Recently, our world came closer together with the development of two very important Advocacy Advisory Committees (AAC): one from the American Dental Hygienists’ Association (ADHA) and the other from the International Federation of Dental Hygienists (IFDH). It’s no coincidence that both committees share the same name: AAC. Isn’t it interesting that at this same point in time, both organizations realized the urgency to purposely advocate for the profession of dental hygiene?

The ADHA’s AAC is designed to streamline and sharpen the organization’s legislative influence. Its creation coincides with a massive shift in how the ADHA operates, following the association’s 2025 transition away from its century-old “House of Delegates” to a more agile, modernized governance model. The AAC acts as the strategic engine room for the ADHA’s advocacy efforts. Its main goals are to:

• Strengthen state and federal influence: Support legislative efforts at both the national level, such as federal loan access for students, and the state level (eg, license portability and practice acts).
• Support professional autonomy: Aligning with the 2026–2028 ADHA Strategic Plan, the committee focuses on advancing dental hygiene as an autonomous, prevention-driven profession.
• Rapid response: Under the new governance structure, the AAC helps the Board of Directors respond quickly to emerging threats, such as policies that propose alternative (and often less rigorous) pathways to licensure.

The IFDH’s AAC is a strategic body whose primary mission is to unify and strengthen the global voice of dental hygiene by monitoring and influencing international health policy. The IFDH committee operates on a global scale, focusing on the profession’s integration into universal healthcare systems. The IFDH AAC acts as the “eyes and ears” for the organization, specifically focusing on:

• Policy monitoring: Keeping watch on global health trends, particularly directives from the World Health Organization regarding noncommunicable diseases and the Global Oral Health Action Plan.
• Professional advancement: Advocating for the recognition of dental hygienists, dental therapists, and oral health therapists as essential primary care providers.
• Strategic guidance: Advising the IFDH Board on how to react to global health crises or opportunities, such as the United Nation’s recent declarations regarding oral health’s role in general well-being.
• Support for member nations: Helping smaller national associations develop their own advocacy toolkits to lobby their respective governments for expanded scopes of practice.

There is no such thing as coincidence. These two committees are synergistic, strategic, and significant. Perfect timing.

For more information visit adha.org/advocacy/federal-efforts and ifdh.org/about-ifdh/committees.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):9

First introduced in the 1990s, handheld portable X-ray devices are used in a variety of settings, from schools to mobile clinics. While not intended to replace the traditional wall units seen in most dental offices, handheld devices are becoming ubiquitous in dentistry.^1,2
       
        Traditional wall-mounted units are installed with structural shielding and protective barriers to protect operators from ionizing radiation in a controlled setting. In contrast, handheld units are typically used in noncontrolled environments, where the standard protective barriers associated with wall-mounted units are not present. Handheld devices are not designed to replace the traditional wall-unit but rather serve as a supplement.^3,4

Handheld X-ray devices are frequently found in military settings, nursing homes, facilities for individuals with special needs, remote or underdeveloped regions lacking dental clinics, community outreach clinics, patients receiving treatment under general anesthesia, and in forensic dentistry.^1,3

Radiation Safety for Dental Hygienists

Oral health professionals must always adhere to the “as low as reasonably achievable” (ALARA) principle when using ionizing radiation. Any exposure to radiation can increase the risk of adverse health effects; however, the exposure encountered in the dental setting is low.⁵

The National Council on Radiation Protection and Measurements (NCRP), a United States-based scientific advisory organization, provides guidance for dental radiographic procedures in NCRP Report No. 177: Radiation Protection in Dentistry and Oral and Maxillofacial Imaging.⁵ The maximum permissible dose (MPD) for occupational exposure is set at 50 mSv per year; however, oral health professionals receive an average annual dose of just 0.06 mSv, approximately 6% of this limit.⁵

Studies evaluating handheld X-ray devices report even lower operator exposure levels, averaging 0.0453 mSv, or about 0.9% of the annual limit.⁶ These values can vary depending on factors such as device type, operator hand positioning, and handling technique.⁶

The NCRP has made the following recommendations for oral health professionals who use handheld devices.^2,3,6

1. All handheld devices must be approved by the US Food and Drug Administration (FDA).^2,3,6
2. Approved units must be equipped with a backscatter shield that is at least 0.25 mm lead/lead equivalent, clear, and not removable from the device.³ The backscatter shield protects oral health professionals by blocking radiation scattered from the patient and surrounding objects. Research shows that with the backscatter shield in place, operator exposures are well within the maximum permissible dose for occupationally exposed individuals.³
3. Rectangular collimation should be used whenever possible. Rectangular collimation reduces the patient-absorbed dose by 50% and also decreases scatter radiation.^1,2
4. Operators of handheld devices must be able to hold the device in place for multiple exposures.
5. Handheld radiographic equipment must be securely stored.
6. When handheld devices are used, all individuals at risk of exposure need to be protected.
7. The operator of an FDA-cleared device is not required to wear a personal radiation protective garment.

Although exposure rates are low, many oral health professionals would prefer to see additional safety protocols implemented. Current studies recommend that operators use lead aprons with thyroid collars, dosimeters, and lead gloves as added protection.^4,6,7 The potential areas of risk to exposure are the eyes, hands, thyroid, and gonads; due to the close proximity to the source of ionizing radiation.^6,7 Future research is needed focusing on the cumulative exposures and to strengthen safety protocols.

Clinical Protocols for Safe Use

To ensure operator safety, correct positioning must be implemented during use. Several manufacturers recommend that the operator’s arms be fully extended and the device held parallel to the patient and perpendicular to the floor.⁴

Proper positioning will provide a maximum safety zone of protection for the operator. Figure 1 shows the correct positioning when exposing a posterior and bitewing dental image. Figure 2 shows both correct and incorrect positioning of the device.

The handheld device should have the backscatter shield at the outer edge of the positioning indicator device (PID) close to the subject. For additional safety, dental staff and patients should stand at least 6 feet away from the primary beam when barrier protection is not available.⁵

Handling the machine with both hands helps with maintaining correct positioning. Due to the weight of the machine, operator arm fatigue over multiple exposures can compromise the ability to keep the device parallel.² In Figure 3, the device is supported with two hands. One hand is held underneath the PID stabilizing the device, while the other is on the exposure button.

The use of beam alignment devices helps clinicians adhere to the ALARA principle by minimizing technique errors and reducing dose exposure. The beam alignment device used for handheld units is different than the one used with the traditional wall-mounted unit. The indicator extension rod used for the handheld device is shorter. The shorter rod helps keep the backscatter shield as close as possible to the patient. Figure 4 shows a comparison of the regular beam alignment indicator extension rod compared to the beam alignment indicator extension rod used for the handheld device.

Although the NCRP no longer recommends the use of lead aprons, manufacturers continue to suggest they may be helpful. In some cases, patient positioning may limit proper operator placement, and altering device positioning can compromise the protective zone. The lead apron is an added safety measure for operator protection.

Operators who face exposure beyond the annual limit of 1 mSv, should consider using a dosimeter, a personal safety device used to measure an individual’s cumulative exposure to ionizing radiation (X-rays, gamma rays, beta particles) over time.⁵ Pregnant operators should adhere to shielding procedures as stated in the facility’s radiation protection protocol in addition to using a dosimeter.⁵

Proper Handling , Storage, and Infection Control

Due to the design and weight of the handheld device, operators should be careful about how they are handled. The devices can be placed in a cart or laid flat on the counter to prevent damage. The device should remain in the locked position until ready for use to prevent accidental discharge of radiation (Figure 5). Units should be stored securely and kept out of each to prevent unauthorized use.⁵

Handheld X-ray devices are disinfected with a nonacetone disinfectant. Only the exterior surfaces and unplugged charger should be wiped down; the device surfaces should never be sprayed. The unit can also be covered with a plastic barrier for added infection control protection.

Quality Assurance

All dental offices need to have a protocol for the use of handheld X-ray devices. Only trained personnel should be using the device. The NCRP states that special training for the operation of the handheld devices is needed for all clinicians and that the manufacturers are responsible for the training.³ Certification may be required before operating a handheld device.

In addition to NCRP recommendations, oral health professionals should know their state regulations and requirements. Information on state radiology regulations is available at the American Society of Radiologic Technologists’ website: asrt.org.⁸

Conclusion

Handheld dental radiation devices offer valuable flexibility in modern dental care, particularly in places where the traditional unit is not possible. As the dental hygiene profession continues to expand to meet the needs of individuals outside of the traditional dental office, dental hygienists must have a working knowledge of how to properly use the equipment safely and limit risks to themselves and their patients.

References

1. Almeida FT, Majeed M, Fossen A, Pacheco-Pereira C. Exploring hand-held dental X-ray devices and their impact on digital dentistry: rationale and best practices. Can J Dent Hyg. 2026;60:64-68.
2. Lurie AG, Kantor ML. Contemporary radiation protection in dentistry: Recommendations of National Council on Radiation Protection and Measurements Report No. 177. J Am Dent Assoc. 2020;151:716-719.
3. Geist JR. Handheld intraoral dental x-ray devices should supplement but not replace conventional radiographic equipment. Oral Surg Oral Med Oral Pathol Oral Radiol. 2021;132:257-259.
4. Martins GC, Rocha TG, de Lima Azeredo T, de Castro Domingos A, Visconti MA, Villoria EM. Hand-held dental X-ray device: Attention to correct use. Imaging Sci Dent. 2023;53:265-266.
5. Benavides E, Krecioch JR, Connolly RT, et al. Optimizing radiation safety in dentistry: Clinical recommendations and regulatory considerations. J Am Dent Assoc. 2024;155:280-293.
6. Altındağ A, Eren H, Orhan K, Görgün S. Evaluation of operator and patient doses after irradiation with handheld x-ray devices. Appl Sci. 2023;13:10414.
7. Abubakr RI, Hajee SI. Occupational radiation exposure from handheld dental x‐ray devices: A quantitative dosimetric study. J Appl Clin Med Phys. 2025;26:e70375.
8. American Society of Radiologic Technologists. ASRT States that Regulate. Available at asrt.org/main/standards-and-regulations/legislation-regulations-and-advocacy/states-that-regulate. Accessed April 21, 2026.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):10-13

As patients seek alternatives to traditional fluoride-based products, oral health professionals are increasingly fielding questions about the best options for preventing dental caries and reducing tooth sensitivity.¹ With ongoing public scrutiny of fluoride use, hydroxyapatite (HA) has emerged as a promising agent due to its unique properties. However, dental provider adoption of HA has been tempered by questions regarding efficacy, safety, and regulatory approval. The prudent clinician is tasked with navigating evidence-based research while considering patient preferences and ensuring efficacy for maximum clinical outcomes.

Fluoride

Fluoride remains the standard for caries prevention and enamel remineralization. Fluoride’s effectiveness is supported by years of research and regulatory endorsement from agencies such as the United States Centers for Disease Control and Prevention,US Food and Drug Administration (FDA), the American Dental Association (ADA), and the American Academy of Pediatrics.^2,3

Fluoride forms a robust, acid-resistant fluorapatite layer on teeth, making the tooth structure stronger and more resistant to acid attacks. By increasing salivary fluoride concentration and raising salivary pH, fluorapatite inhibits the breakdown of the tooth surface.^2,3 Standard recommendations vary by agent and are based on patient needs. Sodium fluoride (NaF) and sodium monofluorophosphate are used for caries prevention, while stannous fluoride is recommended for caries prevention, antimicrobial control, and sensitivity protection. Potassium nitrate can be combined with NaF for sensitivity management and caries protection.⁴

In 1997, the FDA placed warning labels on fluoride-containing toothpastes in response to concerns about fluoride toxicity in young children. In 2014, the ADA recommended lowering the amount of toothpaste to a rice-sized smear for children under age 3 and a pea-sized amount for older children and adults.⁵ However, some evidence-based research has questioned whether a rice-sized smear provides sufficient caries-preventive benefit.⁶

Excess ingestion of fluoride beyond the recommended dose can lead to an upset stomach, enamel fluorosis, and potential neurotoxic effects on the developing brains of children.^3,7 The American Academy of Pediatrics affirms that extensive research validates the safety and efficacy of fluoride when following current dosing regimens. Additionally, community water fluoridation at 0.7 ppm is deemed safe from both fluorosis and adverse neurocognitive effects.^8,9 Yet, patient preferences and public perception continue to drive interest in alternative options.

Hydroxyapatite

Calcium and phosphate are essential minerals present in bones and teeth as carbonated hydroxyapatite. HA is the main inorganic component of both enamel (97%) and dentin (70%). While bone and dentin share many similarities, enamel is considerably harder due to the composition, size, and crystalline structure of HA.^10–12 Research shows that synthetic HA integrates into enamel and dentin defects, builds upon existing crystalline structures, forms a protective mineral layer on the tooth surface, supports ongoing deposition of calcium and phosphate from saliva, and enhances overall tooth hardness.¹

Due to the biocompatibility and osteoconductivity of HA, synthetic HA has been explored for use in medical and dental applications since its development by the US National Aeronautics and Space Administration in the 1970s.^1,10 A Japanese company acquired the patent and developed the first commercially marketed HA dentifrice. Japan formally recognized HA as an anticaries agent in 1993. Broader adoption in Europe, Canada, and the US has been slow to follow.^3,6,7,12-14 In recent years, HA has gained popularity in dentistry and medicine. Current indications for use include bone grafts, tissue repair, sensitivity reduction, repairing and strengthening enamel, medication delivery, and coating dental implants.^1,14,15

Synthetic HA is available in micro (mHA 5-10 microns) and nano (nHA 20-100 nanometers) particle forms. nHA is used more frequently in dental products because the size and structure more closely resemble natural HA , allowing deeper penetration into the enamel and dentin tubules than mHA.¹²

Currently, nHA is not FDA-approved for caries prevention in the US and does not carry the ADA Seal of Acceptance.¹⁶ The Journal of the American Dental Association addressed the ethical considerations of recommending HA products as alternatives to fluoride, noting professional ethics, such as veracity, autonomy, and nonmaleficence, must be integrated with standards of care and clinical practice guidelines. The ADA maintains that fluoride is safe, effective, and recommended for caries prevention, while acknowledging that alternative options, such as HA, may be offered to patients.¹⁶ Patients must be well informed that HA has not been as extensively researched as fluoride.¹

Biofilm and the Microbiome

The oral microbiome maintains symbiosis with the host under healthy conditions. However, local and systemic factors can shift this balance toward dysbiosis, increasing the risk of caries or periodontal disease. In either condition, oral biofilm accumulation on the tooth surface and gingival tissues facilitates the disease process.¹⁷ Given its biocompatibility, HA represents a reasonable alternative or adjunct to traditional methods of biofilm control.^{12,13,18–20}

Although literature is limited, HA binds to bacteria and proteins, disrupting the bacterial growth process. The smaller the particle size, the more surface area available for bacterial interaction, making nHA the preferred formulation. Compared to chlorhexidine, HA is as equally effective at disrupting biofilm accumulation.^{1,12,13,18,21}

Caries Prevention

When combined with zinc, strontium, magnesium, or fluoride, nHa was more effective against S. mutans than nHA alone.²² Additionally, HA can decrease lactic acid production, an important factor in caries prevention.^19,20 While fluoride acts primarily at the enamel surface, nHA can penetrate enamel lesions more deeply, inhibiting further demineralization. Remineralization of caries with a 10% HA toothpaste was as effective as 1,400 ppm stannous toothpaste in preventing caries progression.²³ nHA can penetrate underlying tooth structure for effective enamel repair, sensitivity reduction, and restoration of surface smoothness, independent of salivary conditions.^12,24–26 In comparison to mHA, nHA demonstrates more favorable biocompatibility and bioactivity, making it a safe and effective over-the-counter choice for remineralizing teeth and preventing caries as a fluoride-free option.^12,24

Dentinal Hypersensitivity

Dentinal hypersensitivity (DH) is a common, multifactorial condition, typically occurring near the cementoenamel junction. Causes include toothbrush abrasion due to dentin exposure and demineralization of cementum from an acidic oral environment.⁷ While stannous fluoride and potassium nitrate provide relief from DH, nHA provides both caries protection and sensitivity reduction.²⁷ nHA crystals adhere to the dentin surface, coating the surface and occluding dentinal tubules to prevent temperature or tactile stimuli from reaching the pulp, similar to that of stannous fluoride. One study found HA to be an effective desensitizer and, in some cases, superior to stannous fluoride.⁷ A 2019 meta-analysis identified nHA toothpaste as the best treatment for DH.²⁸

Recommending Hydroxyapatite

Given its biocompatibility, ability to prevent biofilm adhesion, anti-caries properties, desensitizing effects, and capacity to maintain homeostatic balance within the oral cavity, nHA is an option for patients who prefer fluoride-free alternatives. While additional studies are needed, nHA serves as a favorable oral care agent to combat cariogenic bacteria and support oral health.^{12,14,18–20} Ultimately, nHA toothpaste is not definitively superior to fluoride, but stands as a strong alternative. The choice between fluoride and nHA should be guided by patient ingredient preference and specific dental needs, particularly dentinal hypersensitivity or caries risk.

Comparative Effectiveness and Safety

Oral health professionals have expressed concerns about nHA absorption and toxicity. In comparison to fluoride, which has been associated with dental fluorosis, bone weakening, and accidental poisoning from over-ingestion, available evidence indicates that HA is essentially nontoxic and nonimmunogenic.^{6,11,21,29,30} When ingested, HA particles are broken down by stomach acid into calcium and phosphate ions and easily eliminated; thereby making nHA a biocompatible option that is considered safe if swallowed and a preferable option for children.¹

Nano-sized particles are preferred for their bioactivity, larger surface area, and crystalline structure closely resembling enamel.^1,12,15,22 An in vitro study on nHA cytotoxicity found no harm to human gingival cells, specifically fibroblasts. Moreover, cells appeared normal and healthy, with no signs of damage, cell death, oxidative stress, or tissue irritation. nHA-treated cells were more metabolically active than untreated controls.³¹ Systemic cytotoxicity of nHA via oral epithelium exposure is considered unlikely due to cell turnover of nonkeratinized oral mucosa.¹⁴ However, another study found that inhaled nHA particles may interfere with pulmonary surfactant function, though lung cell damage was not observed. The risk of inhalation of nHA from currently available dental products is low.³²

The shape of nHA particles warrants consideration. Different crystalline morphologies, H-sphere, H-needle, H-rod, and H-plate, vary in cytotoxicity. In vitro studies indicate H-plate shapes exhibit the highest and H-rod shapes the lowest levels of cytotoxicity.^12,33 European Union guidelines classify rod-shaped nHA as safe in concentrations < 10% in dentifrices and < 0.465% in mouthrinses.³⁴ While further research is needed, nHA morphology needs to be considered when recommending oral care products to patients.^32,33

Products and Limitations

A variety of nHA oral care products are commercially available, including toothpastes, gels, mouthrinses, gums, and professionally applied varnishes. While marketed to promote remineralization, protect enamel, prevent caries, and decrease hypersensitivity, no nHA dental products currently carry FDA approval.^{3,12,13,21,29,35–41}

Cost, limited manufacturing capacity, and variable regulatory oversight influence the production and availability of nHA. Inconsistencies among brands in particle size, shape, and concentration contribute to differences in product efficacy.⁴⁰ The recommended over-the-counter concentration is 5% to 10% nHA for dentifrices and 0.465% for mouthrinses, yet commercially available products may fall outside these ranges due to limited regulatory oversight. While 10% is optimal for caries prevention and remineralization, higher concentrations provide no additional benefit.^{3,12,14,34,41} Because nHA requires more advanced manufacturing processes and lacks the global scale of fluoride production, raw material and manufacturing costs are higher. This additional cost cascades down to the consumer, reflecting retail prices three to five times higher than fluoride toothpaste.⁴⁰

The body of research supporting nHA is limited in comparison to fluoride, contributing to hesitancy among clinicians.⁴⁰ Best practices include reviewing product labels for nHA concentration, noting where the active ingredient appears in the ingredient list, and identifying pharmaceutical-grade designations. Dental professionals should strive to recommend reputable products supported by clinical studies and known to produce high-quality, appropriately concentrated nHA dental products.⁴¹

Conclusion

Synthetic HA, in either micro or nano formulations, serves as a suitable agent for caries prevention, treatment of hypersensitivity, and the prevention of biofilm adhesion without the potential toxicity concerns associated with fluoride ingestion (Table 1). Its biocompatibility makes nHA a viable option across all ages, particularly those who prefer nonfluoridated products. The higher production cost of nHA is a practical consideration for many patients, and best practice suggests that dental hygienists independently review scientific data to make evidence-based recommendations, regardless of marketing claims about specific products.

References

1. Meyer F, Enax J, Amaechi BT, et al. Hydroxyapatite as remineralization agent for children’s dental care. Front Dent Med. 2022; 3:859560.
2. Yeh CH, Wang YL, Vo TTT, Lee YC, Lee IT. Fluoride in dental caries prevention and treatment: mechanisms, clinical evidence, and public health perspectives. Healthc Basel. 2025;13(17):2246.
3. Naim J, Sen S. The remineralizing and desensitizing potential of hydroxyapatite in dentistry: a narrative review of recent clinical evidence. J Funct Biomater. 2025;16:325.
4. National Institutes of Health (NIH). Fluoride: Fact Sheet for Health Professionals. Availalbe at https://ods.od.nih.gov/factsheets/Fluoride-HealthProfessional. Accessed April 9, 2026.
5. American Dental Association. Fluoride toothpaste use for young children clinical practice guideline. J Am Dent Assoc. 2014;145:190-191.
6. Limeback H, Enax J, Meyer F. Biomimetic hydroxyapatite and caries prevention: a systematic review and meta-analysis. Can J Dent Hyg. 2021;55:148-159.
7. Limeback H, Enax J, Meyer F. Clinical evidence of biomimetic hydroxyapatite in oral care products for reducing dentin hypersensitivity: an updated systematic review and meta-analysis. Biomim 2313-7673. 2023;8(1):23.
8. American Academy of Pediatrics. Fact Checked: Fluoride is a Powerful Tool for Preventing Tooth Decay. Available at aap.org/en/news-room/fact-checked/fact-checked-fluoride-is-a-powerful-tool-for-preventing-tooth-decay/#:~:text=The%20AAP%2C%20the%20Centers%20for,%2C%20focus%2C%20and%20attend%20school. Accessed April 9, 2026.
9. American Academy of Pediatric Dentistry. The Reference Manual of Pediatric Dentistry. Fluoride Therapy. Chicago: American Academy of Pediatric Dentistry; 2023:372-378.
10. Dorozhkin SV, Epple M. Biological and medical significance of calcium phosphates. Angew Chem Int Ed Engl. 2002;41(17):3130-3146.
11. Meyer F, Amaechi BT, Fabritius HO, Enax J. Overview of calcium phosphates used in biomimetic oral care. Open Dent J. 2018; 12:406-423.
12. Chen L, Al-Bayatee S, Khurshid Z, Shavandi A, Brunton P, Ratnayake J. Hydroxyapatite in oral care products—a review. Mater 1996-1944. 2021;14:4865.
13. O’Hagan-Wong K, Enax J, Meyer F, Ganss B. The use of hydroxyapatite toothpaste to prevent dental caries. Odontology. 2022;110:223-230.
14. Pushpalatha C, Gayathri VS, Sowmya SV, et al. Nanohydroxyapatite in dentistry: A comprehensive review. Saudi Dent J. 2023;35:741-752.
15. Juntavee A, Juntavee N, Hirunmoon P. Remineralization potential of nanohydroxyapatite toothpaste compared with tricalcium phosphate and fluoride toothpaste on artificial carious lesions. Int J Dent. 2021;2021:5588832.
16. Ambrosino B. Ethical guidance for dentists about offering nonfluoridated toothpaste to patients who request it. J Am Dent Assoc. 2025;156:338-339.
17. Marsh PD, Zaura E. Dental biofilm: ecological interactions in health and disease. J Clin Periodontol. 2017;44:S12-S22.
18. Meyer F, Enax J. Hydroxyapatite in oral biofilm management. Eur J Dent. 2019;13:287-290.
19. Huang Y, Han Q, Peng X, et al. Disaggregated nano-hydroxyapatite (dnhap) with inhibitory effects on biofilms and demineralization. J Dent Res. 2023;102:777-784.
20. Luo W, Huang Y, Zhou X, et al. The effect of disaggregated nano-hydroxyapatite on oral biofilm in vitro. Dent Mater. 2020;36:e207-e216.
21. Amaechi BT, AbdulAzees PA, Okoye LO, Meyer F, Enax J. Comparison of hydroxyapatite and fluoride oral care gels for remineralization of initial caries: a pH-cycling study. BDJ Open. 2021;6(1):1-7.
22. Imran E, Cooper PR, Ratnayake J, Ekambaram M, Mei ML. Potential beneficial effects of hydroxyapatite nanoparticles on caries lesions in vitro-a review of the literature. Dent J. 2023;11:2.
23. Schlagenhauf U, Kunzelmann K, Hannig C, et al. Impact of a non‐fluoridated microcrystalline hydroxyapatite dentifrice on enamel caries progression in highly caries‐susceptible orthodontic patients: A randomized, controlled 6‐month trial. J Investig Clin Dent. 2019;10:e12399.
24. Mehrjoo M, Haghgoo R, Ahmadvand M. Effect of a nano-hydroxyapatite toothpaste on enamel erosive lesions of third molars induced by exposure to orange juice. Contemp Clin Dent. 2024;15:17-21.
25. Grocholewicz K, Matkowska-Cichocka G, Makowiecki P, et al. Effect of nano-hydroxyapatite and ozone on approximal initial caries: a randomized clinical trial. Sci Rep. 2020;10:11192.
26. Daas I, Badr S, Osman E. Comparison between fluoride and nano-hydroxyapatite in remineralizing initial enamel lesion: An in vitro study. J Contemp Dent Pract. 2018;19:306-312.
27. Smith TL. Tooth remineralization agents: an evidence-based review to make informed patient recommendations. Available at todaysrdh.com/tooth-remineralization-agents-an-evidence-based-review-to-make-informed-patient-recommendations. Accessed April 9, 2026.
28. Hu ML, Zheng G, Lin H, Yang M, Zhang YD, Han JM. Network meta-analysis on the effect of desensitizing toothpastes on dentine hypersensitivity. J Dent. 2019;88:103170.
29. Bossù M, Saccucci M, Salucci A, et al. Enamel remineralization and repair results of biomimetic hydroxyapatite toothpaste on deciduous teeth: an effective option to fluoride toothpaste. J Nanobiotechnology. 2019;17:17.
30. Anil A, Ibraheem WI, Meshni AA, Preethanath RS, Anil S. Nano-hydroxyapatite (nHAp) in the remineralization of early dental caries: a scoping review. Int J Environ Res Public Health. 2022;19:9.
31. Coelho CC, Grenho L, Gomes PS, Quadros PA, Fernandes MH. Nano-hydroxyapatite in oral care cosmetics: characterization and cytotoxicity assessment. Sci Rep. 2019;9:N.PAG.
32. Fan Q, Wang YE, Zhao X, Loo JSC, Zuo YY. Adverse biophysical effects of hydroxyapatite nanoparticles on natural pulmonary surfactant. ACS Nano. 2011;5:6410-6416.
33. Huang L, Sun X, Ouyang J. Shape-dependent toxicity and mineralization of hydroxyapatite nanoparticles in A7R5 aortic smooth muscle cells. Sci Rep. 2019;9:18979.
34. Scientific Committee on Consumer Safety. Opinion on Hydroxyapatite (Nano). Available at https://health.ec.europa.eu/publications/hydroxyapatite-nano-0_en. Accessed April 9, 2026.
35. Patel D. Nano hydroxyapatite toothpaste market research report. Available at https://dataintelo.com/report/nano-hydroxyapatite-toothpaste-market. Accessed April 9, 2026.
36. Amaechi BT, Alshareif DO, Azees PAA, et al. Anti-caries evaluation of a nano-hydroxyapatite dental lotion for use after toothbrushing: An in situ study. J Dent. 2021;115:103863.
37. Cocco F, Salerno C, Wierichs RJ, et al. Hydroxyapatite-fluoride toothpastes on caries activity: a triple-blind randomized clinical trial. Int Dent J. 2025;75:632-642.
38. Limeback H, Enax J, Meyer F. Improving oral health with fluoride-free calcium-phosphate-based biomimetic toothpastes: an update of the clinical evidence. Biomim Basel Switz. 2023;8:331.
39. Hatfield S. Nano-hydroxyapatite varnish: does research support caries prevention efficacy and safety? Available at .todaysrdh.com/nano-hydroxyapatite-varnish-does-research-support-caries-prevention-efficacy-and-safety. Accessed April 9, 2026.
40. Nano-Hydroxyapatite Downsides: Limitations and Important Considerations. Available at https://nanohydroxyapatite.org/article/nano-hydroxyapatite-downsides-limitations-considerations. Accessed April 9, 2026.
41. Toothpaste with Highest Nano-Hydroxyapatite: Complete Concentration Guide. Available at https://nanohydroxyapatite.org/article/highest-nano-hydroxyapatite-toothpaste-concentration-guide. Accessed April 9, 2026.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):16-21

Dental implants do not just fail. We fail them — through a disregard of biological, restorative, and maintenance principles.¹ True implant success tests the resilience of the peri-implant apparatus. Because implants lack a periodontal ligament, exhibit collagen fibers aligned parallel rather than perpendicular to their surface, and host a unique microbiome in which fewer than 10% of species overlap with periodontal niches, they function within their own ecological and immunologic environment.^1,2 This environment is acutely sensitive to both patient self-care and the quality of professional maintenance.

A growing clinical consensus indicates that peri-implant diseases are largely preventable when risk factors are properly managed and robust maintenance protocols are followed.^1,3 Without such support, dysbiotic biofilm accumulates, provoking rapid inflammatory change, implant surface degradation, and nonlinear bone loss.³ Peri-implantitis progresses faster than periodontitis, with lesions nearly twice as large and driven by more aggressive cytokine profiles.³ Early and ongoing recare can safeguard implants from this destructive sequelae. Yet it is the standard of maintenance that shapes their prognoses.

Emerging research has refined the understanding of material-tissue interactions, revealing that titanium is not inert; when its protective dioxide layer is disrupted, ions and particles are released, amplifying a local inflammatory reaction known as metallosis.^3,4 Tribocorrosion from improper hand or power instrumentation can initiate or accelerate tissue breakdown, making surface-safe debridement essential.

Risk Factors Impacting Maintenance

Active or previous periodontitis captures the biological, mechanical, behavioral, and environmental factors that undermine implant health. Numerous longitudinal studies confirm that patients with successfully treated periodontitis had higher rates of peri-implant mucositis, bone loss, and implant failure than periodontally healthy individuals.^3,5 In fact, without maintenance, tissue level implants had a 15-fold increased risk of peri-implant bone loss in periodontally compromised patients in a 20-year follow-up.⁵ Even with successful treatment, these patients remain vulnerable to biological complications, underscoring the importance of structured, ongoing maintenance for implants.

This inherent vulnerability reinforces the role of soft tissue phenotype, as the peri-implant complex depends on sufficient, resilient mucosal tissue to buffer change. Thin mucosal tissues provide less protection against mechanical forces, poor prosthetic design, and plaque accumulation.^1,6 Wider bands of keratinized mucosa are generally associated with improved patient comfort, reduced inflammation, and more stable marginal bone levels, though controversial.^3,6

An often-cited meta-analysis revealed that sites with insufficient keratinized tissue are more prone to bleeding, discomfort during brushing, and biofilm retention, all of which can precipitate disease progression.⁶ When a peri-implant tissue deficiency is identified, augmentation procedures may be performed before implant placement, loading, or during peri-implantitis therapy.

Suboptimal prosthetic designs further complicate maintenance, creating situations where clinicians are unable to diagnose or manage disease effectively. Overcontoured crowns, emergence profiles exceeding 30°, prosthetic splinting, open contacts, and deep restorative margins impede hygiene access and collect biofilm.⁷

A recent systematic review and meta-analysis found strongly associated overcontoured prostheses to peri-implantitis prevalence, with some reports above 80%.⁷ Remnants from cement-retained restorations can trigger persistent inflammation with their detection becoming more difficult among deeper margins or multiple or splinted units.^3,7 Maintenance therefore begins with a well-designed restoration from a properly placed implant.

From there, broader influences come into play. Cigarette smoking, for example, impairs both perioperative and long-term treatment outcomes with a dose-dependent response.^2,3 A 2024 meta-analysis associated vaping with negative esthetic, clinical, and radiographic parameters; it is gaining popularity among young adults.⁸ Even with discontinued use, disease susceptibility may only begin to re-approximate the risk of a nonsmoker after 21 years.^2,3 Early intervention and cessation can be life-changing and should be discussed during subsequent maintenance visits.⁹

Attention must also be given to systemic factors, which exert equally significant biological pressures. Obesity and uncontrolled type 2 diabetes mellitus (T2DM) create a chronically pro-inflammatory, dysregulated host environment that undermines peri-implant health. Findings from the Academy of Osseointegration and American Academy of Periodontology Consensus on Prevention and Management of Peri-Implant Diseases and Conditions suggest that obesity does not consistently reduce implant survival but is associated with deeper peri-implant pockets, more bleeding on probing, and greater marginal bone loss, increasing the risk of peri-implant diseases.³

Poorly controlled T2DM slows and impairs osseointegration, leading to early implant failure and complications compared to healthy or well-controlled patients.^3,9 Nutritional counseling can broaden the impact of recare, supporting not only oral health but mental and systemic wellness.

Yet across all categories, one powerful and modifiable factor remains: adherence to routine professional maintenance. Because even with these comorbidities, patients who were maintained every 3 to 6 months had better therapeutic outcomes.^1,3,5,9 These findings demonstrate that maintenance is not merely beneficial but essential, functioning as the primary defense against disease initiation and escalation.

Maintenance and Self-Care Protocols

Implant maintenance necessitates a shift from traditional instrumentation to more biologically compatible techniques. High-abrasion polishing pastes, stainless steel curettes, and certain ultrasonic tips can scratch or strip the protective dioxide layer of an integrated implant, potentially releasing metal particles and altering cellular responses via metallosis.^2,4,9 Low-abrasion air-polishing techniques with erythritol powder via guided biofilm therapy consistently demonstrated high effectiveness with minimal surface disruption.^4,10 A 2025 randomized clinical trial comparing erythritol-based air polishing with ultrasonic debridement using a polyetheretherketone insert found both modalities reduced probing depths and bleeding on probing, but air polishing achieved patient-preferred comfort with less instrumentation time and greater surface decontamination.¹¹

Self-care instruction should then complement professional therapy. Patients must be taught techniques compatible with their implant prosthesis. For many, conventional wax or unwaxed floss may not be appropriate, as it can lodge around misfit abutments and exposed threads, acting as plaque-retentive foreign bodies in the peri-implant sulcus.¹² Water flossers, by contrast, offer improved plaque removal in both supragingival and subgingival spaces and are more practical for multiple and full-arch implant restorations on a low-to-medium setting.^12,13

Removable locator- and bar-retained implant-assisted overdentures require daily cleaning and periodic replacement of worn attachments. Patients should be encouraged to debride the intaglio surface with a specialized electric brush head, then rinse it in an antimicrobial solution.¹⁴ Fixed full-arch restorations demand meticulous self-care with similar brushing and interproximal aids and should then be removed every 18 months, on average, for complete evaluation and debridement.^13,14 These maintenance routines, though time-intensive, protect difficult-to-reach mucosal tissues beneath larger prosthetic surfaces.

Maintenance should extend through every phase of treatment, independent of the final prosthesis. Because healing follows a predictable biological sequence, implant debridement and recare should be timed to align with each stage as follows:

• Two weeks. Inflammation is prevalent, as the epithelial seal is still forming around the implant collar.¹⁵ Gentle biofilm disruption and reinforcement of self-care with a hygiene team prevent its early breakdown.
• Six to 8 weeks. Woven bone remodeling and connective-tissue organization accelerate along the implant body.¹⁵ Localized debridement prevents deeper plaque penetration and ensures all restorative steps occur in a healthy, stable environment.
• Twelve weeks. Lamellar bone has matured and osseointegration is sufficiently established.¹⁵ Radiographs and gentler clinical measurements should be taken to guide long-term maintenance planning and self-care, with more thorough surface debridement.

Personalized maintenance reduces probing depths, bleeding, and other negative indices, especially for already ailing implants.^1,9,14 Large cohort data continue to confirm higher implant survival rates among patients who remain in regular maintenance programs.^5,14 Implant maintenance is indispensable in preventing disease recurrence and maintaining stability, especially when 60% of treated diseased implants relapse, requiring secondary intervention or removal, in as little as 1 year.¹⁶

Case Report

The following case outlines the management of a failing dentition through comprehensive periodontal and implant therapy. A 59-year-old man presented to a private practice dissatisfied with his smile and experiencing increasing discomfort in the posterior region secondary to long-standing, untreated periodontitis (Figures 1-16). His medical history was noncontributory aside from a penicillin allergy. He reported smoking one pack of cigarettes daily for at least 20 years.

The patient expressed concern about losing additional teeth without a definitive plan in place. Clinical examination revealed generalized pink-red, edematous, and poorly attached periodontal tissues with heavy plaque, calculus, and debris accumulation throughout. Probing depths ranged from 4 to 10 mm with profuse bleeding on probing and/or suppuration. Cone-beam computed tomography (CBCT) imaging revealed generalized moderate-to-severe horizontal bone loss with isolated vertical defects and periapical or furcal lesions.

After a thorough evaluation and discussion of treatment options, a comprehensive plan was developed and informed consent was obtained. Although a removable, implant-assisted prosthesis would have been ideal given his periodontal and smoking histories, the patient declined any removable solution and accepted the associated risks. He agreed to a strict maintenance program. Intraoral scans, CBCT imaging, photographs, and videos, collected as part of his initial consultation, were sent to the laboratory to digitally plan same-day implant placement in the maxillary arch and next-day loading.

1. Initial debridement and self-care instruction with the dental hygiene team was performed to reduce inflammation, lower the bacterial load, and reinforce proper oral hygiene.
2. Digital implant planning for fabrication of tooth-borne reduction and osteotomy guides was completed to ensure implant positioning and accuracy.
3. Full-mouth periodontal and implant therapy was initiated to remove hopeless teeth, control periodontal infection, and prepare the arches for implant-supported rehabilitation.

• Extraction of all remaining maxillary teeth and implant placement for next-day conversion using a digital workflow were carried out to remove nonrestorable teeth and provide an immediate functional and esthetic restoration.
• Osseous resective surgery #19 to 30 with extractions and bone grafting of #18; #31 was performed to correct periodontal defects, remove hopeless teeth, and regenerate adequate bone for periodontal stability.

4. Follow-up visits with localized debridement using guided biofilm therapy at 2, 6, and 12 weeks were scheduled to control biofilm during healing and support peri-implant health.
5. A final integration check and delivery of the final prototype by the restorative dentist were completed to verify implant integration, confirm abutment stability, and finalize the prosthetic design.
6. Periodontal maintenance every 3 months was prescribed to monitor tissue health, maintain implant stability, and prevent recurrence of periodontal disease.

His initial debridement was performed by the dental hygienist, emphasizing the importance of long-term maintenance and patient compliance from treatment onset. He was given a pressure-controlled electric toothbrush with specialized heads, stabilized chlorine dioxide rinse, and a water flosser. Oral hygiene instructions were reviewed and demonstrated at this and subsequent visits. They were provided in written and video formats for improved compliance.

All remaining maxillary teeth were extracted, and alveolar ridge reduction was completed using a prefabricated printed guide to achieve appropriate prosthetic space. Bone-level implants were placed with the aid of a tooth-borne guide for initial osteotomy preparation. Following abutment selection and placement using a denture trough guide, photogrammetry was performed to verify implant position and angulation remotely with the laboratory. Extraction sockets were grafted, flaps were repositioned, and resorbable sutures were placed. A final intraoral scan was taken to initiate fabrication of a milled provisional restoration to enhance form and function. Osseous resective surgery was then completed from #19-30, along with extraction and grafting of hopeless teeth #18 and #31.

The patient returned the next day for delivery of the interim full-arch maxillary restoration. Oral hygiene protocols were reinforced, and he was scheduled for subsequent follow-ups at 2, 6, and 12 weeks for guided biofilm therapy and evaluation. At the final integration check, radiographs confirmed satisfactory healing, and abutments were torqued to their final values. Updated intraoral scans and photogrammetry records were sent to the laboratory to fabricate the final prototype to be delivered by the restorative dentist.

The patient continues to be seen every 3 months for periodontal maintenance. With consistent follow-up, improved oral hygiene practices, and his growing sense of agency and ownership over his oral health, the patient is expected to achieve stable long-term function despite the significant risk factors present at the start of treatment.

Future Directions

A structured post-operative schedule at 2, 6 to 8, and 12 weeks, followed by maintenance every 3 to 6 months depending on risk, reflects tissue healing and is especially important in full-arch implant therapy, where extensive prosthetic surfaces increase hygiene challenges. Early recare enables clinicians to identify inflammation, open contacts, prosthetic convexities, or residual cement before they contribute to irreversible bone loss. Although clinical experience supports this approach, high-quality evidence remains limited. More robust research is needed to evaluate how specific maintenance intervals influence inflammatory markers, microbial changes, radiographic bone stability, and long-term implant survival. Even so, maintenance is as essential to implant therapy as the implant it supports.

References

1. Wang HL, Avila-Ortiz G, Monje A, et al. AO/AAP consensus on prevention and management of peri-implant diseases and conditions: Summary report. J Periodontol. 2025;96:519-541.
2. Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. J Clin Periodontol. 2018;45(Suppl 20):S246-S266.
3. Galarraga-Vinueza ME, Pagni S, Finkelman M, Schoenbaum T, Chambrone L. Prevalence, incidence, systemic, behavioral, and patient-related risk factors and indicators for peri-implant diseases: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:587-633.
4. Kotsakis G, Olmedo D. Peri-implantitis is not periodontitis: Microbiome-biomaterial interactions. Periodontol 2000. 2021;86:231-240.
5. Roccuzzo A, Imber JC, Marruganti C, Salvi GE, Ramieri G, Roccuzzo M. Clinical outcomes of dental implants in patients with and without history of periodontitis: A 20-year prospective study. J Clin Periodontol. 2022;49:1346-1356.
6. Lin GH, Chan HL, Wang HL. The significance of keratinized mucosa on implant health: a systematic review. J Periodontol. 2013;84:1755-67.
7. Lin GH, Lee E, Barootchi S, Rosen PS, Curtis D, Kan J, Wang HL. The influence of prosthetic designs on peri-implant bone loss: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:634-651.
8. Guney Z, Altingoz SM, Has H, Serdar MA, Kurgan S. The impact of electronic cigarettes on peri-implant health: A systematic review and meta-analysis. J Dent. 2024;143:104883.
9. Mojaver S, Zad A, Sarmiento H, Fiorellini JP. Efficacy of supportive peri-implant therapy in the management of peri-implant mucositis and peri-implantitis: A systematic review. J Am Dent Assoc. 2025;S0002-8177:00497-0.
10. Ravidà A, Dias DR, Lemke R, Rosen PS, Bertolini MM. Efficacy of decontamination methods for biofilm removal from dental implant surfaces and reosseointegration: an AAP/AO systematicreview on peri-implant diseases and conditions. Int J Oral Maxillofac Implants. 2025;4:91-160.
11. Maiorani C, Butera A, Pérez-Albacete Martínez C, et al. Effectiveness of erythritol-based air polishing and ultrasonic instrumentation with peek inserts in peri-implant maintenance: a randomized clinical trial including different prosthetic materials. Dent J (Basel). 2025;13:235.
12. Tütüncüoğlu S, Cetinkaya BO, Pamuk F, et al. Clinical and biochemical evaluation of oral irrigation in patients with peri-implant mucositis: a randomized clinical trial. Clin Oral Investig. 2022;26:659-671.
13. Maghsoudi P, Valkenburg C, Ter Gunne LP, van der Weijden FGA. Retrospective evaluation of peri-implant maintenance in patients with implant-supported fixed prostheses. Int J Dent. 2025;2025:9920951.
14. 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.
15. Salvi GE, Bosshardt DD, Lang NP, et al. Temporal sequence of hard and soft tissue healing around titanium dental implants. Periodontol 2000. 2015;68:135-52.
16. Monje A, Barootchi S, Rosen PS, Wang HL. Surgical- and implant-related factors and onset/progression of peri-implant diseases: An AO/AAP systematic review. J Periodontol. 2025;96:542-561.

From Dimensions of Dental Hygiene. May/June 2026;24(3):22-25

My mama always said, “Do what you have always done, and you will get what you have always got.” She was not wrong. Based on the level of disease among our patients, I say it is time for a disruption. A disruption in the way we practice dental hygiene. A disruption in the health outcomes of our patients. And it is time for a disruption in the way we disrupt microbial biofilm.

Most of us learned the “blended approach” in dental hygiene school. Back when calculus removal was king. We now know that periodontal disease is much more complicated than just calculus removal. We also know that we can be more effective, efficient, and cause less damage (especially to the cementum) with ultrasonic instrumentation. So, what’s holding us back? I believe it is simply the comfort of our old habits. We do what we learned in school.

The routine looks like this: we use the ultrasonic around the mouth. We set the ultrasonic down and go back in to scale everything with hand instruments (because we always find calculus the ultrasonic missed). Sound familiar? Me too.

Meanwhile, many of our colleagues don’t even get out the ultrasonic until moderate or heavy deposits are present. Even worse, some gave up the ultrasonic entirely based on unsubstantiated information about it being dangerous for us to use. Or perhaps the office doesn’t stock a variety of tips, so the hardest cases get the 10-year-old bent tip of which there are only four in the whole office. You can see how this is less than ideal even if we are using the blended approach.

A Better Way to Remove Calculus

The blended approach is fine. But just that, fine. It takes a long time, is harder on our bodies, is less comfortable for the patient, and (now with our better microscopic understanding) is inferior. There is a better way.

The solution? Use the ultrasonic to its fullest capability and to completion! Ultrasonic instrumentation removes 50% more biofilm than hand instruments and only one-tenth the cementum.¹

Most of our patients have the largest quantity and most tenacious deposits on their lower anteriors. Start there. If we use the correct tip and setting, the deposit should be tapped, swiped, and otherwise channeled away with ease and speed. Ultrasonic the lower anteriors until all the calculus is removed. Then clean the surfaces facing toward you, followed by the surfaces facing away, to maintain the most efficient chair positioning. Then repeat for the maxillary teeth.

It is at this juncture that dental hygienists want to go back in with hand instruments. However, if we simply switch to a thin ultrasonic tip, we can go back to explore. Research shows that exploring with a thin ultrasonic tip is as effective as using an explorer.² The beauty of using the ultrasonic tip is, if we find deposit, we can simply depress the foot pedal and remove the calculus we miss without switching instruments!

Last, grab your favorite piece of floss and explore everything again and voila! We are done. More biofilm disrupted. Less cementum removed. And with the correct settings, we have a more comfortable and delighted patient. Happily, this is quicker than the blended approach once it is mastered.

Four Tips to Easily Adopt This New Approach

Here are a few more tips for smooth delivery:

1. Know that it takes a little getting used to. The new routine will likely take a few extra minutes the first handful of times we try it.
2. Prep your patients. Tell them how great this instrument is. If we are excited, they will be too.
3. Do not muscle through an ineffective setup. If the tip is too light for the deposit, get a new one. If the tip isn’t working well, get a new one (tips do wear out). If the setting is too high for the conditions, turn it down. Dental hygienists often suffer through what’s on our tray and in our hands. However, if we simply get up and acquire what we need, our bodies, brains, and patients will all be much happier.
4. The slow-speed suction for retraction and evacuation is a dream come true. Rather than tasking our patients with the chore of holding the suction, we can deliver a spa-like experience. This will have them requesting us for all their future recare appointments. I like mine bent at a 90° angle and a full hand grasp to move about freely in conjunction with the ultrasonic. If I need my mirror, I add it to the nondominant suction-holding hand and grasp it with my pinky, ring, and middle fingers.

The Joys of Using a Piezoelectric Ultrasonic

I have one more secret weapon: the piezoelectric ultrasonic! In the past 20 years I have used both piezo and magneto and the piezo is my absolute favorite! The piezoelectric ultrasonic is magnificent for patient comfort and efficacy.^3,4 I don’t think I’ve ever seen a piece of burnished calculus when a piezo was used, while I have found plenty of magnetostrictive deposit burnished by incorrect use. Certainly, we have all missed calculus, but that is why I advocate for exploration with both instruments to remove the deposit as well as floss. And, if there is any question about removal, take an X-ray or use an ODU 11/12, the pigtail, the shepherd’s hook, or explore with anything you prefer.

I love the piezo tips shaped like periodontal probes. They go anywhere and everywhere (just like a periodontal probe). When I use them, it feels like I am using a pencil to color away all the calculus with ease. Tips are available in a wide variety of shapes for different locations and volume of calculus.

Light deposit, healthy tissue? No problem, turn down the setting. Heavy, tenacious, smokers’ calculus that has never been cleaned before? No problem: turn up the power and water, then begin below the bridge of tartar. Watch that gunk blast off the teeth and clog your suction.

As of April 2023, I am an ultrasonic-only clinician roughly 97% of the time. I keep sharp hand instruments nearby for the rare occasion a patient truly does not tolerate the ultrasonic well. I also have a tiny over-sharpened sickle for those crazy tight-under-the contact misaligned teeth that have that last speck of deposit that cannot be reached any other way.

In my practice, I use the Varios 970 by NSK. The settings are easy to adjust so I can be precise with the power for a better result. The Varios is portable, making it easy to use no matter where I am working. The NSK piezo is also easy and smooth for sensitive patients. The water control is fabulous and there is no leakage. It does not heat up at all. All upgrades in my book.

Regardless of the type of ultrasonic you use, I hope you will join me in disrupting patient care and biofilm in the most profound and effective way! Get out that ultrasonic and use it to the fullest. Keep your patients excited, comfortable, and in the chair for as little time as possible. Remove more biofilm and less cementum. Let’s disrupt our way into a healthier next chapter in dentistry for us and for our patients. n

NSK Dental Instruments
www.nskdental.com
888-675-1675

References

1. Parashar A, Bhavsar N. Assessing the effect of piezoelectric ultrasonic scaler tip wear on root surface roughness under influence of various working parameters: A profilometric and atomic force microscopic study. J Indian Soc Periodontol. 2023;27:583-589.
2. Partido B, Webb C, Carr M. Comparison of calculus detection among dental hygienists using an explorer and ultrasonic insert. Int J Dent Hygiene. 2019;17:192-198.
3. Stutzer D, Hofmann M, Eick S, Scharp N, Burger J, Niederhauser T. In-vitro measurement of forces during debridement with a piezoelectric ultrasonic periodontal scaler. Oral Health Prev Dent. 2024;22:223-230.
4. You X, Wu X, Chen S. Effects of a new magnetostrictive ultrasonic scaler and a traditional piezoelectric ultrasonic scaler on root surfaces and patient complaints. Sci Rep. 2024;14:6601.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):26-27

As dental procedures become more sophisticated, potential risks to patients also increase. Adverse events are unintended or harmful incidents that occur during the delivery of dental care, resulting in patient harm or injury. They are the result of medical errors, system failures, or a combination of factors and may cause injury, disability, or even death. Many of these errors occur with regularity in the dental setting, making prevention a priority.

Ethics and Jurisprudence

Healthcare professionals demonstrate their commitment to patient safety by adhering to ethical values that promote the highest level of practice, including:^1-3 nonmaleficence: do no harm; beneficence: doing good and acting in the best interest of others; justice: treating people with fairness and impartiality; veracity: being truthful; autonomy: respecting individuals’ rights to make their own decisions without coercion; confidentiality: keeping each patient’s information private; and trust: acting with integrity to engender trust among patients.

The United States lacks standardized reporting systems and comprehensive data collection in dental settings.⁴ The National Practitioner Data Bank reported that 8,280 adverse reports involving dental hygienists and 34,327 involving dentists were filed between 2000 and 2025.⁵

Many types of adverse events may occur in the dental office (Table 1). Obadan et al⁶ highlight the difficulty of categorizing adverse events, noting that the lack of a standardized dental patient safety taxonomy and wide variation in published case reports make classification challenging. Some of the most cited adverse events are medical errors, which include prescription errors, failure to properly maintain patient records, diagnostic errors, misdiagnosis and failure to refer.⁷ These often stem from negligence or failure to adhere to the standard of care.

Both civil and criminal offenses are perpetrated in the practice of dentistry. Contract law and tort law are two types of civil offenses. Contracts are legally binding agreements to keep a promise in exchange for something of value. The contract binds both parties to fulfill their committed responsibilities. Torts are civil wrongs resulting from the breach of legal duty. Negligence is an unintentional tort that involves the failure to act as a reasonable, prudent person would under similar circumstances. Dental malpractice is a form of professional negligence by an oral health professional that results in injury, harm, or damage to a patient.

Diagnostic Errors

The National Academy of Medicine defines a diagnostic error as a failure to establish an accurate and timely understanding of a patient’s condition or to effectively communicate that information. More broadly, it encompasses mistakes in the diagnostic process that result in missed, delayed, or incorrect diagnoses.⁹

Diagnosis-related issues were the leading cause of serious adverse events in dentistry, accounting for 23% of all reported incidents in a review of 270 US case reports.⁶ The researchers further categorized the extent of harm, reporting that 24% of patients experienced temporary harm significant enough to require a transfer to the emergency department or hospitalization and 24% experienced permanent harm.⁶

A 2025 study found the most common type of diagnostic dental practice malpractice claims was missed diagnoses (78.6%), followed by delayed diagnoses (13.4%), and wrong diagnoses (8.0%).⁹ In the review of 58,229 paid dental claims, missed diagnoses (78.6%) were the most common.⁹ A recent study used a sophisticated record review instrument that uses a list of triggers to alert reviewers to the potential presence of a wrong diagnosis and found that periodontal diseases were misclassified in one third of patients.¹⁰

The failure to diagnose or delayed diagnosis of oral cancer is a documented issue in US dental practices. Close to 58,500 Americans each year are diagnosed with oral or oropharyngeal cancer, causing 12,250 deaths.¹¹ This high rate is, in part, due to the late diagnosis of lesions, which are then in advanced stages with poor prognoses.

A definitive diagnosis of oral cancer can only be made via biopsy, which few general dentists perform.¹² Clinicians and patients should be aware of the most significant risk factors for oral cancer, including alcohol and tobacco use and sun exposure. A recent study evaluated 65 lawsuits regarding oral cavity cancer malpractice from 2000 to 2019. A total of 17 cases had a dentist defendant but no information on the exact judgments was provided.¹³ Still, Epstein et al¹⁴ emphasize the serious medicolegal consequences associated with delayed or incorrect diagnoses, noting that oral health professionals may face litigation when oral cancer is not identified, often due to routine oral examinations being omitted or performed inadequately.

Medication Errors

A medication error refers to any preventable incident that can lead to or result in inappropriate medication use or patient harm while the medication is under the control of a healthcare professional, patient, or consumer.¹⁵ Globally, dentists represent the second largest group of prescribers, including antibiotics, analgesics, anesthetics, anti-inflammatories, and high-fluoride content toothpastes, and antiseptics such as chlorhexidine.¹⁵ It is difficult to quantify the harm resulting from medication errors, especially since research consistently reports widespread misuse of these drugs.¹⁶

Errors associated with anesthetic delivery include administering too much or too little, not waiting long enough for the anesthetic effect to begin, administering an anesthetic known to cause nerve toxicity, accidental intravascular injection, improper needle placement, needle penetration into the orbit, and needle or cartridge breakage.¹⁷

Informed Consent

Oral health professionals must obtain valid consent before starting any treatment. The concept of informed consent is based on the ethical principle of autonomy, which asserts the right of a competent individual to self-determination. A competent person has the right to consent to or refuse any course of treatment. Consent can be given only after a patient has been fully advised of:

• Diagnosis (or suspected diagnosis)
• Nature and purpose of the proposed treatment or procedure; a concise description of what is to be done
• Risks and benefits of the proposed treatment (including common and serious/rare but significant risks)
• Prognosis if the treatment is successful or if it fails
• All alternatives, including the option of no treatment, and the risks and benefits of the alternatives.

Informed consent (Table 2) is generally categorized into three main types, distinguished by the level of formality and documentation required.¹⁸

Informed consent forms should be used for all procedures and should be specific to the procedure, especially if the practice frequently performs complex procedures. The patient must always sign the consent form before treatment is provided.¹⁹

The legal definition and application of consent to treatment are facing increased scrutiny. Failure to obtain valid informed consent can lead to two types of legal claims: negligence and battery. Failing to disclose any risk that ultimately occurs is a breach of the standard of care and is considered negligence. Performing a procedure without consent constitutes battery. Consequently, any healthcare provider who fails to adequately prove that a patient has given valid, proper consent for a procedure is significantly increasing his or her vulnerability to litigation and malpractice lawsuits.

Documentation and Dental Patient Records

Maintaining secure, detailed, and accurate records is an ethical and legal obligation of all oral health professionals. The dental record is a legal document that includes patient’s assessment findings, treatment rendered, outcomes, and notations regarding communications between the patient and office staff.²⁰ Oral health professionals provide the treatment, including dentists, dental hygienists, dental therapists, and dental assistants; however, a nonprovider may also enter information in the dental record. Patients also have responsibilities to their providers. Noting “no show,” “canceled”, or “came late ” is important to indicate patients’ noncooperation as well as patients’ failure to perform self-care or follow referrals as noted in an informed refusal. This will help show contributory negligence.

The dental record clearly states what work was previously completed on the patient and plays a critical role in the event of a malpractice insurance claim. Often, the dental record has absolved providers of responsibility in court cases. While written consent is not always necessary, it is an unequivocal source of proof of an event. Relying on verbal consent is not ideal in proving (or disproving) an event occurred. Dental records are also important when submitting dental benefit claims and help providers monitor progress of treatment.

There is no mandatory way to maintain a dental record. Providers record treatment using whatever format they choose. For example, providers choose different abbreviations for treatment. One dentist may choose to write the word lidocaine while another may choose to use the common abbreviation “lido.”Additionally, most offices now have electronic health records with custom-made templates that allow for ease in completing progress notes.

State laws and participating provider contracts generally specify the time following the last patient visit during which records must be maintained. Different requirements typically exist for the retention of children’s records.

The Privacy Rule and the Security Rule of the Health Insurance Portability and Accountability Act (HIPAA) also affect recordkeeping requirements. While there is no stipulation as to how long patient medical records must be kept (this is usually determined by state law), it does require that certain HIPAA compliance documents must be retained for at least 6 years from their date of creation or the date they were last in effect. The dental office should have a records retention policy and all staff should understand it. Poor documentation and record-keeping errors are a major contributing factor in dental malpractice lawsuits.

Patient Safety Initiatives

Evident from the lack of literature related to dental patient safety, standardized safety conventions and initiatives in dentistry are slowly starting to materialize. In 1999, Congress created the Agency for Healthcare Research and Quality (AHRQ) to support patient safety research and state-of-the-art data analytics tools to analyze and improve the US healthcare system.²⁰ The organization has proposed a four-element patient safety framework to reduce treatment-related harm:²¹

1. Identifying patient safety threats through rigorous chart reviews and assessing organizational patient safety cultures using the Medical Office Survey on Patient Safety Culture. This has been adapted for use in dentistry, in dental schools, specifically. It requires considerable resources.
2. Identifying and evaluating effective patient safety practices using root-cause analysis and health are failure mode and effect analysis.
3. Disseminating and implementing best practices while enlisting the help of organizations and stakeholders.
4. Monitoring threats to patient safety to encourage a positive safety culture.

In 2005, AHRQ was further empowered, through the Patient Safety and Quality Improvement Act, to create and maintain a Network of Patient Safety Databases, which provides interactive, evidence-based management resources for healthcare providers, patient safety organizations (PSOs) listed by AHRQ, and others.²² The Dental Patient Safety Foundation gathers data on adverse incidents, publishes case reviews, and provides real-time data.²³ Additionally, the American Dental Association established the Dental Quality Alliance to promote safety.²⁴

A single provider can do a lot to ensure patient safety, such as creating a safety culture that includes infection prevention and control, ensuring medical histories are thoroughly reviewed, use of safety checklists, maintaining clear, accurate records to ensure continuity of care and prevent miscommunication, obtaining informed consent, and participating in continuing dental education.

Conclusion

The underreporting of adverse events coupled with the lack of scientific research creates an imperative to enhance patient safety. Ethical principles along with informed consent and meticulous recordkeeping form the foundation from which all oral health professionals practice. The lack of a standardized reporting system and patient safety taxonomy continues to put patient safety at risk. Ultimately, reducing patient harm requires a conscious, daily commitment from every oral health professional.

References

1. American Dental Association. Principles of Ethics and Code of Professional Conduct. Available at ada.org/about/principles/code-of-ethics. Accessed April 14, 2026.
2. American Dental Hygienists’ Association (ADHA). ADHA Code of Ethics. Available at adha.org/about-adha/policies-bylaws/. Accessed April 14, 2026.
3. American Dental Assisting Association (ADAA). ADAA Principles of Professional Ethics. Available at https://adaausa.org/about/about-adaa/. Accessed April 14, 2026.
4. Kalenderian E, Obadan-Udoh E, Maramaldi P, et al. Classifying adverse events in the dental office. J Patient Saf. 2021;17:e540-e556.
5. Division of Practitioner Data Bank. Data Analysis Tool. Available at npdb.hrsa.gov/analysistool. Accessed April 14, 2026.
6. Obadan EM, Ramoni RB, Kalenderian E. Lessons learned from dental patient safety case reports. J Am Dent Assoc. 2015;146:318-326.
7. Grober ED, Bohnen JM. Defining medical error. Can J Surg. 2005;48:39-44.
8. Obadan-Udoh E, Howard R, Valmadrid LC, Walji M, Mertz E. Patients’ experiences of dental diagnostic failures: a qualitative study using social media. J Patient Saf. 2024;20:177-185.
9. Singhania R, Obadan-Udoh E. Dental diagnostic errors and characteristics associated with claims in the United States, 1990-2020. J Am Dent Assoc. 2025;156:563-570.
10. Tokede B, Yansane A, Brandon R, et al. The burden of diagnostic error in dentistry: a study on periodontal disease misclassification. J Dent. 2024;148:105221.
11. Oral Cancer Foundation. Oral Cancer Facts. Available at https://oralcancerfoundation.org/facts/. Accessed April 14, 2026.
12. González-Moles MÁ, Aguilar-Ruiz M, Ramos-García P. Challenges in the early diagnosis of oral cancer, evidence gaps and strategies for improvement: a scoping review of systematic reviews. Cancers. 2022;14:4967.
13. Wong A, Zhu D, Tong JY, et al. The jaw-dropping costs of oral cavity cancer malpractice. Head Neck. 2021;43:2869-2875.
14. Epstein JB, Sciubba JJ, Banasek TE, Hay LJ. Failure to diagnose and delayed diagnosis of cancer: medicolegal issues. J Am Dent Assoc. 2009;140(12):1494-1503.
15. Eriksen N, Kleva S, Shpati D, Xhizdari R. Medical errors in dentistry, improving by knowing and accepting the reality. Eur J Med Nat Sci. 2024;7.
16. Lockhart PB, Thornhill MH, Zhao J, et al. Factors that affect dentists’ use of antibiotic prophylaxis: findings from the National Dental Practice-Based Research Network questionnaire. J Am Dent Assoc. 2022;153(6):552-562.
17. Nagelberg R. Medical errors in dentistry. RDH. 2015;35:79-85.
18. Kakar H, Gambhir RS, Singh S, Kaur A, Nanda T. Informed consent: corner stone in ethical medical and dental practice. J Family Med Prim Care. 2014;3:68-71.
19. American Dental Association. Types of Consent. Available at ada.org/resources/practice/practice-management/types-of-consent. Accessed April 14, 2026.
20. Agency for Healthcare Research and Quality. AHRQ: A Brief History. Available at ahrq.gov/cpi/about/brief-history.html. Accessed April 14, 2026.
21. Yansane A, Walji MF, Kalenderian E. Introducing safety in dentistry: perspectives and directions. J Calif Dent Assoc. 2019;47:433-437.
22. Agency for Healthcare Research and Quality. What is the Network of Patient Safety Databases? Availabel at ahrq.gov/npsd/what-is-npsd/index.html. Accessed April 14, 2026.
23. Dental Patient Safety Foundation. Enhance Our Culture of Safety. Available at dentalpatientsafety.org/. Accessed April 14, 2026.
24. American Dental Association. Dental Quality Alliance. Available at ada.org/resources/research/dental-quality-alliance. Accessed April 14, 2026.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):28-31

Dental hygienists are uniquely positioned to identify, assess, and contribute to the management of complex oral manifestations of systemic diseases and their treatments. Among the most debilitating complications encountered in oncology patients is oral mucositis (OM), an inflammatory response of the oral mucosa marked by ulcerations caused by cytotoxic cancer therapies. OM profoundly impacts quality of life, often leading to severe pain, compromised nutrition, increased risk of systemic infection, and even interruption or modification of cancer treatment.

While medical oncologists, radiation oncologists, and oncology nurses collaborate to manage the primary disease and its systemic effects, cancer therapies can also significantly affect the oral cavity and require dedicated management. By understanding the intricate pathophysiology of OM, its clinical presentations, and evidence-based management strategies, dental hygienists can help alleviate patient suffering, improve treatment adherence, and contribute to better overall outcomes.

OM can result in erythema, edema, and ulcerative lesions of the oral mucosa and may range from mild to severe including small ulcerations and those large enough to impair oral function (Table 1). For patients undergoing chemotherapy, approximately 40% will develop OM at some stage during treatment, typically 5 to 7 days after starting medication. For those receiving both chemo- and radiation therapy, this percentage increases to approximately 90%.^1-3

OM is a complex biological process of cellular injury, inflammation, and tissue breakdown (Figure 1). This intricate process is typically divided into five phases (Table 2), regardless of whether the etiology is chemotherapy or radiation.^1-5

Phase 1. The initiation phase begins immediately upon exposure to chemo- or radiation therapies. Cancer treatments, which are designed to target rapidly dividing cancer cells, also damage rapidly proliferating healthy cells, including the basal epithelial cells of the oral mucosa.

Phase 2. The signaling phase occurs after the cellular damage is initiated and activates several molecular pathways. Signaling molecules amplify the initial damage leading to further cell death and an escalating inflammatory response. The subepithelial connective tissue and vasculature are impacted in this phase, contributing to the overall tissue injury.

Phase 3. In the amplification phase, pro-inflammatory cytokines released in the signaling phase continue to recruit inflammatory cells and perpetuate the cycle of tissue damage. This leads to a further decrease in epithelial cell proliferation and a thinning of the oral mucosal lining. The delicate balance between cell death and cell renewal is severely disrupted, making the mucosa increasingly vulnerable.

Phase 4. During the ulceration phase, symptoms present clinically with the breakdown of the oral epithelial barrier. As the basal epithelial cells are destroyed and their regenerative capacity is compromised, the overlying mucosa thins and eventually sloughs, exposing the underlying connective tissue. This leads to the formation of painful, erythematous, and often pseudomembranous ulcers. The loss of mucosal integrity provides a direct pathway for oral microorganisms to enter the compromised tissues, thus significantly increasing the risk of local and systemic infections. This phase typically peaks around 7-14 days after the start of chemotherapy, or 2-3 weeks into radiation therapy.^1-5

Phase 5. The healing phase begins as the cancer therapy is discontinued, or the mucosal cells have had a chance to recover. This phase involves the proliferation and migration of surviving epithelial cells, re-epithelialization of the ulcerated areas, and resolution of inflammation. The duration of healing can vary widely, from a few weeks to several months, depending on the severity of the mucositis and the patient’s overall health and immune status.

Impact of Oral Mucositis on the Patient

The effects of oral mucositis extend far beyond the oral cavity. Arguably, the most dominant symptom is pain. Interference with virtually all oral functions occurs as the palate, tongue, cheeks, floor of mouth, lips, and pharynx are damaged. Pain ranging from mild discomfort to debilitating pain can require strong opioid analgesics.

Chemotherapy and radiation often cause dysphagia, odynophagia, and dysgeusia. This, combined with pain, severely reduces appetite.⁵ Inadequate oral intake results in weight loss, nutritional deficiencies, and dehydration. Malnutrition can further impair immune function and delay wound healing, initiating a pattern of deterioration. In severe cases, patients may require enteral (feeding tube) or parenteral (intravenous) nutrition.⁶

The affected oral mucosa now functions as an entry point for opportunistic pathogens. Patients undergoing cancer treatment are often profoundly immunocompromised (neutropenic) because of therapy.⁷ This combination dramatically increases the risk of local oral infections and, more dangerously, systemic infections (sepsis). Oral sepsis originating from mucositis-related ulceration can be life-threatening and may require hospitalization.^6,8

OM also negatively affects quality of life, limiting patients’ ability to perform activities of daily living and hindering their emotional well-being and social interactions.⁹ Speech may be impaired, affecting the patient’s communication. Patients may experience anxiety, depression, and frustration. This decreased quality of life may reduce the desire to continue with prescribed therapy.¹⁰

Severe OM is a common reason for delaying or reducing doses of cancer therapy.^1,6 While these modifications aim to alleviate suffering and prevent life-threatening complications, they can compromise the efficacy of the cancer treatment. Effective OM management to support treatment adherence is critical. The management of OM, depending on the severity, may include hospitalizations, increased clinic visits, medications, and nutritional support. All of which can impose a significant economic burden on patients and healthcare systems.^6,8,11

Etiology of Oral Mucositis

While the underlying mechanism of OM involves damage to rapidly dividing cells, specific cancer treatments and patient-related factors significantly influence the incidence and severity of OM. Certain chemotherapeutic agents are more cytotoxic than others. Antimetabolites and certain alkylating agents are particularly notorious for inducing severe OM.^4,12 High-dose chemotherapy regimens, especially those used in preparation for hematopoietic stem cell transplantation (HSCT), are associated with a remarkably high incidence and severity of OM (70% to 100%).^6,7 The use of multiple chemotherapeutic agents concurrently, or chemotherapy combined with radiation therapy, significantly increases the risk and severity of OM.⁶

Radiation to the head and neck region, particularly when the oral cavity is within the treatment field, is a primary cause of OM. The severity is related to the volume of oral mucosa irradiated and the total cumulative dose.⁶ Hypofractionated regimens (larger doses per fraction) can sometimes lead to more acute, severe mucositis compared to conventional fractionation.¹³

Patients undergoing HSCT receive extremely high doses of chemotherapy (myeloablative conditioning regimens), often followed by total body irradiation. This combination invariably leads to severe, often Grade 3 or 4, oral mucositis, which is frequently cited by patients as the most distressing side effect of their transplant.⁶

Proactive, Preventive, and Palliative

The dental hygienist is uniquely positioned to impact the comprehensive care of oncology patients at risk for or experiencing OM. Expertise in oral health assessment, preventive strategies, patient education, and supportive care make dental hygienists invaluable members of the interdisciplinary team. The role encompasses proactive intervention, vigilant monitoring, and empathetic palliative care. Optimizing oral health before the initiation of cancer therapy is paramount in reducing the incidence and severity of OM.

Pretreatment assessment and intervention are arguably the most critical phases. A detailed history of the patient’s cancer diagnosis, planned treatment regimen (chemotherapy, radiation, HSCT), anticipated side effects, current medications (including over-the-counter and herbal supplements), allergies, and any history of previous oral complications should be obtained. Clinically, a thorough examination of the head, neck, lymph nodes, lips, buccal mucosa, labial mucosa, gingiva, tongue (dorsal, ventral, lateral borders), floor of the mouth, hard and soft palate, and oropharynx should be performed. Documentation of any existing lesions, infections, or abnormalities is necessary. Intraoral photographs are an excellent form of documentation for this step.

Next, the patient’s periodontal status should be evaluated, including probing depths, bleeding on probing, clinical attachment loss, and presence of calculus. Active periodontal disease is a significant risk factor for OM. Prescribed periodontal therapy should be performed to reduce inflammation and bacterial load. Review of recent radiographs to identify periapical lesions, impacted teeth, or other bony pathologies that may pose a risk during immunosuppression.

An examination of the hard tissue is important to identify any existing carious lesions, especially those approaching the pulp or causing sensitivity. Restoration of carious lesions should be completed, and extraction of nonrestorable teeth considered, especially those with periapical lesions or severely periodontally involved teeth. These procedures need to be completed prior to head and neck radiation or bone marrow transplant during which the risk of osteoradionecrosis or osteonecrosis of the jaw is high.

Extractions should ideally be completed with sufficient time (7 to 14 days for healing) before the start of cancer therapy.¹⁴ If a patient uses a removable prosthesis of any kind, the fit and condition should be assessed to identify areas of irritation or potential trauma. Ill-fitting appliances can exacerbate OM, so sharp cusps should be smoothed, adjustments made, or temporary denture discontinuation may be recommended. While daily oral hygiene is crucial, routine  preventive visits should also be maintained. Prophylactic steps taken with an oral healthcare provider can reduce the risk of mucositis by more than 25%.¹⁵

When speaking to the patient, define OM, why it occurs, and what symptoms it may cause. Use simple language and visual aids if available. Stress the critical importance of maintaining meticulous oral hygiene before, during, and after treatment.

Recommend an extra-soft toothbrush, emphasizing gentle, thorough brushing at least two to four times daily, especially after meals and before bed. Advise the patient to replace the toothbrush frequently (every 3-4 weeks, or after an infection). Toothbrush storage is also important. Patients may become immunocompromised; an improperly stored toothbrush may introduce new risks. Recommend storing the toothbrush in an area away from family toothbrushes that will allow air flow.¹⁶

Suggest a nonabrasive, fluoride-containing toothpaste with a mild flavor (avoid strong mints or whitening agents that can irritate). Encourage daily flossing but advise patients to stop if it causes excessive pain or bleeding that doesn’t subside within a couple of minutes. If patients were not consistent flossers prior to their diagnosis, now may not be the time to start. Instruct them to consult with their oncology team if platelet counts are low, as flossing may be contraindicated.

Nonirritating mouthrinses may be recommended. A sodium bicarbonate rinse is ideal. The standard recipe is 1 teaspoon of salt and 1 teaspoon of baking soda mixed into 4 cups of warm water. Advise rinsing frequently (four to six times daily, especially after meals and before bed, and even hourly if symptoms are severe). Patients should make their sodium bicarbonate rinse daily. Emphasize swishing for at least 30 seconds and spitting out. Patients with OM should avoid alcohol-containing hydrogen peroxide, chlorhexidine (unless specifically prescribed by the oncology team for a targeted infection), and highly acidic or irritating commercial mouthrinses. The Multinational Association of Supportive Care in Cancer recommends benzydamine mouthrinse for the prevention of OM. Note: This rinse is only available by prescription in the United States through a compounding pharmacy.²

Advise regular application of water-soluble or lanolin-based lip lubricants to prevent dryness and cracking.

Patients who wear dentures should remove them for at least 8 hours daily ( overnight) and clean them thoroughly after each meal. If mucositis develops, advise wearing dentures only during meals or discontinuing them altogether if they cause irritation or pain.

Guidance on appropriate dietary choices during mucositis onset should be provided. Recommend soft, bland, moist foods that are easy to chew and swallow, such as mashed potatoes, scrambled eggs, yogurt, smoothies, pureed fruits, and cooked cereals. Encourage adding gravies or sauces to foods to make them easier to consume.

Patients should be advised against eating acidic, spicy, hot, and crunchy foods as well as consuming carbonated beverages. Suggest lukewarm or cool foods and beverages, as extreme temperatures can increase pain. Encourage patients to take frequent sips of water throughout the day to keep the mouth moist and aid in cleansing.

Patients should understand when it is time to reach out to their oncology team; for instance, in light of worsening pain, inability to eat or drink, fever, signs of infection, and bleeding.

Emerging Therapies

While supportive care is still the cornerstone of OM management, research continues to explore new preventive and therapeutic interventions. Palifermin (recombinant human keratinocyte growth factor-1) is the only US Food and Drug Administration-approved medication for reducing the incidence and duration of severe OM in patients undergoing HSCT for hematologic malignancies. It works by promoting the growth and repair of epithelial cells.²

Growing evidence supports the use of lower-level laser therapy (LLLT) for the prevention and treatment of OM, particularly in head and neck cancer patients receiving radiation and in HSCT patients. LLLT is thought to reduce inflammation, promote cell proliferation and provide analgesic effects.^2,8

Used during chemotherapy, cryotherapy can reduce the severity of OM due to vasoconstriction reducing the amount of drug delivered to the oral mucosa. Continued research is exploring the precise timing and duration for maximal benefit.⁸ Understanding the role of the oral microbiome in the pathogenesis and resolution of OM may lead to novel probiotic or prebiotic interventions.

Conclusion

OM demands a comprehensive and interdisciplinary approach to care. By thoroughly understanding the etiology, pathophysiology, impact, and evidence-based management of OM, dental hygienists can provide invaluable pretreatment preparation, vigilant monitoring during therapy, and empathetic palliative care.

References

1. Pulito C, Cristaudo A, Porta CL, et al. Oral mucositis: the hidden side of cancer therapy. J Exp Clin Cancer Res. 2020;39:210.
2. Blakaj A, Bonomi M, Gamez ME, Blakaj DM. Oral mucositis in head and neck cancer: Evidence-based management and review of clinical trial data. Oral Oncol. 2019;95:29-34.
3. Wong HM. Oral complications and management strategies for patients undergoing cancer therapy. ScientificWorldJournal. 2014;2014:581795.
4. Basile D, Di Nardo P, Corvaja C, et al. Mucosal injury during anti-cancer treatment: from pathobiology to bedside. Cancers. 2019;11:11060857.
5. Kutuk T, Atak E, Villa A, Kalman NS, Kaiser A. Interdisciplinary collaboration in head and neck cancer care: optimizing oral health management for patients undergoing radiation therapy. Curr Oncol. 2024;31:2092-2108.
6. Gugnacki P, Sierko E. Is there an interplay between oral microbiome, head and neck carcinoma and radiation-induced oral mucositis? Cancers (Basel). 2021;13:5902.
7. Raber-Durlacher JE, Elad S, Barasch A. Oral mucositis. Oral Oncol. 2010;46:452-456.
8. Lalla RV, Saunders DP, Peterson DE. Chemotherapy or radiation-induced oral mucositis. Dent Clin North Am. 2014;58:341-349.
9. Al-Rudayni AHM, Gopinath D, Maharajan MK, Menon RK. Impact of oral mucositis on quality of life in patients undergoing oncological treatment: A systematic review. Transl Cancer Res. 2020;9:3126-3134.
10. Jung YS, Park EY, Sohn HO. Oral health status and oral health-related quality of life according to presence or absence of mucositis in head and neck cancer patients. J Cancer Prev. 2019;24:43-47.
11. Tang X, Li W, Zhong Q, Wan L. Effects of omega-3 fatty acids on oral mucositis induced by anticancer therapy: a meta-analysis. Nutr Cancer. 2025;77:600-609.
12. Liu M, An R, Wu Z, Dai L, Zeng Q, Chen W. The trajectory of oral mucositis in head and neck cancer patients undergoing radiotherapy and its influencing factors. Ear Nose Throat J. 2025;104:NP257-NP269.
13. Nahum AE. The radiobiology of hypofractionation. Clin Oncol. 2015;27:260-269.
14. Strobl J, Ballicas N, Wachter B, et al. Dental health, conditioning and oral mucositis in allogeneic hematopoietic stem cell transplantation: a single-center study. Cytotherapy. 2025;27:1130-1136.
15. Brown TJ, Gupta A. Management of cancer therapy-associated oral mucositis. JCO Oncol Pract. 2020;16:103-109.
16. Dayoub MB, Rusilko D, Gross A. Microbial contamination of toothbrushes. J Dent Res. 1977;56:706.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):32-35

The Epstein-Barr virus (EBV), a member of the human herpesvirus IV family, is a widespread and impactful pathogen with a complex history.¹ Recognized in 1968, EBV is the etiological agent of infectious mononucleosis, commonly referred to as mono.^. EBV primarily spreads through saliva, which led to its nickname “the kissing disease,” though its modes of transmission are not limited to this pathway. Sharing drinks, eating utensils, or any other contaminated object with infected saliva can facilitate transmission, making it a master of subtle spread.^2–10

Dental hygienists are easily exposed in clinical settings through routine procedures that involve saliva, especially those that generate aerosols. Dental hygienists are not only at risk for EBV exposure, they are uniquely positioned to recognize its oral manifestations and guide patients on proper management.

Signs and Symptoms

EBV is typically asymptomatic in most individuals; however, it can cause visible signs and symptoms in cases of infectious mononucleosis (Table 1).^2–7,9,11 These include fatigue, fever, swollen lymph nodes, rash, oral candidiasis, oral hairy leukoplakia, gingivitis, and periodontitis.¹²

Oral candidiasis, also known as “oral thrush,” arises from an overgrowth of Candida albicans fungi, appearing as soft, creamy white patches on the tongue, buccal mucosa, and the soft and hard palate (Figure 1).^8,13 These fungal plaques can be easily scraped away. C. albicans is a commensal species, meaning that it benefits from the oral environment but does not harm it. However, in large amounts, C. albicans can become pathogenic, thus causing denture stomatitis. Oral candidiasis is commonly found in patients with oral prostheses.^14,15 Immunocompromised patients, especially those with human immunodeficiency virus, are at risk for infections from C. albicans.¹⁵

EBV may also cause oral hairy leukoplakia to develop in the oral cavity, which may be misdiagnosed as oral candidiasis.^2-4,16 Hairy leukoplakia presents as persistent white patches or lesions firmly attached to the ventral, dorsolateral, and lateral borders of the tongue, soft palate, floor of the mouth, and oropharynx. This manifestation is extremely resistant to scraping and will continue until the viral source is addressed.^8,17 Like oral candidiasis, oral hairy leukoplakia is more often found in immunosuppressed individuals.¹⁶ Oral hairy leukoplakia is contagious, and oral candidiasis is typically not.¹³

Research shows EBV is associated with increased risk of periodontitis, specifically chronic periodontitis.^9,18–20 Zeng et al¹⁹ infected human gingival fibroblasts with levels of EBV. This resulted in high levels of inflammatory cytokines. Inflammatory cytokines are associated with periodontal inflammation, which explains how EBV may cause gingivitis.

Pathophysiology

A thorough understanding of the pathophysiology of EBV enables clinicians to comprehend how the virus targets the body and how the body responds. EBV first crosses the body’s physical barriers, then activates both the innate and adaptive immune responses. The virus specifically infects B lymphocytes and epithelial cells in the oropharynx, particularly the tonsils. The adaptive immune response is activated, targeting the specific antigens involved. B cells attach to the antigens, processing them and initiating an immune response locally in the tonsils. This activation of B cells results in IgG, IgM, and IgA antibody production. Additionally, B cells and macrophages stimulate cytotoxic T cell (CD8) activity, which identifies and eliminates infected B cells.^{2,3,5-7,21-23}

After the initial infection, EBV establishes latency through memory B cells. The virus produces latency-associated transcripts, which enable the virus to remain undetectable, with the opportunity to reactivate. This can lead to the recurrence of symptoms and contribute to chronic conditions. Specific factors, such as stress, immunosuppressants, and environmental influences, can trigger this viral reactivation, perpetuating its impact on the body.^2-4,6,7,9,22

Chronic periodontitis and EBV continue to rise globally, with correlations found between the two. Current evidence suggests a potential link between EBV reactivation and butyric acid (BA) found in oral fluids, likely influenced by BA-producing bacteria such as Porphyromonas gingivalis and Fusobacterium nucleatum.^9,24 Although more mechanistic research and larger clinical studies are still needed, progress has been limited by the fact that EBV infects only humans, making traditional animal models unsuitable. To address this challenge, a new humanized-mouse model is being developed, and early findings show EBV-positive B-cell infiltration and osteoclast induction in periodontal tissues, with validation ongoing.⁹

Co-Infection With Periodontally Involved Bacteria

The periodontal pathogens that correlate with EBV-reactivation are: P. gingivalis, Aggregatibacter actinomycetemcomitans, F. nucleatum, Prevotella intermedia, Helicobacter pylori, Streptococcus pyogenes, Treponema pallidum, and Tannerella forsythia.^9,24

4. gingivalis, a red-complex bacteria, is highly prevalent in EBV-positive patients with periodontal diseases. In patients with chronic periodontitis, EBV DNA and P. gingivalis were detected together more often in deeper periodontal pockets than when either organism was present alone.²⁰ This EBV-P. gingivalis coexistence occurred in approximately 40% of chronic periodontitis patients with probing depths ≥ 5 mm, and the associated odds ratio of 4.67 was higher than that of either microorganism individually. These findings indicate that the combined presence of EBV and periodontopathic bacteria may significantly elevate the risk of periodontitis.^8,9,20
5. actinomycetemcomitans is a Gram-negative anaerobic bacterium associated with periodontitis, previously referred to as aggressive periodontitis. A. actinomycetemcomitans triggers reactivation of EBV into its productive viral cycle.²⁴ P. intermedia is an obligate anaerobic, rod-shaped bacterium that is known for causing periodontal diseases. Unlike other periodontal pathogens, this bacterium does not secrete high concentrations of BA. This suggests that it does not create an EBV reactivation through the histone deacetylases pathway, ultimately, facilitating an alternate mechanism. Because P. intermedia produces lipopolysaccharides (LPS) that drive inflammatory responses in periodontal diseases, it also contributes to structural and molecular changes mediated by pro-inflammatory interleukins. Additionally, the LPS in P. intermedia in host immune cells activates dependent pathways through cell-surface receptors. Ultimately, these signaling pathways lead to lytic gene expression that results in the reactivation of EBV.^24-26

Although S. pyogenes is primarily recognized for causing pharyngitis, skin infections, and various systemic complications, its behavior offers meaningful insight into how bacterial pathogens can influence oral and periodontal health. This organism has been shown to enhance EBV reactivation by activating B cells and disrupting normal immune regulation, emphasizing how bacterial-viral interactions can contribute to broader inflammatory responses within the oral cavity.²⁴

Coinfection with group A Streptococci (GAS) and EBV has also been documented in pharyngitis, where GAS-derived superantigens nonspecifically stimulate T cells and further amplify inflammation.²⁴ While S. pyogenes is not classified as a traditional periodontal pathogen, its capacity to modulate host immunity, promote inflammatory cascades, and increase salivary viral loads suggests that similar mechanisms may intensify periodontal inflammation and accelerate tissue breakdown.²⁴

Dental Hygienists’ Role in Patients With Epstein-Barr Virus

Comprehensive medical and dental histories must be taken to identify if a patient has any potential or known diagnosis of EBV infection or infectious mononucleosis. A thorough patient interview will help with the collection of all relevant information. The dental hygienist should document all findings by noting any signs or symptoms. Because EBV is so contagious, dental hygienists should not treat an infected patient but rather encourage him or her to reschedule the appointment. However, providing appropriate guidance on managing symptoms is vital to supporting patients’ well-being.

In some cases, patients may be unaware of their EBV infection and present to their dental hygiene appointments. Dental hygienists should complete a thorough extraoral and intraoral examination and connect the signs, symptoms, and oral manifestations discussed in Table 1, specifically ulcerations in the oral cavity, swollen lymph nodes in the neck, and hairy leukoplakia/oral candidiasis. Once these conditions have been identified, further questioning of other symptoms, such as fatigue, fever, and sore throat, should be done, as well as the history and duration of symptoms.^3–6,11,21 Further questioning of the patient to identify duration is critical because the incubation period of infectious mononucleosis can last for 4 to 6 weeks.²⁷ Once symptoms resolve, patients are safe to resume dental hygiene services.²⁸ Patients should seek their primary care provider for an official diagnosis, but can be educated on EBV management in the dental setting.

In terms of oral hygiene instruction, patients with oral lesions, particularly painful ones, should monitor symptoms closely and seek a referral to the proper healthcare professional, such as physicians or medical virology specialists, if symptoms persist or worsen.^5,29 For pain relief associated with EBV, over-the-counter medications, such as acetaminophen or ibuprofen, can be recommended, as well as brushing gently using a soft-bristled toothbrush to minimize irritation. Staying hydrated, the use of saline rinses to soothe throat discomfort, and fluoride treatments to protect tooth enamel in cases of xerostomia are all helpful strategies for patients with EBV.¹² Once recovered, patients should replace oral hygiene products to prevent reinfection. Patients currently or previously infected with EBV should be educated about proper self-care to reduce the likelihood of gingivitis and periodontitis.

When caring for patients affected by both EBV and periodontitis, the dental hygienist’s role centers on comprehensive assessment, prevention, and strategic patient education. Due to EBV’s ability to increase inflammatory pathways and interact with periodontal pathogens, clinicians must closely monitor overall periodontal status. This includes meticulous periodontal charting, efficient debridement, and targeted biofilm disruption while remaining aware that viral-related immune dysregulation may negatively influence healing responses. Effective collaboration with medical providers is essential to ensure coordinated management and timely referral when inflammation does not resolve as expected, including referral to a periodontist when deeper probing depths persist. Through this integrated approach, dental hygienists help support improved periodontal outcomes in patients whose disease may be complicated by EBV reactivation and its associated symptoms.

Dental hygienists can provide psychosocial support by listening and acknowledging concerns and encouraging stress-reducing techniques to manage EBV symptoms.^22,30 Patients need providers who practice active listening to help empower them, especially with this type of condition.³¹ Dental hygienists can also help by offering patients resources, including community support and educational resources from organizations such as the National Organization for Rare Disorders.³²

Conclusion

EBV poses significant implications for both general and oral health. Dental hygienists play a crucial role in recognizing important oral manifestations, guiding patients in managing symptoms, and providing preventive care. Dental hygienists need to be careful in the event that patients are unaware of a potential infection, so maintaining standard precautions is crucial. Early identification of EBV-related symptoms, along with time-effective referrals to healthcare providers, is essential for effective patient care.

Consideration of a patient’s immunosuppressed health status and potential re-infection with EBV is essential for dental hygienists to identify, especially in patients with periodontitis. The coinfection of EBV with periodontitis intensifies tissue breakdown due to the pro-inflammatory cytokines. These cytokines impair the host’s immune response by triggering a synergistic relationship that contributes to deeper periodontal pockets and advanced loss of soft tissue. Understanding the complexities of EBV, its co-infection rate with periodontal pathogens, and its impact on oral health enables oral health professionals to deliver comprehensive, patient-centered care that addresses both the physical and emotional aspects of the infection.

References

1. Sangueza-Acosta M, Sandoval-Romero E. Epstein-Barr virus and skin. An Bras Dermatol. 2018;93:786–799.
2. Yu H, Robertson ES. Epstein-Barr virus history and pathogenesis. Viruses. 2023;15:714.
3. Damania B, Kenney SC, Raab-Traub N. Epstein-Barr virus: Biology and clinical disease. Cell. 2022;185:3652–3670.
4. Chakravorty S, Afzali B, Kazemian M. EBV-associated diseases: Current therapeutics and emerging technologies. Front Immunol. 2022;13:1059133.
5. Hoover K, Higginbotham K. Epstein-Barr Virus. Treasure Island, Florida: StatPearls Publishing; 2023.
6. Houen G, Trier NH. Epstein-Barr virus and systemic autoimmune diseases. Front Immunol. 2021;11:587380.
7. Dasari V, McNeil LK, Beckett K, et al. Lymph node targeted multi-epitope subunit vaccine promotes effective immunity to EBV in HLA-expressing mice. Nat Commun. 2023;14:4371.
8. Slots J, Saygun I, Sabeti M, Kubar A. Epstein-Barr virus in oral diseases. J Periodontal Res. 2006;41:235–424.
9. Imai K, Ogata Y. How does Epstein-Barr virus contribute to chronic periodontitis? Int J Mol Sci. 2020;21:1940.
10. Khanna R. Kissing the Epstein-Barr virus goodbye? Available at science.org.au/curious/people-medicine/epstein-barr-virus. Accessed April 2, 2026.
11. Naughton P, Healy M, Enright F, Lucey B. Infectious mononucleosis: diagnosis and clinical interpretation. Br J Biomed Sci. 2021;78:107–116.
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13. Talapko J, Juzbašić M, Matijević T, et al. Candida albicans—The virulence factors and clinical manifestations of infection. J Fungi (Basel). 2021;7:79.
14. Devcic M, Simonic-Kocijan S, Prpic J, et al. Oral candidal colonization in patients with different prosthetic appliances. J Fungi (Basel). 2021;7:662.
15. Manikandan S, Vinesh E, Selvi D, Kannan R, Jayakumar A, Dinakaran J. Prevalence of Candida among denture wearers and nondenture wearers. J Pharm Bioallied Sci. 2022;14(Suppl 1):S702–705.
16. Mahalakshmi SKJ, Safreen V, Sivaraj R, Haripriya G, Deepasree B. Oral candiasisis mimicking leukoplakia in an immunocompetent male: A rare case report. Int J Pharm Sci. 2025;3:5343–5346.
17. Mohammed F, Fairozekhan AT. Oral Leukoplakia. Treasure Island, Florida: StatPearls Publishing; 2023.
18. Gao Z, Lv J, Wang M. Epstein–Barr virus is associated with periodontal diseases. Med (Baltimore). 2017;96:e5980.
19. Zeng W, Liu G, Luan Q, et al. Epstein-Barr virus promotes inflammatory cytokine production in human gingival fibroblasts. Int Dent J. 2024;74:607–615.
20. Kato A, Imai K, Ochiai K, Ogata Y. Higher prevalence of Epstein–Barr Virus DNA in deeper periodontal pockets of chronic periodontitis in Japanese patients. PLoS One. 2013;8:e71990.
21. Che Y, Ding X, Xu L, et al. Advances in the treatment of Hodgkin’s lymphoma (Review). Int J Oncol. 2023;62:61.
22. Chen CJ. Epstein-Barr virus reactivation and disease flare of systemic lupus erythematosus. Taiwan J Obstet Gynecol. 2024;63:161–164.
23. Lamont R, Hajishengallis G, Koo H, Jenkinson H. Oral Microbiology and Immunology. 3rd ed. Washington, DC: ASM Press; 2019:480.
24. Indari O, Ghosh S, Bal A, et al. Awakening the sleeping giant: Epstein-Barr virus reactivation by biological agents. Pathog Dis. 2024;82:ftae002.
25. Nørskov-Lauritsen N, Claesson R, Jensen A, Åberg C, Haubek D. Aggregatibacter actinomycetemcomitans: clinical significance of a pathobiont subjected to ample changes in classification and nomenclature. Pathog. 2019;8:243.
26. Könönen E, Fteita D, Gursoy U, Gursoy M. Prevotella species as oral residents and infectious agents with potential impact on systemic conditions. J Oral Microbiol. 2022;14:2079814.
27. Mayo Clinic. Mononucleosis. Mayo Clinic; 2022. Available at mayoclinic.org/diseases-conditions/mononucleosis/symptoms-causes/syc-20350328. Accessed April 2, 2026.
28. College of Dental Hygienists of Ontario. Fact Sheet: Mononucleosis. Available at https://cdho.org/factsheets/mononucleosis. Accessed April 2, 2026.
29. Cleveland Clinic. Virologist. Available at https://my.clevelandclinic.org/health/articles/25116-virologist. Accessed April 2, 2026.
30. Ackerman B. Communication skills for dental professionals: Do you hear me now? Available at https://www.todaysrdh.com/communication-skills-for-dental-professionals-do-you-hear-me-now. Accessed April 2, 2026.
31. Pieren J, Gadbury-Amyot C. Darby and Walsh: Dental Hygiene Theory and Practice. 6th ed. New York: Elsevier; 2024.
32. National Organization for Rare Disorders. Community Support. Available at https://rarediseases.org/community-support. Accessesd April 2, 2026.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):36-39

Pediatric obstructive sleep apnea (POSA) occurs in 1% to 6% of children, making it a significant public health concern.¹ POSA can be linked to a variety of developmental delays and chronic health issues, including cardiovascular concerns and overall failure to thrive. Additionally, POSA can lead to problems with skeletal, jaw, and dentition development.² POSA also may contribute to neurocognitive and emotional developmental delays, including attention-deficit/hyperactivity disorder (ADHD).

Because early detection of POSA and related conditions can significantly improve oral and general health outcomes in children, oral health professionals should screen for signs and symptoms of POSA during routine exams.³

Obstructive sleep apnea (OSA) is a partial or complete airway obstruction during sleep that interrupts normal sleep patterns and nighttime breathing. This includes episodes of intermittent hypoxia (lack of oxygen) and frequent sleep arousal.² OSA usually occurs when the pharyngeal airway soft tissue relaxes during sleep. When an individual inhales, the airway can be partially or completely obstructed, thereby inhibiting oxygen flow. OSA is the most common type of sleep-disordered breathing in children.⁴

A major complication of untreated POSA is strain on the heart and vascular system, which can increase the risk of chronic cardiovascular disease. Episodes of apnea (breathing pauses) can trigger intermittent hypoxia (a drop in blood oxygen levels). That drop in oxygen levels activates the sympathetic nervous system, increasing heart rate and blood pressure. Repeated episodes over time can lead to cardiac remodeling. These effects are more pronounced in children who are obese or have elevated blood pressure.^1,5,6

Another complication of POSA is its impact on physical growth and development. Children with POSA may experience poor weight gain, growth delays, and failure to thrive. Cognitive, learning, and behavior issues can also be linked to untreated POSA. The lack of oxygen resulting from apnea can significantly affect neurocognitive development, attention deficits, memory, and academic performance. Unsurprisingly, these complications of POSA may inhibit a child’s ability to learn and function well in school, causing behavioral difficulties, irritability, and social issues.²

POSA in children may also affect craniofacial development. Children with POSA may have differences in their dental arch dimensions when compared with healthy children. These include narrower maxilla, deeper palatal height, receding mandible (deficient chin), crossbites, overjets, and dental malposition. These alterations are believed to result from chronic postural adaptations of the head, jaw, and tongue aimed at maintaining an open airway during sleep.⁷ These abnormalities can affect dental crowding, breathing patterns, bite, and facial structure. Additionally, chronic mouth breathing can lead to xerostomia, increasing the risk of dental caries and periodontal diseases.⁸

Causes and Risk Factors

The leading cause of OSA in children is thought to be adenotonsillar hypertrophy, or enlarged tonsils and/or adenoids. This enlargement can narrow the upper airway, especially during sleep, leading to airflow obstruction.⁹ This correlates with the fact that peak prevalence of childhood OSA occurs between the ages of 2 and 5, when the size of even a healthy child’s adenoids and tonsils are large relative to their developing airway size.¹⁰

Obesity in young children also can be an important risk factor for POSA, leading to fat deposits in the neck and throat that narrow the upper airway, making it more prone to collapse during sleep. This fat deposition also reduces the effectiveness of muscles that help keep the airway open.¹¹ However, unlike in adults, obesity in children is not the most significant risk factor for POSA.^10,11

Neuromuscular and functional risk factors for POSA include weakness in the muscles of the upper airways, impaired upper airway reflexes during sleep, abnormal central arousal mechanisms, and weak protective airway responses. These conditions reduce airflow and can cause apneas and/or hypoxia during sleep. These symptoms may appear in isolation or may occur with neuromuscular diseases such as spinal muscular atrophy, muscular dystrophy, and congenital myopathies.¹²

Craniofacial abnormalities, such as retrognathia (small or recessed jaw) and/or high-arched or narrow palate, can be risk factors for POSA because they physically restrict the upper airway. As a smaller or constricted airway is more prone to collapse during sleep, this can lead to the breathing interruptions. Nasal obstructions (allergic rhinitis, deviated septum) also play a role in POSA for the same reasons. These craniofacial and nasal factors may be congenital, developmental, or secondary to chronic mouth breathing. All of these can contribute to a constricted airway.^2,13

Other factors to consider when evaluating potential for POSA are exposure to allergens and second-hand smoke, which can contribute to nasal inflammation. Additionally, POSA more frequently occurs in boys, children between the ages of 2 and 8, and those with a family history of sleep apnea.¹⁰

Signs and Symptoms

Most children with OSA experience symptoms that include snoring and difficulty breathing during sleep. Because it can be challenging to differentiate OSA from snoring, parents should be on the lookout for symptoms including restless sleep, night sweats, bedwetting, and morning headaches.¹⁰

Some children with OSA may also exhibit signs of daytime sleepiness, although this is less commonly reported in children than in adults. Children may also exhibit behavior issues similar to ADHD, as well as loss of appetite, learning difficulties, aggressive behavior, and poor academic performance.^9,10 Additional physical signs and symptoms of POSA include recessed or retrognathic jaw and receding chin, and forward head posture, as well as dark undereye circles and an overall look of fatigue compared with healthy children.¹⁰

POSA exhibits many physical signs, such as enlarged tonsils, bruxism, and signs of tooth wear such as abrasion, attrition, erosion, and abfraction. Duran-Cantolla et al¹⁴ found a statistically significant association between apnea episode frequency and tooth wear severity. Additional symptoms within the mouth include high arched or narrow palate, enlarged tongue, and ankyloglossia (tongue ties) or untreated short lingual frenum. Untreated ankyloglossia can impair tongue function early in life, leading to abnormal orofacial growth, some types of which can increase risk of upper airway collapse during sleep (Figure 1).¹⁵

Diagnosis and Treatment

POSA can only be diagnosed by a qualified physician before beginning any treatment. Therefore, patients experiencing symptoms of OSA should seek diagnosis by a physician, preferably one specializing in sleep disorders. They use specific techniques including endoscopy, laryngoscopy, and pharyngometry, and computed tomography or magnetic resonance imaging to evaluate airway narrowing or other structural concerns.¹⁰

Polysomnography (PSG) is considered the gold standard for diagnosing OSA.¹⁰ This is usually done in a clinical setting where the patient is monitored to measure sleep patterns, breathing, and oxygen levels. The PSG will provide an apnea-hypopnea index (AHI), which represents the number of apneas and hypopneas divided by the hours the individual sleeps. While a minimum of five apneas is considered evidence of OSA in adults, children can be diagnosed with an AHI of greater than one and less than five.¹⁰

The right treatment plan depends on individual risk factors and symptoms, but the most common approaches are surgery, positive airway pressure (PAP) therapies, myofunctional therapy (MFT), and orthodontic treatments. For most children, treatment for POSA includes a procedure to remove enlarged adenoids and tonsils via adenotonsillectomy. Although this is the first line of treatment, surgical therapy sometimes fails to provide a long-term solution.¹⁰

Used to improve air flow and reduce nighttime apneas, PAP therapies generally are effective for adults, but present challenges when used to treat children.¹⁶ The use of PAP therapy masks in children can potentially affect midfacial growth and cause maxillary retrognathia over time.¹⁷ Other concerns include mask fit, anxiety, and embarrassment. Questions surrounding whether pediatric patients will use the therapy consistently and whether children who use continuous PAP therapy will need it indefinitely create uncertainty as to its long-term effectiveness.¹⁸

MFT, used to strengthen muscles and improve tongue and facial muscle function,  increases patient proprioception (body awareness) and improves airway health. Myofunctional therapists help patients use exercises to improve nasal breathing, lip tone, and lip seal. They may also recommend a lingual frenectomy. According to Bandyopadhyay et al,¹⁹ studies show that MFT decreased AHI by 43% in children and increased oxygen saturations in children with mild to moderate OSA. As with other therapies, MFT’s effectiveness relies on the patient’s ability to consistently follow directions for completing exercises. Compliance can be an issue with MFT in children and therefore requires continuous parental involvement to increase effectiveness.¹⁵

Orthodontic treatments are used to expand the upper and/or lower jaw to create room for the tongue and open the airway. Rapid maxillary expansion (RME) is used to expand the upper jaw and open the airway to alleviate the breathing obstruction (Figure 2). Studies show that RME can be effective beyond 2 years following treatment, and when combined with adenotonsillectomy, RME resolves POSA in most children.¹⁰

Mandibular repositioning appliances (MRAs) expand the oropharynx in a lateral direction to protrude the mandible, which opens the airway and promotes healthy skeletal development (Figure 3). MRAs are more often used in adults and limited evidence is available to suggest their effectiveness in children.¹⁰ Children and adults with oral appliances of any kind should have regular and thorough dental examinations, periodontal examinations, and temporomandibular joint evaluations to ensure optimal tooth alignment, periodontal health, and proper joint function.¹⁰

Tobacco smoke, allergens, and pollutants that irritate the airway and contribute to congestion should be avoided. Though obesity is more commonly associated with OSA in adults, an unhealthy weight can also be a contributing factor in children and teenagers experiencing OSA.²⁰

Oral health professionals are uniquely situated to help detect early signs of POSA and identify patients who may benefit from seeing a sleep specialist. Oral health professionals may see children more frequently than physicians. In addition, their specialized oral health expertise can help them spot abnormalities that general practitioners may overlook.^3,10

Interprofessional practice is important to treating the whole patient. By screening for POSA and collaborating with other healthcare providers, oral health professionals can improve long-term health outcomes for children.²¹ For this reason, the American Academy of Pediatric Dentistry recommends children be screened for sleep disorders at the first dental visit.⁸

The Ask, Look, Refer Method

When clinicians are educated about the signs of sleep disorders, they can efficiently identify potential concerns by adding a simple three-step process to the already existing clinical assessment. We propose the ask, look, refer (ALR) method to support the accurate detection of POSA.

Ask. A thorough health history that includes common POSA symptoms can help providers assess the potential need for referral. Dental hygienists can ask parents/caregivers about specific daytime symptoms, including sleepiness, mouth breathing, and behavior problems, as well as nighttime symptoms such as snoring, gasping for air, grinding teeth, and bedwetting.⁸ A sleep questionnaire or screening form can help parents/caregivers and providers spot signs of disordered sleep they may not otherwise notice.

Look. Dental hygienists should first note visible signs of POSA, including retrognathic jaw, receding profile, dark undereye circles, and signs of obesity. During the intraoral assessment, the presence of enlarged tonsils should be noted. The Mallampati tongue classification system can be used to visually assess tongue size and airway obstruction (Figure 4).^{10, 22} Untreated tongue tie, high arched or narrow palate, as well as bruxism, mouth breathing, and shiny or swollen gums should be noted.^8,14

Refer. Once the assessment is complete, the dental hygienist, with consultation and approval of the dentist, should determine whether to recommend a referral based on the number and combination of potential POSA symptoms. The dental hygienist can then educate the parent/caregiver and patient by discussing noted signs and symptoms, as well as explaining the risks of untreated POSA. The dentist may then refer the parent/caregiver to a sleep specialist. The parent/caregiver should be informed that POSA must be diagnosed by a physician, but that treatments may occur in a dental or orthodontic office depending on the physician’s treatment plan.

The ALR method simplifies POSA screening by giving clinicians a structured, simple evaluation process that can be  integrated into the processes already in place during preventive care visits.

Conclusion

POSA can have serious long-term health consequences if left untreated. Dental hygienists can screen for POSA during routine exams, educate caregivers/parents and patients, and, with the help of the dentist, refer patients to physicians, all of which can significantly improve the overall health and well-being of children.

References

1. Baker-Smith C, Amal I, Melendres MC, et al. Sleep-disordered breathing and cardiovascular disease in children and adolescents: a scientific statement from the American Heart Association. J Am Heart Assoc. 2021;10:022427.
2. Alsubie HS, BaHammam AS. Obstructive sleep apnea: children are not little adults. Paediatr Respir Rev. 2017;21:72-79.
3. Levine B, Patterson F, Covington L. Pediatric dentists: frontline public health providers leading the way in identifying and preventing childhood obstructive sleep apnea syndrome. Del J Public Health. 2024;10:44-45.
4. Chang SJ, Chae KY. Obstructive sleep apnea syndrome in children: epidemiology, pathophysiology, diagnosis, and sequelae. Korean J Pediatr. 2010;53:863-871.
5. Hanlon CE, Binka E, Garofano JS, Sterni LM, Brady, TM. The association of obstructive sleep apnea and left ventricular hypertrophy in obese and overweight children with history of elevated blood pressure. J Clin Hypertens. 2019;21:984-990.
6. Maniaci A, Lavalle S, Parisi FM, Barbanti M, Cocuzza S, Iannella G, et al. Impact of obstructive sleep apnea and sympathetic nervous system on cardiac health: a comprehensive review. J Cardiovasc Dev Dis. 2024;11:204.
7. Al-Hammad NS, Hakeem LA, Salama FS. Oral health status of children with obstructive sleep apnea and snoring. Pediatr Dent. 2015;37:35-39.
8. American Academy of Pediatric Dentistry. Policy on obstructive sleep apnea (OSA). The Reference Manual of Pediatric Dentistry. Chicago: American Academy of Pediatric Dentistry; 2023:137-140.
9. Gupta, S, Sharma, R. Pediatric obstructive sleep apnea: diagnostic challenges and management strategies. Cureus. 2024;16:1-19.
10. Stauffer J, Okuji DM, Lichty GC II, et al. A review of pediatric obstructive sleep apnea and the role of the dentist. J Dent Sleep Med. 2018;5:111-130.
11. Kanney M, Harford KL, Raol N, Leu RM. Obstructive sleep apnea in pediatric obesity and the effects of sleeve gastrectomy. Semin Pediatr Surg. 2020;29:150887.
12. Chidambaram AG, Jhawar S, McDonald CM, Nandalike K. Sleep disordered breathing in children with neuromuscular disease. Children. 2023;10(:1675.
13. Cielo CM, Marcus CL. Obstructive sleep apnoea in children with craniofacial syndromes. Paediatr Respir Rev. 2015;16:189-196.
14. Durán-Cantolla J, Alkhraisat MH, Martínez-Null C, Aguirre JJ, Rubio Guinea E, Anitua E. Frequency of obstructive sleep apnea syndrome in dental patients with tooth wear. J Clin Sleep Med. 2015;11:445-450.
15. Huang YS, Quo S, Berkowski JA, Guilleminault C. Short lingual frenulum and obstructive sleep apnea in children. Int J Pediatr Res. 2015;1:273.
16. Stevens, D, Title, M, Spurr, K, Morrison, D. Positive airway pressure therapy adherence and outcomes in obstructive sleep apnea: an exploratory longitudinal retrospective randomized chart review. Can J Respir Ther. 2024;60:28-36.
17. Bariani, RCB, Guimaraes, TM, Cappellette Jr, M, Moreira, G, Fujita, RR. The impact of positive airway pressure on midface growth: a literature review. Braz J Otorhinolaryngol. 2020;86:647-653.
18. Carmody JK, Duraccio KM, Krietsch KN, Simmons DM, Byars KC. Factors affecting pediatric adherence to positive airway pressure: Patient and caregiver reported treatment barriers and sleep difficulties. Sleep Med. 2023;101:58-65.
19. Bandyopadhyay A, Kaneshiro K, Camacho M. Effect of myofunctional therapy on children with obstructive sleep apnea: a meta-analysis. Sleep Med. 2020;75:210-217.
20. Salzano G, Maglitto F, Bisogno A, et al. Obstructive sleep apnoea/hypopnoea syndrome: relationship with obesity and management in obese patients. Acta Otorhinolaryngol Ital. 2021;41:120-130.
21. Fagundes NCF, Flores-Mir C. Pediatric obstructive sleep apnea—dental professionals can play a crucial role. Pediatr Pulmonol. 2022;57:1860-1868.
22. O’Brien SM. Understanding the Mallampati score. Available at clinicaladvisor.com/features/understanding-the-mallampati-score. Accessed April 3, 2026.

From Dimensions of Dental Hygiene. May/June 2026; 24(3):40-45

When presenting scaling and root planing to a patient, offering a prophylaxis as an alternative may not be the central concern. The focus should be on maintaining consistent care, reinforcing the need for periodontal treatment, and closely monitoring the patient’s oral health. Providing ongoing care allows for continued education, relationship-building, and improved communication. Patients should never feel pressured into treatment. Some patients may need additional time to fully comprehend and process the proposed treatment. Maintaining open communication and offering continued care may eventually lead to acceptance of recommended treatment.

Refusing to provide care to patients who have declined treatment may result in a lost opportunity to guide them toward better health. Patients faced with the choice between immediate periodontal therapy or being referred elsewhere may opt to forgo treatment altogether. In such cases, they may no longer have access to an oral health professional who is actively working to encourage necessary care.

Patients often face barriers, such as financial concerns, insurance limitations, fear, pain, shame, or lack of trust. These obstacles can take time to address. We need to recognize that our ideal treatment goals may not always align with what the patient is initially ready to accept. Offering an alternative treatment may provide the necessary time to address barriers, build rapport, and educate the patient effectively.

In cases where a patient declines ideal periodontal treatment, an informed refusal document should be completed, signed by both the patient and the dentist. This document should confirm that:

• The patient has been diagnosed with periodontal disease.
• Recommended treatment options have been explained.
• The patient acknowledges the risks of refusing treatment and understands that alternative procedures will not address the diagnosed disease.
• The patient’s condition will be re-evaluated at each ensuing visit.
• The patient should also be placed on a shorter recare schedule to facilitate closer monitoring.
• The patient has been informed that if his or her periodontal condition worsens, the dentist may discontinue treatment in accordance with appropriate legal protocols and without patient abandonment.

Dental hygienists play a critical role in identifying periodontal disease, working closely with patients, and supporting the dentist’s recommended treatment plan. By advocating for alternative solutions when appropriate and maintaining clear communication, dental hygienists can help ensure that patients have autonomy in their care. Ultimately, while not all patients will accept ideal treatment right away, providing alternative care options, fostering trust, and maintaining open communication can support the goal of guiding patients toward optimal oral health in the long term.

From Dimensions of Dental Hygiene. May/June 2026;24(3):46