Reconnecting Practicing Hygienists with the Nation's Leading Educators and Researchers.

Promote Healthy Aging

How to effectively address the oral health issues faced by older adults.

PURCHASE COURSE
This course was published in the August 2011 issue and expires August 2014. The authors have no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated.

 

EDUCATIONAL OBJECTIVES

After reading this course, the participant should be able to:

  1. Discuss individual and environmental risk factors for dental caries, periodontal diseases, oral cancer, and edentulism among mature adults.
  2. Discuss behavioral and therapeutic regimens for oral disease prevention in mature adults.periodontal diseases, oral cancer, and edentulism among mature adults.
  3. Identify the principles of risk assessment and strategies for health promotion among mature adults.

When treating mature adults, the goal of all health care professionals is to improve function, maintain independence, and promote quality of life. Successful aging is an individualized experience influenced by behavior, culture, environment, gender, biology (genetics), and socioeconomic class.1 Common chronic systemic conditions experienced by older adults place great demands on individuals, families, and the health care delivery system. More than 80% of Medicare beneficiaries are living with one chronic disease, and at least 20% suffer from five or more chronic conditions.2 Most chronic systemic conditions and oral diseases share common risk factors (eg, diet, tobacco, alcohol, stress, socioeconomic status).1 Dental caries, periodontal diseases, and oral cancer are three common oral conditions that challenge the health status of older adults.

Mature adults often experience conditions that affect multi-organ systems and involve different medical disciplines. Oral systemic approaches typically do not address the variability of diseases in older adults. Consequently, management of dental conditions presented by mature adults is below the acceptable standard of care. Risk assessment with targeted disease prevention is one method to improve the oral health of mature adults at greatest risk of disease.

DENTAL CARIES

Unlike previous generations, today’s independent older adults retain their natural teeth. With age comes an increased risk of coronal and root caries, as well as vertical tooth fractures of endodontically and nonendodontically treated teeth.3,4 Nonshedding natural and restored tooth surfaces, past caries experience, elevated levels of cariogenic bacteria, and limited salivary flow provide an environment for biofilm accumulation and bacterial colonization. Higher bacterial counts and lower buffering capacity contribute to coronal caries development.5 The risk of dental disease is a complex interaction of individual genetics, polypharmacy, systemic conditions, limitations in activities of daily living (ADLs), difficulty with maintaining optimal oral hygiene, cariogenic dietary intake, oral health literacy, and access to oral health care.
Although etiological factors responsible for tooth enamel demineralization and breakdown of tooth structure are similar for people of all ages, unique biological, behavioral, and socioenvironmental factors alter the risk status for mature adults.6,7 Root surface caries is associated with gingival recession of the susceptible root portion of the tooth, which creates a hospitable environment for bacterial plaque accumulation.

Root caries is an asymmetrical-shaped soft lesion either confined to the root surface or undermining the enamel at the cementoenamel junction. Longitudinal studies have found that synergistic virulence and high salivary counts of Streptococcus mutans, Lactobacillus, and Actinomyces increase the risk of root caries.8,9 Other studies suggest Candida albicans contributes to dentin and root caries formation.10

The prevalence of coronal and root caries in younger and older adults is higher with increased frequency of fermentable carbohydrate consumption, poor oral hygiene practices, and lack of fluoride exposure. Vulnerable and socioeconomically challenged mature adults are six times more likely to have untreated carious lesions in comparison to school-aged children.11 Mature adults with a history of smoking have a higher prevalence of untreated coronal and root caries that increase the incidence of coronal and root fracture and, ultimately, tooth extraction.12 Polypharmacy-induced xerostomia, functional limitations in ADLs, and cognitive impairment alter the oral ecosystem. Increased putative pathogen counts result in higher risk for caries activity. Risk reduction, early detection, diagnosis, prescription of preventive regimens (Table 1), as well as appropriate recare intervals will prevent the progression of dental caries.

PERIODONTAL DISEASES

Periodontal diseases are nonage-related multifactorial chronic diseases caused by the accumulation of select Gram-negative anaerobic organisms on tooth retentive surfaces that develop into bacterial infections.13 Manifestation of the disease and rate of progression are influenced by host susceptibility, sociobehavioral factors, genetic factors, and local and systemic conditions. Etiological anaerobic microorganisms have been identified as Porphyromonas gingivalis, Tannerella forsythusTreponema denticola, and Aggregatibacter actinomycetemcomitans.13 Periodontal diseases are slow, relatively painless bacterial challenges that destroy host tissues and result in loss of attachment and bone that ultimately leads to tooth mortality. Attachment loss may be evident throughout adulthood and it progresses over the course of life at different rates, but age is not a predictor of attachment loss.14

The complex course of periodontal diseases has been linked as a potential risk factor in the development of systemic conditions such as hypertension, obesity, cardiovascular disease, type 2 diabetes, osteoporosis, negative birth outcomes, and vitamin D deficiency. Other risk factors for periodontal disease progression include a compromised immune response, polypharmacy, xerostomia, poor oral health literacy, low socioeconomic status, functional limitation in ADLs, and depression.11 Timely reduction of risk, diagnosis of periodontal diseases, prescription of preventive regimens (Table 1), and timely recare intervals can help alter periodontal disease progression and severity.

ORAL CANCER

The most common sites for oral cancer are the lips, tongue, salivary glands, floor of the mouth, gums, oropharynx, and tonsilar areas. Clinically, oropharyngeal cancer is more visible and deforming than other cancers. Unfortunately, it is often detected and diagnosed at advanced stages. Delayed diagnosis has been attributed to a gap in knowledge among oral health professionals and other primary health care providers. Lack of national oral cancer screening standards, little public awareness, and limited health literacy regarding risk factors and symptoms contribute to stagnant morbidity and mortality rates over the past 15 years in the United States.15

Risk factors for oral cancer are a complex interaction of behavioral, social, hereditary, systemic, economic, and environmental conditions.16 Pathogenesis includes social habits such as a history of tobacco use, alcohol use, unprotected exposure to ultraviolet radiation, and exposure to sexually-acquired human papillomavirus (HPV), especially HPV-16, as well as inadequate consumption of grains, fruits, and vegetables. Recent studies have shown individuals who are seropositive for HPV-16 have a 15-fold increased risk of oropharyngeal cancer.17 HPV vaccination early in life may prevent HPV mediated oropharyngeal cancer.17 Early signs of oropharyngeal cancer are fairly asymptomatic with minimal discomfort and indiscernible tissue changes. Some early symptoms may include recurring mouth sores and persistent white or red patches on the tongue, lining mucosa, gums, and tonsilar area. Leukoplakia (white patch) is common in individuals with a history of tobacco and alcohol use, cheek biting/bruxism, and denture wearers, and has the potential to progress to oral cancer. Intraoral red patches (erythoplakia) are rarer lesions with a greater potential to become malignant.18

Clinical symptoms of advanced stages of oral cancer include: chronic mouth pain; sore throat; voice alteration; difficulty swallowing, chewing, moving tongue and jaw; and swelling of the edentulous areas, which causes prosthetic devices to no longer fit. Numbness in the mouth, teeth with excessive clinical mobility, loss of weight, lumps in the neck, and persistent bad breath are additional indicators of possible advanced oral cancer. Improved prognosis is possible with: risk reduction; early detection, diagnosis, and staging of oral cancer; and comprehensive follow-up. Preventive strategies for oral cancer should include interdisciplinary training of oral and primary health care providers about comprehensive oral cancer examination, especially for high-risk patients. Community-based education for patients to improve oral health literacy is also imperative.

EDENTULISM

Advanced age is not a risk factor for edentulism. Chronic oral infection of the teeth and supporting structures may lead to tooth mortality and edentulism. Extraction of natural dentition diminishes masticatory function, limits nutritional intake, reduces dietary options, promotes social isolation, and negatively impacts cognitive status and quality of life.

Demographic studies indicate that the incidence of edentulism is dependent on race, oral health literacy, access to and utilization of dental services, and sensory impairment that can impact daily self-care.19 Poor access to oral health care as well as limited financial resources may preclude some treatment options for mature adults. Because dental insurance is frequently lost upon retirement and Medicare does not offer dental benefits, older adults may have to rely on limited economic resources for needed dental services.20 Mature adults challenged with edentulism, chronic systemic conditions, and/or social habits of tobacco and/or alcohol use should be offered frequent follow-up visits. Lesions that do not heal shortly after denture adjustments and use of preventive regimens (Table 1) should be addressed as potential malignancies.

Denture stomatitis and angular chelitis are preventable complications (Table 1) of the partial or totally edentulous. Candida-induced inflammatory processes of the edentulous mucosal tissues is a source infection and irritation and can contribute to the formation of intraoral lesions. Nonpathogenic members of the microflora grow, proliferate, and become opportunistic pathogens in response to imbalance of the host’s immunologic and physiologic state of equilibrium. These organisms inhabit the oral cavity shortly after birth, however, colonization and pathogenicity increase with advanced age and decline in host immunity.21 Functional limitations, inability to maintain oral self-care, lack of daily cleansing of oral prosthesis, and behavioral habits (eg, tobacco and alcohol use) promote the pathogenicity of these organisms.

The microporous tissue surface of the acrylic resin prothesis provides an environment for growth and proliferation of opportunistic pathogens. Mature adults who rely on caregivers for oral hygiene experience a higher incidence of Candida infections.11 Continuous swallowing or possible aspiration of these pathogens from denture plaque is a risk for pleuropulmonary and gastrointestinal infections. Denture plaque naturally adheres and accumulates on the dental prosthesis, forming a dense microbial layer. The biofilm composition of this layer is similar to dental plaque with the exception of an elevated Candida albicans count identified as the causative factor in denture-induced stomatitis.

Continuous wearing of the denture as well as functional oral traumatic habits and medication-induced habits, such as tardive dyskinesia, can result in traumatic ulceration. Permeation of the oral mucosa alters the oral environment and opportunistic pathogens line the tissue surface of the prosthesis, which results in irritation and increased risk of Candida infection. Salivary proteins, primarily histatins (antimicrobial peptides), provide fungicidal and bactericidal activity that inhibits the pathogenicity of Candida, and can control drug resistant antifungal infections.22 Good oral hygiene of the edentulous mucosa and the prosthesis, preventive regimens (Table 1), and eliminating the use of the prosthesis when resting will prevent the proliferation of these pathogens.

CLINICAL IMPLICATIONS

As the baby boomer generation ages, people will be increasingly challenged by chronic systemic conditions. The principles of risk assessment are to: assess the risk of the individual patient for future development of disease; identify the individual etiologic factors of the existing disease; create a personalized plan to help reduce the patient’s risk factors and prevent disease; communicate and facilitate needed change in behavior; and evaluate the success of the preventive plan or the need to modify the prevention plan.

Strategies for health promotion require: assessment of patient behavioral, psychosocial, oral, and physical factors; identification of risk factors for chronic systemic and oral disease; clear communication with patients, their interdisciplinary health care teams, and family or caregivers to reinforce health education; and direction of care that is patient-centered with an individualized follow-up plan. The dental team needs to develop processes to address and improve the oral health of an expanding number of mature patients. The ideas discussed here will contribute to a framework for success.

BONUS WEB CONTENT

 


REFERENCES

  1. Watt RG. Strategies and approaches in oral disease prevention and health promotion. Bull World Health Organ. 2005;83:711-718.
  2. Berenson RA, Horvath J. Confronting the barriers to chronic care management in Medicare. Health Aff (Millwood). 2003;Suppl Web Exclusives:W3-37-53.
  3. Murray PE, Stanley HR, Matthew JB, Sloan AJ, Smith AJ. Age-related odontometric changes of human teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;93:474-482.
  4. Wahl MJ, Schmitt MM, Overton DA, Gordon MK. Prevalence of cusp fractures in teeth restored with amalgam and with resin-based composite. J Am Dent Assoc. 2004;135: 1127-1132.
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  6. Eldarrat AH, High AS, Kale GM. Age-related changes in ac-impedance spectroscopy studies of normal human dentin: further investigations. J Mater Scie Mater Med. 2010;21:45-51.
  7. Brown JP, Dodds MWJ. Risk based prevention. In: Cappelli DP, Mobley CC, eds. Prevention in Clinical Oral Health Care. St. Louis; Elsevier/Mosby; 2008:45-55.
  8. Scheinin A, Pienihäkkinen K, Tiekso J, Holmberg S, Fukuda M, Suzuki A. Multifactorial modeling for root caries prediction: 3-year follow-up results. Community Dent Oral Epidemiol. 1994;22:126-129.
  9. Ellen RP, Banting DW, Fillery ED. Streptococcus mutans and Lactobacillus detection in the assessment of dental root surface caries risk. J Dent Res. 1985;64:1245-1249.
  10. Zaremba ML, Stokowska W, Klimiuk A, et al.Microorganisms in root carious lesions in adults. Adv Med Sci. 2006;51Suppl 1:237-240.
  11. McClain M, Dounis G. Prevention strategies for special populations. In Cappelli DP, Mobley CC, eds. Prevention in Clinical Oral Health Care. St. Louis: Elsevier/Mosby; 2008:269-271.
  12. Featherstone JDB. The caries balance: The basis for caries management by risk assessment. Oral Health Prev Dent. 2004;2(Supplement 1): 259-264.
  13. Novak KF. Periodontal disease and associated risk factors. In: Cappelli DP, Mobley CC, eds. Prevention in Clinical Oral Health Care. St. Louis: Elsevier/Mosby; 2008:56-67.
  14. Löe H, Anerud A, Boysen H, Morrison E. Natural history of periodontal disease in man. J Clin Periodontol. 1986;13:431-440.
  15. American Cancer Society. Cancer Facts and Figures 2011. Atlanta: American Cancer Society; 2011.
  16. Jones DL, Rankin KV. Oral cancer and associated risk factors. In: Cappelli DP, Mobley CC, eds. Prevention in Clinical Oral Health Care. St. Louis: Elsevier/Mosby, 2008:68-77.
  17. D’Souza G, Kreimer AR, Viscidi R, et al. Casecontrol study of human papillomavirus and oropharyngeal cancer. N Engl J Med. 2007;356: 1944-1956.
  18. American Cancer Society. Signs and Symptoms of Oral Cavity or Oropharyngeal Cancer. Available at: www.cancer.org/Cancer/OralCavityand OropharyngealCancer/DetailedGuide/oral-cavityand- oropharyngeal-cancer-diagnosis. Accessed July 14, 2011.
  19. Starr JM, Hall R. Predictors and correlates of edentulism in healthy older people. Curr Opin Clin Nutr Metab Care. 2010;13:19-23.
  20. Dounis G, Ditmyer MM, McClain MA, Cappelli DP, Mobley CC. Preparing the dental workforce for oral disease prevention in an aging population. J Dent Educ. 2010;74:1086-1094.
  21. Soll DR. Candida commensalism and virulence the evolution of phenotypic plasticity. Acta Trop. 2002;81:101-110.
  22. Kavanagh K, Dowd S. Histatins: antimicrobial peptides with therapeutic potential. J Pharm Pharmacol. 2004;56:285-289.

From Dimensions of Dental Hygiene. August 2011; 9(8): 16-19.

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