanent damage. Treatment typically involves the administration of hyaluronidase, warm compresses, and gentle massage to break down the occluding filler and restore blood flow and oxygen to the tissues.^9,10 However, without immediate treatment, patients have been subjected to unrepairable tissue necrosis and vision loss due to filler occluding the ophthalmic artery.¹¹

Emerging technologies, such as vascular mapping and ultrasound visualization, can assist clinicians in identifying superficial blood vessels, helping to avoid intravascular trauma and further decreasing the likelihood and severity of bruising. Educating patients about expected post-procedure changes, the normal timeline for bruising resolution, and strategies to manage discoloration not only improves safety but also enhances patient confidence and satisfaction with the procedure.² However, these tools used to enhance visualization of the underlying tissue and vascularity should supplement, not replace, clinical knowledge, advanced training, and sound judgment.

Dental Hygienists’ Preparedness and Practice Integration

While some view the administration of dermal fillers as outside the traditional boundaries of dentistry, dental hygienists possess the combination of anatomical knowledge, clinical judgment, and patient-centered chairside experience necessary to successfully inject dermal fillers. Although several states permit dentists to administer both dermal fillers and neuromodulators, only a small number of states currently authorize dental hygienists to inject dermal fillers or administer neuromodulators.^12-17

While scope of practice and the stipulations for the administration of dermal fillers vary considerably from state to state, these regulatory limitations do not reflect the profession’s capabilities. Dermal fillers can be a valuable addition to the dental hygienist’s therapeutic arsenal to better serve their patients.

Dental hygienists are uniquely prepared to contribute to the safe and effective delivery of facial esthetic services. Their foundational education includes training in head and neck anatomy, pharmacology, pain control, and recognition/management of medical emergencies. Combined with hands-on experience administering intraoral injections, monitoring patient responses, and delivering chairside care, dental hygienists bring high-level competence and patient-centered focus to facial esthetic procedures.²

Even where state regulations preclude hygienists from administering fillers themselves, their contributions to facial esthetic services remain substantial. Hygienists can support these procedures through patient intake, education, pre- and post-operative photos, and medical history review. This collaborative approach enhances efficiency, improves patient experience, and allows dental providers to focus on technical aspects of filler administration.

References

1. de Castro Costa M, Andrade CA, Dantas RVF, Germani M, Buzalaf MAR, Soares DG. Clinical durability of hyaluronic acid-based dermal fillers for facial application: a systematic review. Aesthetic Plast Surg. 2026;50:1971-1993.
2. Maci M, Fanelli C, Lorusso M, Ferrara D, Caroprese M, Laurenziello M, et al. Botulinum toxin type A and hyaluronic acid dermal fillers in dentistry: a systematic review of clinical application and indications. J Clin Med Res. 2024;16:273-283.
3. Ruiz-de-León G, Cortés-Eslava D, Hernández-Pacheco E, Serrera-Figallo MÁ, Torres-Lagares D, Baus-Domínguez M. Biopolymers in facial aesthetics: gel-based applications, safety, effectiveness, and future prospects—a systematic review of the literature. Gels. 2025;11:455.
4. Haddad S, Galadari H, Patil A, Goldust M, Al Salam S, Guida S. Evaluation of the biostimulatory effects and the level of neocollagenesis of dermal fillers: a review. Int J Dermatol. 2022;61:1284-1288.
5. Kalimeri E, Roccuzzo A, Stähli A, et al. Adjunctive use of hyaluronic acid in the treatment of gingival recessions: a systematic review and meta-analysis. Clin Oral Investig. 2024;28:329.
6. Malcangi G, Inchingolo AD, Trilli I, Ferrante L, Casamassima L, Nardelli P, et al. Recent use of hyaluronic acid in dental medicine. Materials (Basel). 2025;18:1863.
7. Hong GW, Hu H, Chang K, et al. Adverse effects associated with dermal filler treatments: part II vascular complication. Diagnostics (Basel). 2024;14:1555.
8. Soares DJ. Bridging a century-old problem: the pathophysiology and molecular mechanisms of HA filler-induced vascular occlusion (FIVO)—implications for therapeutic interventions. Molecules. 2022;27:5398.
9. Wang R, Li Y, Li Z, Yao H, Zhai Z. Hyaluronic acid filler-induced vascular occlusion—three case reports and overview of prevention and treatment. J Cosmet Dermatol. 2024;23:1217-1223.
10. Fabi SG, Desyatnikova S, Dayan SH. Prevention and management of dermal filler complications: a review. Facial Plast Surg Aesthet Med. 2025;27:120-124.
11. Mehta P, Kaplan JB, Zhang-Nunes S. Ischemic complications of dermal fillers. Plast Aesthet Res. 2022;9:57.
12. New Mexico. Administration of Botulinum Neurotoxin (Botox) and Dermal Fillers, NM Admin Code § 16.5.14.8. Available at https://www.srca.nm.gov/parts/title16/16.005.0014.html. Accessed August 18, 2026.
13. Oregon Board of Dentistry. Scope of Practice. Available at oregon.gov/dentistry/Pages/scope-practice.aspx. Accessed August 18, 2026.
14. Permit for the Use of Dermal Fillers and Botulinum Toxin for Dental Use. Available at ndlegis.gov/information/acdata/pdf/20-02-01.pdf. Accessed August 18, 2026.
15. State of Alabama. Administration of Botulinum Toxin and Similar Treatments by Dentists. Available at https://dentalboard.org/wp-content/uploads/2024/09/BDEAL-APA3-270-X-2-.25-Administration-of-Botulinum-Toxin-and-Similar-Treatments-by-Dentists.pdf.
16. Oklahoma State Board of Dentistry. Advanced Procedures for Dental Hygienists: Neuromodulator Administration. Available at law.cornell.edu/regulations/Oklahoma/OAC-195-15-1-6.1. Accessed August 18 2026.
17. Arizona State Dental Board. Recent Rules Approved. Available at https://dentalboard.az.gov/rules. Accessed August 18, 2026.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):32-35

As life expectancy increases, age-related conditions, such as neurodegenerative diseases and periodontitis, are becoming more prevalent.^1,2 Mild cognitive impairment is one of the earliest signs of declining brain function, affecting memory, language, and judgment. These changes indicate an increased likelihood of developing neurodegenerative diseases, such as dementia.^1,3

Dementia is an umbrella term used to describe progressive loss of cognitive abilities that interferes with daily life. Alzheimer disease (AD), the most common type of dementia, accounts for 60% to 80% of all dementia diagnoses. AD is characterized by progressive cognitive decline and currently no curative treatment exists, leaving early intervention as the most effective strategies for managing daily life.⁴

Oral health represents one potentially modifiable factor. Periodontitis affects nearly half of adults in the United States and remains the leading cause of tooth loss.^5–8 While largely preventable, periodontitis cannot be reversed once established, but it can be managed through professional care and improved oral hygiene.⁸ This disease contributes to a persistent proinflammatory state through bacterial dysbiosis and host immune responses, creating potential systemic effects. As evidence increasingly associates systemic inflammation with accelerated cognitive decline, the intersection of periodontitis and dementia has gained attention.^2,5,9 Understanding this relationship may help refine preventive strategies and clarify how cognitive decline impacts periodontal health and vice versa.

How Periodontitis Impacts Dementia

Chronic inflammation is a common feature of both periodontitis and dementia. Gram-negative periodontal pathogens stimulate a sustained host immune response, prompting the release of proinflammatory cytokines. These cytokines may circulate systemically and affect distant organ systems, including the central nervous system. Multiple studies suggest that elevated systemic inflammation can increase the permeability of the blood-brain barrier (BBB). Once the BBB is compromised, cytokines may enter neural tissue, activating glial cells and contributing to the type of neuroinflammation seen in AD.^10–13 Although more studies are needed, this pathway represents a biologically plausible connection between the two conditions.

Another potential mechanism of etiologic crossover is the migration of oral pathogens into the brain. Inflammatory changes may make the BBB more permeable, allowing oral pathogens to enter neural tissue. Lipopolysaccharide (LPS) endotoxins produced by the periodontal pathogen Porphyromonas gingivalis have been identified in the brain tissue of individuals with AD.^14,15 LPS is known to trigger neural cell responses that can worsen cognitive dysfunction, including the dysfunction seen in AD.¹⁰ The presence of LPS in brain tissue alone does not clearly indicate that higher levels are associated with more severe stages of periodontitis, because the samples studied were only obtained from individuals with moderate to severe disease.¹⁴

Further research suggests an alternative pathway for oral microbial invasion of the brain. Oral bacteria, such as P. gingivalis, Treponema denticola, and Tannerella forsythia, have been identified in post-mortem brain samples, suggesting a connection between these sites. Researchers have proposed that these pathogens may reach neural tissue through systemic circulation and peripheral nerves, like the trigeminal nerve.^2,10–12 While this theory is still emerging, the presence of oral bacteria within neural tissue reinforces the possibility of a direct oral-brain link.

Amyloid beta (Aβ) protein dysregulation, a hallmark of AD, may also be influenced by periodontal inflammation. In healthy brains, Aβ is continually removed through lymphatic flow during sleep, but chronic inflammation may impair this process.^{9,11,12,15,16} Healthy older adults with periodontitis have been shown to exhibit higher Aβ deposition in brain regions vulnerable to AD, including the posterior cingulate cortex/precuneus, prefrontal cortex, lateral temporal lobe, middle frontal gyrus, and parietal lobule. Because peripheral inflammation influences Aβ accumulation in these regions, chronic inflammation associated with periodontitis may further contribute to neurodegeneration.^11,12,15

Although inflammatory signaling, microbial translocation, and Aβ dysregulation are often discussed as separate processes, current literature suggests these mechanisms may occur concurrently rather than independently. Chronic periodontal inflammation may contribute to a sustained systemic immune response that can increase BBB permeability and influence exposure of neural tissue to inflammatory mediators and microbial byproducts.^10–12,15 Repeated exposure to these factors may promote microglial activation and ongoing neuroinflammatory responses, processes commonly observed in dementia.^5,10–12 Regardless of the mechanisms, the substantial evidence in support of periodontitis impacting neurodegeneration is significant.

Clinical Evidence Supporting the Connection

The use of standardized cognitive testing provides additional support for these relationships. In one clinical trial, patients with active periodontitis demonstrated a greater decline on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale over 6 months compared with those without periodontitis.¹⁷ Another study using the Mini-Mental State Examination cognitive test found that individuals with P. gingivalis present in their saliva were at an increased risk for developing AD.² Similarly, additional research suggests that periodontitis may increase the risk of developing AD by 1.7-fold.^12,18

When considered collectively, findings from epidemiological studies, standardized cognitive assessments, and proposed biological mechanisms indicate an association between periodontitis and dementia.^5,7,11,12,17 Even though a causal relationship has not been established, the consistency of observations across multiple study designs supports continued attention to periodontal health as one factor relevant to cognitive aging and neurodegenerative disease risk.^6,12,18 While the above mechanisms describe how periodontitis may influence cognitive decline, it is also important to explore the impact dementia may have on periodontal health.

How Dementia Impacts Periodontal Health

Dementia frequently alters behavior, communication, and daily functioning.^7,19 As dementia progresses, individuals often become increasingly dependent on caregivers for oral hygiene. This loss of autonomy can contribute to agitation or refusal of care, complicating efforts to provide consistent daily plaque removal. Not surprisingly, these behavioral barriers can lead to poor oral hygiene and increase susceptibility to periodontitis.¹⁹

Many individuals with cognitive impairment are unable to verbalize oral pain or discomfort, so caregivers must rely on nonverbal cues such as facial expressions, vocalization, or changes in behavior. Unfortunately, this often leads to delayed or insufficient treatment. More frequent dental examinations for older adults with dementia, as well as proper oral health education provided by oral health professionals, can be methods to combat behavioral barriers to oral care.¹⁹

Physical impairments, such as declining coordination and fine motor control, develop as AD progresses, limiting patients’ ability to brush effectively, manipulate floss, or rinse and expectorate. Research shows that oral hygiene performance worsens with increasing dementia, even when individuals remain motivated to care for their teeth due to the associated physical impairments.^7,20 These limitations contribute to an increase in plaque accumulation and subsequently raise the risk for periodontitis.²⁰

Because these functional limitations impact a patient’s ability to perform routine oral hygiene self-care, leading to increased plaque accumulation and a higher risk for periodontitis, adaptive self-care tools can help compensate for diminished motor control. Guided brushing or supervised oral hygiene care may also reduce frustration for both caregivers and patients. Tailoring oral hygiene recommendations to a patient’s abilities is essential for maintaining periodontal stability and supporting patients in ways that preserve independence as much as possible.^20,21

Salivary dysfunction is another contributing factor to periodontitis. Reduced salivary flow, or xerostomia, may arise from commonly prescribed medications for dementia, including antidepressants and sedatives, or may result from general aging and disease-related physiological changes.^21,22 Reduced saliva increases the risk of dental caries, candidiasis, oral malodor, and plaque retention, all of which contribute to periodontal breakdown.²¹ Understanding the multifactorial causes of xerostomia allows clinicians to personalize preventive strategies.

Genetic susceptibility and age appear to shape the relationship between periodontitis and neurodegeneration. The APOE4 allele, a major genetic risk factor for AD, increases vulnerability to periodontal pathogens and intensifies infection-driven neuroinflammation. Toxic enzymes produced by P. gingivalis known as gingipains can cleave APOE4, amplifying Aβ pathology. Young adults with dementia have the highest risk of developing periodontitis, likely due to greater biological susceptibility and more rapid functional decline. Similarly, bidirectional evidence suggests that chronic periodontitis increases risk for dementia across the lifespan, but the association is often more pronounced in younger groups.^6,7,12

Systemic comorbidities further magnify these relationships. Conditions such as hyperlipidemia, diabetes, stroke, cardiovascular disease, chronic obstructive pulmonary disease, and hypertension, increase the risk of periodontitis in populations with dementia, with hyperlipidemia emerging as one of the strongest modifiers of risk. More severe or progressing periodontitis, reflected by tooth extraction or surgical treatment, is also linked to higher dementia risk.^7,11,12 Together, these genetic, age-related, and systemic factors suggest that periodontitis functions as a modifiable contributor within the broader neuroinflammatory landscape of dementia.^6,7,11,12

The Role of the Dental Hygienist

Dental hygienists play a vital role in preventing and managing oral diseases and may indirectly influence health outcomes. Uniquely positioned within healthcare to identify early signs of periodontal inflammation,⁸ dental hygienists routinely perform clinical evaluations of the periodontium. Also, dental hygienists provide consistent professional care, including periodontal assessments, nonsurgical periodontal therapy when indicated, and ongoing periodontal maintenance, all of which are essential for controlling chronic inflammation and limiting systemic disease.¹⁸

Moreover, dental hygienists may be among the first healthcare providers to observe changes that could indicate declining cognitive or physical functional status. Patterns such as missed appointments, decreased oral hygiene effectiveness, or increased caregiver involvement may suggest the need for adjusted care strategies or further evaluation.^7,19,20 When working with patients who have diminished decision-making capacity, informed consent may need to involve family members with healthcare proxy or medical power of attorney, or legal caregivers. In these situations, dental hygienists can encourage communication between patients, caregivers, and other healthcare professionals when concerns related to cognitive function arise. These considerations ensure both ethical and effective care.^19–21

In addition to providing routine clinical care, dental hygienists are well-positioned to educate patients and caregivers about risk factors for disease, as well as supporting patients in adopting effective preventive behaviors.⁸ Self-care recommendations should be individualized to the needs of patients, as well as patient and caregiver abilities. Adaptive devices, such as electric toothbrushes, modified toothbrush handles, and water flossers, can support patients with reduced dexterity. However, dental hygienists must assess the patient’s ability to swallow before recommending mouthrinses or water flossers to avoid aspiration risk.^20,22

As cognitive impairment progresses, responsibility for daily oral hygiene often shifts to caregivers who may have limited experience or training.^19,22 Clear instructions, simplified techniques, and realistic expectations may support greater consistency with oral care while reducing caregiver burden.^19,20 Reinforcement through demonstration, written materials, and follow-up during maintenance visits may further support long-term oral health outcomes.^20,22

While the presence of periodontitis alone is not the sole contributing factor to dementia, chronic, sustained systemic inflammation and host immune response may play a significant role in cognitive decline.^5,6 Ultimately, understanding the oral systemic connection empowers dental hygienists to provide care that supports not only oral health but also overall quality of life. By adapting preventive and supportive strategies to individual patient capabilities, dental hygienists can assist in maintaining periodontal stability while addressing the practical challenges associated with dementia.^18–22 This approach reflects the broader oral-systemic relationship and supports interdisciplinary care for patients experiencing cognitive decline.^6,19

Conclusion

Current evidence suggests a meaningful relationship between periodontitis and neurodegenerative diseases supported by proposed mechanisms involving inflammation dysregulation, microbial migration, and Aβ interactions. Conversely, dementia introduces behavioral, physical, and salivary challenges that increase periodontal susceptibility. Although the precise nature of this bidirectional relationship has yet to be determined, the implications for dental hygienists are clear: preventive care, patient-specific education, and adaptation to functional limitations are essential.

While existing research describes an association between periodontitis and dementia, several limitations should be considered when interpreting these findings. Much of the available evidence is observational, which limits the ability to establish causality. Differences in study design, definitions of periodontitis, cognitive assessment methods, and population characteristics also make direct comparison across studies challenging. For these reasons, periodontitis is best understood as one of several potentially modifiable factors within a complex and multifactorial disease process, rather than as an independent cause of dementia.

Despite these limitations, findings across studies consistently suggest a relationship between oral inflammation and cognitive decline exists. Preventive periodontal care, early identification of disease, and individualized maintenance may help manage chronic inflammatory burden over time. Additional research is needed to further clarify underlying mechanisms and to determine the potential impact of sustained periodontal management on cognitive outcomes. However, understanding these interconnected processes allows dental hygienists to more effectively support patients and caregivers, and potentially contribute to strategies that lessen the broader impact of dementia.

References

1. National Institute on Aging. What Is Mild Cognitive Impairment? Available at alzheimers.gov/alzheimers-dementias/mild-cognitive-impairment. Accessed August 22, 2026.
2. Leblhuber F, Huemer J, Steiner K, Gostner JM, Fuchs D. Correction to: Knock-on effect of periodontitis to the pathogenesis of Alzheimer’s disease? Wien Klin Wochenschr. 2020;132:549-550.
3. Mayo Clinic. Mild Cognitive Impairment: Symptoms and Causes. Available at mayoclinic.org/diseases-conditions/mild-cognitive-impairment/symptoms-causes/syc-20354578. Accessed August 22, 2026.
4. United States Centers for Disease Control and Prevention. About Dementia. Available at cdc.gov/alzheimers-dementia/about/index.html. Accessed August 22, 2026.
5. Farsi DN, Abadalkareem R, Linden GJ, et al. Periodontitis and incident cognitive decline and dementia: A 15-year prospective cohort study of older men residing in Northern Ireland. J Alzheimers Dis. 2026;109:980-995.
6. Harding A, Singhrao SK. Periodontitis and dementia: a bidirectional relationship? J Dent Res. 2022;101:245-246.
7. Ma KS, Hasturk H, Carreras I, et al. Dementia and the risk of periodontitis: a population-based cohort study. J Dent Res. 2022;101:270-277.
8. Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primer. 2017;3:17038.
9. Laugisch O, Johnen A, Buergin W, et al. Oral and periodontal health in patients with alzheimer’s disease and other forms of dementia – a cross-sectional pilot study. Oral Health Prev Dent. 2021;19:255-261.
10. Said-Sadier N, Sayegh B, Farah R, et al. Association between periodontal disease and cognitive impairment in adults. Int J Environ Res Public Health. 2023;20:4707.
11. Hwang G, Lee SH, Han SW, et al. Longitudinal association of chronic periodontitis with all-cause dementia, Alzheimer disease, vascular dementia, and mild cognitive impairment: a distributed network analysis. GeroScience. 2026;48:3151-3163.
12. Wagaskar P, Gaikwad S, Suryawanshi M, Patil A. The link between oral health and neurodegeneration: a review of periodontitis in Alzheimer’s and Parkinson’s disease and dementia. Inflammopharmacology. 2025;33(9):5023-5036.
13. Chen CK, Wu YT, Chang YC. Association between chronic periodontitis and the risk of Alzheimer’s disease: a retrospective, population-based, matched-cohort study. Alzheimers Res Ther. 2017;9:56-57.
14. Guo H, Chang S, Pi X, et al. The effect of periodontitis on dementia and cognitive impairment: a meta-analysis. Int J Environ Res Public Health. 2021;18:6823.
15. Kamer AR, Pirraglia E, Tsui W, et al. Periodontal disease associates with higher brain amyloid load in normal elderly. Neurobiol Aging. 2015;36:627-633.
16. Keil SA, Jansson D, Braun M, Iliff JJ. Glymphatic dysfunction in Alzheimer’s disease: A critical appraisal. Sci Am Assoc Adv Sci. 2025;389:8269.
17. Ide M, Harris M, Stevens A, et al. Periodontitis and cognitive decline in alzheimer’s disease. PloS One. 2016;11:e0151081.
18. Leira Y, Vivancos J, Diz P, Martín Á, Carasol M, Frank A. The association between periodontitis and cerebrovascular disease, and dementia. Scientific report of the working group of the Spanish Society of Periodontology and the Spanish Society of Neurology. Neurol Barc Engl Ed. 2024;39:302-311.
19. Lauritano D, Moreo G, Della Vella F, et al. Oral health status and need for oral care in an aging population: a systematic review. Int J Environ Res Public Health. 2019;16:4558.
20. Shirobe M, Edahiro A, Motokawa K, et al. Association between dementia severity and oral hygiene management issues in older adults with alzheimer’s disease: a cross-sectional study. Int J Environ Res Public Health. 2023;20:3841.
21. Gao SS, Chu CH, Young FYF. Oral health and care for elderly people with alzheimer’s disease. Int J Environ Res Public Health. 2020;17:5713.
22. Foley NC, Affoo RH, Siqueira WL, Martin RE. A systematic review examining the oral health status of persons with dementia. JDR Clin Transl Res. 2017;2:330-342.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):36-39

Erythema multiforme (EM) is an acute, immune-mediated dermatologic condition characterized by distinctive target-like lesions of the skin and (Figures 1 and 2), in more severe cases, painful erosions of the mucous membranes. Because EM may involve both cutaneous and mucosal surfaces, nurses play a critical role in comprehensive patient assessment, including evaluation of pain, hydration status, nutritional intake, and the risk for secondary infection. In cases with extensive oral or respiratory involvement, vigilant monitoring for potential airway compromise is essential.

Effective management of EM often requires interprofessional collaboration (IPC) among nurses, physicians, and oral health professionals.¹ Nurses serve as key facilitators of communication between medical and dental teams, particularly when mucosal disease compromises oral health and quality of life.

The World Health Organization defines IPC as a process in which multiple healthcare professionals work together with patients, families, caregivers, and communities to deliver coordinated, patient-centered care.² This collaborative network commonly includes mental health providers, primary and specialty care physicians, nurse practitioners, registered dietitians, social workers, psychologists,and pharmacists.^3,4 Oral health professionals are also essential members of this team, contributing to disease prevention, early detection, and health promotion across the lifespan.

Erythema Multiforme Major and Minor

Erythema multiforme is traditionally categorized into EM minor and EM major, with EM minor defined by typical target lesions with minimal or no mucosal involvement, while EM major includes both target lesions and significant mucosal involvement. These forms of EM are most commonly associated with infectious triggers, particularly herpes simplex virus, and are distinguished by their characteristic raised, targetoid morphology.

In contrast, mycoplasma pneumoniae–induced rash and mucositis (MIRM) and reactive infectious mucocutaneous eruption (RIME) have emerged as related but distinct post-infectious mucocutaneous syndromes. The classification of MIRM and RIME, and their relationship to EM, remains debated. Some experts consider these conditions to fall within the broader EM spectrum, whereas others regard them as separate entities. Clinically and histopathologically, MIRM and RIME share notable overlap with EM major, particularly in their mucosal involvement, though their cutaneous manifestations are typically sparse or atypical compared with the classic target lesions of EM.

Mycoplasma pneumoniae infection may also precipitate an epidermal necrolysis pattern, and some patients demonstrate overlapping features of EM and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN). Differentiating MIRM/RIME from SJS/TEN is essential because management strategies differ significantly, especially given the more severe course and drug-associated etiology typical of SJS/TEN.

Although EM is most commonly infection related and SJS/TEN is usually drug-induced, the clinical presentation remains the most reliable method of distinguishing these syndromes. EM is defined by typical or atypical raised target lesions, whereas SJS/TEN is characterized by flat purpuric macules that progress to vesicles, bullae, and widespread epidermal detachment. Skin detachment in EM is generally limited, and outcomes are more favorable than in SJS/TEN. Nonetheless, the nosology of these disorders remains complex, as epidermal necrolysis can occur in both EM-related conditions and SJS/TEN, contributing to diagnostic uncertainty.

Rather than relying on the traditional major/minor classification, a more practical approach categorizes acute EM as severe or nonsevere, based on the extent and severity of mucosal involvement. Chronic EM can be severe if it includes prominent mucosal disease (EM major). It is nonsevere if it remains primarily a skin-limited condition (EM minor).

Chronic EM may be recurrent or persistent, often presenting with recalcitrant lesions that intensify during disease flares. Recurrent EM is defined by repeated episodes over several years, with studies reporting an average of approximately six episodes annually and a disease duration of 6 to 10 years. Persistent EM is characterized by the continuous presence of typical or atypical target lesions without periods of complete resolution. Bullous lesions are frequently observed, and mucosal involvement may occur but is not universal.

Diagnostic Confusion with Pemphigus Vulgaris

Pemphigus vulgaris (PV) is a chronic autoimmune mucocutaneous blistering disorder caused by autoantibodies targeting desmogleins, resulting in intraepithelial blister formation. Oral lesions are the initial manifestation in approximately 50% to 70% of cases, and the condition may clinically resemble EM, particularly when painful mucosal erosions are present.

According to the British Association of Dermatologists, management of PV consists of two phases: induction, aimed at controlling disease activity, and maintenance, focused on preventing relapse while minimizing drug exposure.⁵ Systemic corticosteroid dosing is guided by disease severity, with mild cases treated at 0.5 to 1 mg/kg/day and severe cases requiring up to 2 mg/kg/day.⁵ Once disease activity is controlled, corticosteroids are tapered gradually.

Systemic steroids are often combined with immunosuppressive agents, such as azathioprine, mycophenolate mofetil, cyclophosphamide, or methotrexate, as well as immunomodulatory therapies including intravenous immunoglobulin or immunoadsorption.⁶ Oral lesions may be managed with topical corticosteroids or intralesional injections for refractory disease.⁷

Misdiagnosing PV as EM can significantly affect patient outcomes. EM is typically self-limiting and often requires supportive care, whereas PV necessitates prolonged immunosuppressive therapy. Therefore, thorough clinical evaluation and appropriately performed biopsies remain essential in patients presenting with persistent mucosal lesions.

Medication-Induced Erythema Multiforme

The skin is the organ most frequently affected by adverse drug reactions, occurring in up to 10% of hospitalized patients and approximately 1% to 3% of individuals taking multiple medications. Nearly 30 distinct cutaneous drug reaction patterns have been described, ranging from mild eruptions to life-threatening conditions such as SJS/TEN.

Managing drug-induced skin reactions is particularly complex in older adults with polypharmacy. These cases highlight the need for heightened vigilance, especially when prescribing psychiatric or high-risk medications. Early recognition and prompt discontinuation of the offending agent are essential to prevent progression to severe cutaneous adverse reactions.⁸

Norimatsu and Norimatsu⁹ described an elderly woman who developed a drug-induced reaction after initiation of raloxifene for osteoporosis. A drug-induced lymphocyte stimulation test confirmed raloxifene as the causative agent, underscoring the importance of diagnostic testing in complex presentations.

Relationship Between Herpes and Erythema Multiforme

EM is primarily mediated by a cell-mediated immune response, with infections accounting for approximately 90% of cases. Herpes simplex virus (HSV) type 1 is the most common trigger, followed by HSV-2 and mycoplasma pneumoniae, particularly in pediatric populations.

The pathogenic mechanisms differ between infection-triggered and drug-induced EM. In HSV-associated EM, autoreactive T-cells target keratinocytes expressing viral DNA polymerase, resulting in epidermal injury.^10,11 In contrast, drug-induced EM is mediated by cytokines such as tumor necrosis factor-α, perforin, and granzyme B, leading to widespread epidermal damage.^10,11

Clinically, HSV-associated EM typically presents with classic target lesions, minimal mucosal involvement, and a self-limited course with no reported mortality.¹⁰ Drug-induced EM, however, often begins with a flu-like prodrome and progresses to blistering lesions with prominent mucosal involvement.¹²

External factors, such as trauma and ultraviolet exposure, may also influence lesion distribution, as lesions may appear in previously sunburned areas.¹³ Early recognition of severe cutaneous adverse reactions is essential to prevent progression to life-threatening conditions such as SJS/TEN.^14-16

Photobiomodulation Therapy

Photobiomodulation therapy (PBM) has been utilized in the management of fluconazole‑ induced oral EM, offering a noninvasive approach that supports healing and symptom reduction. Reports describe the laser parameters commonly used, along with positive treatment outcomes such as decreased pain, accelerated lesion resolution, and improved patient comfort. Proposed mechanisms include PBM’s ability to modulate inflammation, enhance cellular repair, and promote tissue regeneration. Practical clinical guidelines emphasize proper laser settings, consistent application protocols, and careful monitoring to ensure safe and effective integration of PBM into EM management.¹⁷

Clinical outcomes reported with this approach include immediate and significant pain reduction following the first treatment session, along with marked edema reduction within 48 to 72 hours. Patients typically experience partial mucosal healing within the first few days, ultimately achieving complete resolution of lesions upon completion of therapy.¹⁷

Clinical application guidelines for dental practice emphasize initiating PBM therapy as early as possible once EM lesions are identified. A point-by-point technique should be used across all ulcerated and inflamed areas, ensuring consistent energy delivery throughout the treatment sites. Thorough documentation of each session, including wavelength, power, time, spot size, and total energy, is essential for accuracy and reproducibility. PBM should also be combined with supportive measures such as adequate hydration, appropriate analgesics, and careful oral hygiene to optimize healing and patient comfort.¹⁷

Analgesic support commonly includes systemic agents such as acetaminophen or non-steroidal anti‑inflammatory drugs to manage discomfort during the acute phase. Oral health professionals should also reinforce oral hygiene instructions, including the use of soft‑bristled toothbrushes, alcohol‑free antimicrobial rinses, and avoidance of spicy or acidic foods, to reduce irritation and promote mucosal healing.

The mechanism of action of PBM involves increasing mitochondrial adenosine triphosphate production, which enhances cellular energy availability. It also reduces pro-inflammatory cytokines and oxidative stress, helping to moderate the inflammatory response.¹⁷ Additionally, PBM stimulates fibroblast activity and supports tissue repair while improving microcirculation and promoting angiogenesis, all of which contributes to accelerated healing and improved clinical outcomes.

Interventions and Treatments

Treatment strategies are dictated by the disease’s chronicity (acute vs recurrent) and severity.¹⁸ Treatments focus on identifying the cause, managing pain, and preventing secondary infections.

Acute management focuses on symptomatic relief, including topical corticosteroids, antihistamines, and antiseptic or anesthetic washes for painful oral lesions.^19,20

Recurrent EM often requires antiviral prophylaxis (eg, acyclovir or valacyclovir) if HSV is the suspected trigger. For those unresponsive to antivirals, second-line therapies include immunosuppressants such as dapsone, azathioprine, or antimalarials.^18,19

Recent case studies highlight the success of antimicrobial photodynamic therapy and PBM. These noninvasive laser-based treatments have shown significant improvement in pain reduction and lesion healing within 24 to 48 hours for severe oral EM. ²¹

Topical steroids are used for acute skin and wound care. Medium-to-high potency topical corticosteroids should be applied to cutaneous (skin) lesions to reduce inflammation and itching. For blistered areas, use nonadherent dressings and saline compresses to soothe the skin and maintain a moist healing environment. Signs of secondary bacterial infection (purulent discharge, foul odor, or increasing heat) should be noted and strict hand hygiene during dressing changes is a must.

For oral and mucosal care, analgesic rinses are helpful. Compounded mixtures containing lidocaine, diphenhydramine, and antacids will numb the area before meals. If oral lesions make swallowing difficult, monitor fluid intake and output and advocate for intravenous fluids if the patient is at risk for dehydration.

If HSV is the confirmed trigger, a nurse will administer antiviral medications (eg, acyclovir). Antihistamines can be used to manage pruritus (an uncomfortable, irritating feeling that encourages scratching of the skin), which can be distressing and leads to skin breakdown from scratching.

In oncology settings, nurses must distinguish EM from toxic erythema of chemotherapy. This requires careful review of the patient’s medication history and the timing of chemotherapy cycles to ensure the correct supportive care is initiated.

Conclusion

EM is a complex mucocutaneous disorder with diverse clinical presentations, fluctuating severity, and a broad range of infectious or medication-related triggers. Understanding the distinctions among EM, MIRM, RIME, and SJS/TEN is essential, as overlapping features frequently lead to diagnostic uncertainty and delays in appropriate treatment. Clear classification based on mucosal involvement and lesion morphology supports timely recognition and helps clinicians differentiate EM from life threatening conditions such as SJS/TEN or autoimmune blistering disorders like PV.

Because EM affects both skin and mucosal tissues, optimal management requires coordinated interprofessional collaboration among nurses, physicians, oral health professionals, dermatology specialists, and allied health professionals. Nurses play a particularly critical role through early assessment, airway monitoring, wound care, medication management, patient education, and identification of red flag symptoms that suggest severe disease progression. Complex cases, including chronic, recurrent, or persistent EM, often require long-term antiviral therapy, immunomodulatory regimens, and ongoing reassessment to prevent flares and improve quality of life.

Emerging therapies, such as PBM and antimicrobial photodynamic therapy, offer promising adjunctive options for patients with painful oral lesions, reflecting broader advancements in supportive dermatologic care. Additionally, attention to medication safety, especially in older adults with polypharmacy, remains essential to reducing the risk of drug induced EM and more severe cutaneous adverse reactions.

Ultimately, improving outcomes for patients with EM depends on three pillars: accurate and timely diagnosis, evidence-based therapeutic strategies tailored to disease severity and chronicity, and effective interprofessional communication across all points of care. Continued research is needed to further define the immunologic mechanisms of EM, refine diagnostic criteria, and develop targeted therapies that address both the cutaneous and mucosal manifestations of this multifaceted condition.

References

1. Hung M, Birmingham WC, Tucker M, Schwartz C, Mohajeri A. Integrating dentistry into interprofessional healthcare: a scoping review on advancing collaborative practice and patient outcomes. Healthcare. 2025;13(21):2780.
2. World Health Organization. Framework for Action on Interprofessional Education Collaborative Practice. Available at who.int/publications/i/item/framework-for-action-on-interprofessional-education-collaborative-practice. Accessed August 21, 2026.
3. Rawlinson C, Carron T, Cohidon C, et al. An overview of reviews on interprofessional collaboration in primary care: barriers and facilitators. Int J Integr Care. 2021;21:32.
4. Kattach L, Singleton H, Ersser S, Holley D, Pearson I, Shadeed A. Nurse-led models of service delivery for skin cancer detection: a systematic review. J Adv Nurs. 2025;81:8432-8456.
5. Harman KE, Brown D, Exton LS, et al. British Association of Dermatologists’ guidelines for the management of pemphigus vulgaris. Br J Dermatol. 2017;177:1170–1201.
6. Kridin K, Zelber-Sagi S, Bergman R. Pemphigus vulgaris and pemphigus foliaceus: differences in epidemiology and mortality. Acta Derm Venereol. 2017;97:1095–1099.
7. Al-Harbawee A, Kassam K, Patel AN, Cottom H, Cheng L. Oral pemphigus vulgaris: dentists take-home message. Clin Case Rep. 2021;9:e04494.
8. Rezapour, M., Mesgarankarimi, A. Low-dose venlafaxine-induced erythema multiforme: a case report. J Med Case Reports. 2025;19:188 (2025).
9. Norimatsu Y, Norimatsu Y. First report of erythema multiforme minor caused by raloxifene hydrochloride. Case Rep Dermatol. 2021;13:445–449.
10. Aurelian L, Ono F, Burnett J. Herpes simplex virus (HSV)-associated erythema multiforme (HAEM): a viral disease with an autoimmune component. Dermatol Online J. 2003;9:1.
11. Ono F, Sharma BK, Smith CC, Burnett JW, Aurelian L. CD34+ cells in the peripheral blood transport herpes simplex virus DNA fragments to the skin of patients with erythema multiforme (HAEM). J Invest Dermatol. 2005;124:1215–1224.
12. Samim F, Auluck A, Zed C, Williams PM. Erythema multiforme: a review of epidemiology, pathogenesis, clinical features, and treatment. Dent Clin North Am. 2013;57:583–596.
13. Huff C, Weston WL. The photodistribution of erythema multiforme. Arch Dermatol. 1980;116:477.
14. Demoly P, Adkinson NF, Brockow K, et al. International Consensus on drug allergy. Allergy. 2014;69:420–437.
15. Sassolas B, Haddad C, Mockenhaupt M, et al. ALDEN, an algorithm for assessment of drug causality in Stevens-Johnson Syndrome and toxic epidermal necrolysis: comparison with case-control analysis. Clin Pharmacol Ther. 2010;88:60–68.
16. Lazarević VV. Diagnosis, investigation and management of non-immediate (type iv) cutaneous adverse drug reactions. Acta Dermatovenerol Croat. 2024;32:88–95.
17. Silva de Souza F, Palma VM, Lonni N, Rabelo GD. Photobiomodulation therapy as an effective approach for fluconazole-induced oral erythema multiforme: a case report. Lasers Dent Sci. 2026;10:4.
18. Soares A, Sokumbi O. Recent updates in the treatment of erythema multiforme. Medicina. 2021; 57:921.
19. Hafsi W. Erythema multiforme. Available at ncbi.nlm.nih.gov/books/NBK470259. Accessed August 21, 2026.
20. Copp LB. Erythema multiforme. Journal of the Dermatology Nurses’ Association. 2024;16(6):224–227.
21. Martins F, Pallos D, Candeia J, Zerbinati R, Braz-Silva PH, Campos L. Noninvasive techniques for management of erythema multiforme. Case Rep Dent. 2023;2023:9938939.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):40,43-45

Between scrolling, streaming, tidying up, and preparing for the next day, Americans are juggling more than ever before at bedtime. New research from Philips Sonicare suggests that oral care is often just one more task competing for attention and that may be affecting how effectively people brush. As patients look for ways to maintain healthy habits amid increasingly busy routines, technologies that help guide brushing and identify missed areas may play an important role in supporting a more thorough clean.

A survey by Philips Sonicare (conducted by Wakefield Research) included 1,000 United States adults ages 18 and older who completed an online survey in May 2026. Results showed that 82% of Americans multitask while getting ready for bed, rising to 92% among adults younger than 40. Nearly half (47%) admit they sometimes rush through brushing, while 82% multitask during their nighttime routine. These findings point to a broader trend: oral care is increasingly being squeezed into busy schedules rather than treated as a dedicated moment of self-care.

While 91% of Americans say their teeth feel clean after brushing, 66% believe they miss certain teeth or areas when they brush. This reveals a disconnect between perception and performance. Even when brushing leaves people feeling clean, many are not fully convinced they’re reaching every surface effectively.

Nighttime remains a vulnerable moment for oral care routines. Nearly half (47%) of Americans who brush regularly say they may skip brushing before bed because they are too tired or fall asleep before doing so, making fatigue the most common reason for missing a nighttime brushing session. However, after learning more about overnight bacteria and plaque buildup, 81% say they would be likely to change their oral care routine.

The Big Takeaway

Americans aren’t abandoning oral care, they’re trying to fit it into increasingly busy lives. But as multitasking becomes the norm, the survey suggests that many people are questioning whether they’re getting the thorough clean they want. For oral health professionals, this is an opportunity to rethink not only how often patients brush, but also how effectively they brush.

The Solution

Philips Sonicare Next-Generation DiamondClean 9900 Prestige is designed to help bridge that gap between feeling clean and cleaning thoroughly.

With SenseIQ technology that adapts to individual brushing habits, real-time smart coverage feedback that helps identify missed areas, and a 12-segment Mouth Map that shows where additional attention may be needed, the toothbrush is built to support more effective brushing even during busy, distracted routines. The smart pressure feedback helps users avoid brushing too hard, scrubbing detection to improve technique, and personalized coaching through the Sonicare App, which offers real-time guidance and progress tracking

Beyond helping improve brushing habits, the DiamondClean 9900 Prestige delivers proven oral health benefits, removing up to 20 times more plaque* and delivering up to 15 times healthier gums.**

Together, these features help address one of the survey’s clearest findings: in a world of multitasking and rushed routines, patients are looking for greater confidence that they’re reaching every tooth, every surface, and every corner of their smile.

* Compared to a manual toothbrush

** In Clean mode vs a manual toothbrush; measured by MGI at 6 weeks

Philips Oral Healthcare

usa.philips.com/professionals/dental

800-422-9448

From Dimensions of Dental Hygiene. September/October 2026; 24(5):25

Profisil Fluoride Varnish Plus contains the minerals calcium, phosphate, and hydroxyapatite that are found naturally in tooth enamel and offer a distinct advantage for remineralizing enamel and strengthening teeth. Profisil also contains 5% sodium fluoride (22,600 ppm), which continues to release up to 24 hours after application.

Fluoride, calcium, and phosphate work together to remineralize tooth structure and form fluorapatite, a mineral that is even stronger and more resistant to acid than hydroxyapatite, which helps prevent caries. Additionally, the calcium fluoride crystals in Profisil occlude dentinal tubules, making it ideal for patients who need sensitivity relief.

Profisil stands apart from other fluoride varnishes because it is free of ethyl alcohol and colophony (rosin). The absence of ethyl alcohol may help minimize bitter taste, burning sensations, and tissue irritation, while the colophony-free formulation reduces the potential for rosin-related allergic reactions. In lieu of rosin, Profisil contains the mucosa-friendly dimethicone gel, which helps the fluoride adhere to teeth for up to 24 hours without clumping or stickiness.

Patient Benefits

The Profisil formula is hypoallergenic and 100% free of dyes, color pigments, gluten, wheat, soy, sesame, corn, shellfish, egg, and dairy. Additionally, the fluoride varnish is available in three flavors: mint, berry, and unflavored. Mint and berry offer a pleasant hint of flavor while unflavored can be a great option for patients who have a sensitivity to smells or tastes. All versions of the Profisil Fluoride Varnish are completely transparent and colorless after application for optimal esthetics (Figure 2). The texture of the varnish is smooth and not sticky, making it well suited for all patients, including children (Figure 3).

Clinician Benefits

Profisil Fluoride Varnish provides several benefits to clinicians. First, oral health professionals do not need to dry the teeth or a perform a prophylaxis prior to use. Additionally, Profisil can be applied in any direction on the teeth, as it flows into interproximal and difficult-to-reach areas. The lubricous, nonclumping formula makes application easy and efficient.

Another benefit is its constant viscosity, which makes it easy to spread. The colorless esthetic also offers an advantage for workflow efficiency as a comprehensive exam can be performed after application without an impeded view of the teeth or surrounding tissues.

Conclusion

Profisil Fluoride Varnish Plus offers oral health professionals an evidence-based, patient-centered fluoride varnish that remineralizes and strengthens enamel with calcium, phosphate, and hydroxyapatite. Using high-quality ingredients free of ethyl alcohol and rosin commonly found in other varnishes, Profisil prioritizes patient comfort and safety. The ability to be applied to wet or dry teeth and appearing colorless after application give clinicians ultimate flexibility and can improve workflow efficiency. Profisil provides an innovative approach to fluoride varnish that provides an effective, safe, and esthetic treatment to enhance patient care.

Kettenbach Dental

kettenbachusa.com

877-532-2123

From Dimensions of Dental Hygiene. September/October 2026; 24(5):26

A recently presented clinical study offers strong evidence supporting the use of a baking soda–based whitening dentifrice as an effective option for managing extrinsic stain.¹ The findings suggest that this formulation represents a meaningful option in over-the-counter whitening for managing extrinsic stain by combining measurable efficacy with safety and ease of integration into daily routines.

Extrinsic stains form on the enamel surface through repeated contact with chromogenic agents and become incorporated into the acquired pellicle. Because these stains reside on the outermost layer of the tooth, their removal depends largely on mechanical and chemical disruption. As a result, dentifrice formulation plays a critical role in determining how effectively daily brushing can address discoloration.

A Rigorous Clinical Evaluation

An Investigational Review Board–approved, randomized, double-blind, parallel-group clinical trial evaluated a baking soda–containing fluoride toothpaste compared to a standard sodium fluoride control 6 weeks.¹ Participants included healthy adults ages 18 to 65 with measurable levels of extrinsic stain. Subjects brushed twice daily for 2 minutes using their assigned toothpaste and were evaluated at baseline and on days 7, 14, 28, and 42. Stain accumulation was measured using the Modified Lobene Stain Index, which assesses both stain intensity and surface area to generate a total stain score.

The study demonstrated statistically significant reductions in extrinsic stain for the baking soda toothpaste at all evaluated time points. Compared with the control dentifrice, total stain reduction reached 35% at day 7; 48% at day 14; 56% at day 28; and 65% at day 42. Improvements were observed across both stain area and intensity, with highly statistically significant differences between groups (p < 0.0001).

Mechanism of Action

The effectiveness of baking soda–based dentifrices is attributed to a dual mechanism. Sodium bicarbonate serves as a mild abrasive to remove pellicle-bound stains while its buffering properties enhance debris removal and help neutralize acids. When combined with fluoride, the formulation supports both esthetic and anticaries benefits.

No adverse events were reported, supporting the suitability of baking soda toothpaste for daily use and reinforcing its role as a well-tolerated whitening option.

Clinical Implications

These findings support recommending baking soda–based dentifrices as part of a comprehensive approach to stain management. They can help maintain whitening results between professional cleanings while promoting consistent oral hygiene habits.

This clinical investigation demonstrates that TheraBreath Whitening Toothpaste, formulated with baking soda, can deliver a meaningful reduction in extrinsic stain within just 1 week of regular use, with progressive improvements up to 6 weeks with continued use. With strong efficacy data, excellent safety outcomes, and ease of integration into daily routines, this product represents a practical solution for patients seeking gentle yet effective stain removal and whitening.

TheraBreath

hygienesquad.com/therabreath

800-447-6666

Reference

1. Vazquez J, Mateo LR, Peters G, et al. Baking soda toothpaste reduces extrinsic stain to whiten teeth. Presented at: International Association for Dental, Oral, and Craniofacial Research General Session and Exhibition; March 25–28, 2026; San Diego.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):27

QMy office manager was inquiring about charging for oral hygiene instruction (OHI) at every recare appointment. We review and discuss OHI in great detail with every patient, but is this something that we can bill for?

Appropriate situations for billing D1330 include patients at high caries risk, those beginning orthodontic treatment, individuals with advanced periodontal diseases who require significant self-care changes, and patients with special needs or physical limitations that necessitate adaptive techniques. Examples include teaching modified brushing and interdental cleaning for a patient with gingival inflammation and recession, instructing a patient on care around braces or other appliances, demonstrating the use of an interdental brush for open embrasures, or explaining the correct use of a prescription antimicrobial or remineralizing agent.

Accurate, detailed documentation is essential when billing D1330. Because this service involves individualized and often measurable education, clinical notes should go beyond a generic template. On the date of service, document the specific reason the instruction was necessary, the oral hygiene challenges identified, and goals of the session. Record which techniques were demonstrated and why they were chosen. Include the method and sequence used during demonstrations. For example: “Demonstrated modified Bass technique with a soft bristled toothbrush for improved gingival margin cleaning due to buccal recession and localized inflammation” and note the patient’s response and competence with the technique.

List any products, aids, or prescription recommendations provided and explain their intended purpose. For instance, document if chlorhexidine rinse was recommended for short-term gingival healing and the instructions given for frequency and duration, or if a fluoride varnish, prescription fluoride toothpaste, or remineralization agent was supplied or prescribed for caries management. When special tools are introduced, such as interdental brushes, floss threaders, powered toothbrushes, water irrigators, or adaptive handles for patients with limited manual dexterity, note the size, model, or type demonstrated and the instruction provided for effective use.

If self-care goals or a follow-up plan were established, document those details. Examples include assigned daily routines, short-term adjunctive therapies, expected improvement timelines, and plans for reassessment at subsequent appointments. Also record any patient education materials given (written instructions, videos, product samples) and whether the patient demonstrated comprehension or technique mastery during the visit.

Insurance coverage for D1330 varies considerably. Many insurance carriers may consider oral hygiene instruction part of routine preventive care and therefore deny separate reimbursement, regardless of the depth or necessity of the instruction. Always verify benefits before billing: confirm whether the carrier recognizes D1330, how frequently it may be billed for the same patient, and whether supporting clinical notes need to accompany the claim. Inform patients in advance about the likelihood of coverage denial and any potential out-of-pocket costs so they can make an informed decision about proceeding.

From Dimensions of Dental Hygiene. September/October 2026; 24(5):46