Optimizing Oral Health in Women: More than Just Lip Service

By Susan T. Marcolina, MD, FACP, and Pamela A. Fenstemacher, MD, FAAFP. Dr. Marcolina is a board-certified internist and geriatrician in Issaquah, WA; Dr. Fenstemacher is a board-certified family practitioner and geriatrician in Jenkintown, PA. Dr. Marcolina and Dr. Fenstemacher report no consultant, stockholder, speaker's bureau, research, or other financial relationships with companies having ties to this field of study.

Part 1 of a Series on Oral Health

Dental caries and periodontitis are infectious, communicable diseases that cause significant public health problems in the United States. Periodontitis, an infection of the tissues that support the teeth, has been shown in several studies to be a risk factor for poor health beyond the oral cavity. An increased risk of preterm low birth weight infants, aspiration pneumonia, coronary disease, stroke, and poor glycemic control in diabetics are all seen with poor oral health. This burden of disease is disproportionately carried by persons who are poor and uninsured, medically and developmentally disabled, immunocompromised, and elderly, both home-bound and institutionalized. Because women constitute the majority of the elderly population and the entire child-bearing population, it is clear that throughout their lifespan they are vulnerable to periodontal and dental disease.

National Initiatives in Oral Health

Oral Health in America: A Report of the Surgeon General David Sachter in May 2000 alerted the American public to the importance of oral health to their overall general health at every stage of their lives, highlighted the profound and consequential oral health disparities that exist within populations of the United States, and called upon policymakers, community leadership, private industry, health professionals, the media, and the public to implement strategies to mitigate these disparities.1

Since the publication of this report, the Centers for Disease Control and Prevention (CDC) has required acute care hospitals "to develop and implement a comprehensive oral hygiene program" for patients at risk for health care-associated pneumonia, which includes ventilator-associated and aspiration pneumonias.2

Access Problems

Medical and dental insurance are strong determinants of dental care access. In the United States, dental coverage is provided either through commercial insurance (employer-based or individual purchase) or Medicaid/State Children's Health Insurance. Only about 50% of the U.S. population is covered by a third party dental plan. For each child without medical insurance, at least 2.6 children are without dental insurance.1 The latest U.S. Census Bureau data on poverty, income, and health insurance coverage show that economic security for women and their families has eroded over the past six years. The real median income for female-headed households with children has declined from $24,800 in 2000 to $23,100 in 2005 and the percentage of women without health insurance grew from 13.8% in 2000 to 15.6% in 2005, a faster increase than for the overall population. More than one in five (20.8%) elderly women living alone in 2005 was poor.

Dental caries affect 20% of 2-4 year olds, 50% of 5-9 year olds, 67% of 12-17 year olds, and 94% of adults. In 1996, only 28% of people with a yearly income of $32,000 or less reported a dental visit in the preceding year vs. 56% of persons with a yearly income of $64,000 or more. As a result, 33% of poor adults have untreated dental decay as compared to 11% of adults in higher income brackets. Such untreated decay causes pain, compromised nutrition, poor appearance, and diminished productivity, which perpetuates poverty.3-5

In 1999, the United States General Accounting Office surveyed Medicaid program officials in all 50 states regarding dentists' participation. Of the 39 states that provided this information, 23 reported that less than 50% of their states' dentists saw at least one Medicaid patient in 1999.6 Newacheck et al, using the 1994-1995 National Health Interview Survey on Disability, found that approximately one of 12 children with special health care needs was unable to get necessary dental care.7 Dental providers cite low reimbursement rates, missed appointments, and administrative paperwork burden as obstacles to accepting Medicaid patients. For geriatric patients, Medicare specifically excludes routine dental preventive and restorative services.

The fact that tooth decay and periodontitis are both treatable and preventable through a regular regimen of brushing, flossing, and professional dental care suggests that there is a need to get back to the basics. Primary care physicians, who see patients daily in the office for routine and urgent care, are uniquely positioned to notice these problems, educate their patients about routine preventive oral self-care, and refer them to dental professionals before costly, painful problems arise. Ultimately, collaboration between medical, dental, and public health professionals is necessary for the integration of oral health into general medical health because the oral cavity, as a major portal of entry into the body, both reflects and influences general health and well-being.

Microbiology of Dental Caries and Periodontitis

A diverse bacterial flora inhabits the oral cavity due to the ideal humidity, temperature, and availability of nutrients. Although more than 300 types of bacteria reside here, only a few cause dental caries and the tissue destruction of periodontitis. The oral cavity is sterile prior to birth. Subsequently, Streptococcus mutans becomes the predominant cariogenic bacteria in plaque and high counts are associated with increased risk of tooth decay.8 Bacterial typing of S. mutans has shown that mothers are a major source of oral infection in their infants.9

Although adult periodontitis is strongly associated with Bacteroides gingivalis, several other types of anaerobic bacteria such as Fusobacterium nucleatum also cause periodontitis. Actinobacillus actinomycetamcomitans is the pathogen primarily responsible for an early-onset, rapidly progressive juvenile periodontitis.10

Pathophysiology of Dental and Periodontal Disease

Oral hygiene is the efficient removal of plaque and tartar (calcified plaque) from the surface of the teeth. Plaque is a sticky layer of oral bacteria that combines with food residue and causes tooth decay and periodontal disease. Plaque bacteria metabolize dietary sugars into acids, which penetrate the tooth enamel and damage the internal structure as well as the surrounding gum and ligamentous tissue that anchor the tooth in bone of the jaw. Damage to the ligaments and gum tissue is measured with a calibrated probe and thus the clinical attachment level can be quantified in millimeters of depth.

Plaque accumulates in the subgingival space causing gingivitis, the early manifestation of periodontal disease, which appears as gum puffiness and inflammation. If untreated, deep pockets form between the tooth and gum margin. This process destroys the bony and ligamentous support of the tooth and results in loss of dentition.10 Moss et al found increased serum levels of tumor necrosis factor-alpha to be associated with the extent of disease progression in periodontitis patients with active attachment loss.

The elaboration of lipopolysaccharides by the predominately gram-positive anaerobic bacteria in the gingival pockets causes inflammatory cell proliferation in large arteries and stimulates hepatic synthesis of clotting factors, which contribute to atherogenesis and thromboembolic events.11 Several periodontal pathogens such as Streptococcus sanguis induce platelet aggregation and thus may be thrombogenic when hematogenously disseminated.12 The relationship between dental procedures and transient bacteremia has been well documented and must be considered whenever there is a diagnosis of endocarditis or infections of prosthetic implants. Additionally, periodontitis also influences the serum levels of well established cardiovascular risk factors such as lipids, fibrinogen, and C-reactive protein by modifying them toward a more atherogenic profile.13

The pro-inflammatory cytokine interleukin-1 (IL-1) is a key regulator of host responses to microbial infection. McDevitt et al report that variations in the IL-1 gene cluster on chromosome 2 are associated with increased susceptibility to severe adult periodontitis.14,15

Factors Predisposing to Oral Hygiene Problems

Hyposalivation. Although plaque causes periodontal disease and tooth decay, systemic conditions and health habits exacerbate these problems. Autoimmune illness and drug- or radiation-induced xerostomia, which lead to permanent or temporary reductions in salivary flow, dramatically alter the natural oral bacterial ecosystem, resulting in an increase in oropharyngeal colonization with gram-negative bacteria.

Under normal circumstances, saliva produced by salivary glands is a buffer for acids formed by plaque. Saliva also lubricates the mouth and facilitates clearance of food particulates from the oral cavity. It is supersaturated with calcium and phosphorus and serves as an abundant source of these ions for the remineralization of early tooth surface lesions. Bacteriostatic compounds such as lysozyme, lactoferrin, lactoperoxidase, and secretory immunoglobulins are also contained in saliva.16 The secretory immunoglobulins, primarily IgA, are important for the prevention of adherence of the S. mutans bacteria on the tooth surface.10 Kapsimalis et al found an inverse correlation in humans between the amount of saliva produced and the number of coronal caries present.17 Hyposalivation has also been linked to root cavities (cavities below the gum surface), increased gingivitis severity, loss of taste acuity, increased risk of infection, and reduced denture retention.

Many commonly used medications cause hyposalivation as a side effect. A large cross-sectional study by Beck et al showed that 47% of elderly patients receive drugs that decrease salivary flow.18,19 Common medication classes that diminish salivary flow and put patients at risk for poor oral hygiene are listed in the Table.20

Table
The most common drug classes
that cause xerostomia

  Anticholinergics/Antispasmodics
  Antihypertensives
  Anticonvulsives
  Chemotherapeutic agents
  Antipsychotics
  Antibiotics
  Antidepressants
  Antihistamines
  Decongestants
  Sedative-hypnotics
  Acne medications (Accutane)

Adapted from: Sreebny LM, Schwartz SS. A reference guide to drugs and dry mouth. Gerodontology 1986;5:75-99.

Diabetes. Both Type 1 and Type 2 diabetes and perio-dontal disease have reciprocal effects since uncontrolled diabetes is a risk factor for periodontal disease and periodontal problems complicate the management of diabetes. The long-term microvascular complications of diabetes have important oral manifestations including increased susceptibility of oral tissues to trauma, xerostomia, delayed wound healing, and opportunistic infections such as candidiasis.

Sreebny et al conducted a prospective trial of 40 ambulatory adult diabetic outpatients (82% female) with an equal number of age- and sex-matched controls to determine the prevalence of dry mouth and to compare salivary and lacrimal fluid flow rates in patients with and without this complaint.21 Dry mouth was reported by 43% of the diabetic study patients. The oral dryness was not associated with age or the type or duration of diabetes. Although the resting and whole saliva flow rates were abnormally low in the diabetic patients who complained of dry mouth, no significant differences were observed for the stimulated salivary and the lacrimal flow rates. Significant inverse relationships were demonstrated, however, between salivary flow and hemoglobin A1C levels, suggesting that oral dryness in diabetics may be due to disturbances in glycemic control. Persons with Type 1 and Type 2 diabetes appear to be equally susceptible to periodontal disease.22

Tobacco Use. The use of tobacco products exacerbates dental and periodontal disease. Tobacco produces potent local inflammatory effects on the oral mucosa that cause tissue damage and xerostomia. Moore et al, in a prospective, epidemiologic cohort study of Type 1 diabetics, found that smoking increases risk of periodontal disease almost 10-fold.23 Smoking is also a risk for nondiabetic periodontal disease. Haber et al, in a randomly selected cross-sectional population study of young (19-40 years of age) diabetic and nondiabetic patients, found the odds ratio for development of periodontitis for nondiabetic smokers was 8.6 compared to nonsmokers; the odds ratio for the development of periodontitis in diabetic smokers was 6.9 relative to diabetic nonsmokers.24

Dietary Sugars. The consumption of sugars in beverages and snacks, especially sucrose, contributes to tooth decay problems as well. S. mutans preferentially metabolizes this disaccharide as it accumulates on tooth surfaces. The relationship between sugars in the diet and caries, however, is complex and related to many factors including the frequency of eating and the amount of retained food in critical areas of the tooth surface and the gingival tooth sulcus.25

Gastric Acid Exposure. Enamel erosions called perimylolysis can be seen as a result of regular contact with regurgitated stomach acid either from gastroesophageal disease (GERD) or eating disorders such as bulimia. Such abnormalities are primarily seen on the posterior maxillary molars and are one of the initial signs of the eating disorder bulimia and often precede other overt clinical symptoms of GERD. Acid exposure also causes the soft tissues of the mouth to become swollen and dry with resultant halitosis. Once teeth abnormalities are recognized, underlying illness can be treated and dental sealants can be applied to protect the affected teeth from decay.26

Substance Abuse. Drug abuse with crystal methamphetamine produces the characteristic stigmata of "meth mouth" with numerous darkened caries located along the gum lines. The etiology of the tooth decay is multifactorial as the methamphetamine causes xerostomia, abuse results in neglect of personal hygiene and health, and the caustic substances used directly damage dental enamel, predisposing the tooth to decay. This has been recognized over the past 10 years and results in severe dental decay which often requires tooth extractions. Alcoholism and other substance abuse problems, which have as sequelae severe dental neglect and poor nutrition, can also be recognized by symptoms that appear in the oral cavity.27

Fluoride Use. In contrast to factors that exacerbate dental and periodontal disease, Dean et al observed a strong inverse correlation between the natural fluoride concentration in community water supplies and the number of decayed, missing, and filled teeth in children aged 12-14 years.28 After these studies were reported, the United States began large-scale community water fluoridation programs in the 1950s, which resulted in a decline in the prevalence and severity of dental caries.

Conclusion

Examination of the above clinical study data in conjunction with the pathophysiological processes that are consequences of periodontal and dental disease provides adequate evidence that careful attention to daily oral hygiene is an essential part of improving and maintaining good general health for women at all stages of their lives. For physicians, examination of the oral cavity may reveal the presence of systemic conditions that require further investigation and treatment. The challenges to achieving optimal oral health in common clinical situations found throughout a woman's lifespan will be discussed in Part 2 as well as strategies which improve oral health in these populations.

References

1. U.S. Department of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, MD: National Institutes of Health. Available at: www2.nidcr.nih.gov/sgr/sgrohweb/home.htm. Accessed June 18, 2006.

2. Tablan OC, et al. Guidelines for preventing healthcare—associated pneumonia, 2003: Recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep 2004;53(RR03):1-36.

3. Kaste LM, et al. Coronal caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-1991. J Dent Res 1996;75(Spec No):631-641.

4. U.S. Department of Health and Human Services. Healthy People 2010—Understanding and Improving Health. 2nd ed. Washington, DC: U.S. Government Printing Office; November 2000:21-28.

5. Edelstein B. Policy issues in early childhood caries. Community Dent Oral Epidemiol 1998;26(1 Suppl):96-103.

6. General Accounting Office. Report to Congressional Requesters. Factors Contributing the Low Use of Dental Services by Low Income Populations. September 2000. Available at: www.gao.gov/archive/2000/he00149.pdf. Accessed Oct. 2, 2006.

7. Newacheck PW, et al. Access to dental care for children with special health needs. Pediatrics 2000;105:760-766.

8. Newman MG, et al. Studies of the microbiology of perio-dontosis. J Periodontol 1976;47:373-379.

9. Shaw JH. Causes and control of dental caries. N Engl J Med 1987:317:996-1004.

10. Williams RC. Periodontal disease. N Engl J Med 1990;322:373-382.

11. Moss M, et al. Progressive periodontitis is associated with increased serum tumor necrosis alpha. J Dent Res 1995;74(special issue):158.

12. Herzberg MC, Meyer MW. Effects of oral flora on platelets: Possible consequences in cardiovascular disease. J Periodontol 1996;67(10 suppl):1138-1142.

13. Herzberg, MC, et al. Aggregation of human platelets and adhesion of Streptococcus sanguis. Infect Immun 1983;39:1457-1469.

14. McDevitt MJ, et al. Interleukin-1 genetic association with periodontitis in clinical practice. J Periodontol 2000;71:156-163.

15. Wu T, et al. Examination of the relation between periodontal health status and cardiovascular risk factors: Serum total and high density lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen. Am J Epidemiol 2000;151:273-282.

16. Bertram U. Xerostomia. Clinical aspects, pathology, pathogenesis. Acta Odontol Scand 1967;25(Suppl 49):1-126.

17. Kapsimalis P. The relationship between caries activity, flow rate, total nitrogen and mucin content of saliva. J Oral Med 1966;21:107-110.

18. Beck JD. The epidemiology of dental disease in the elderly. Gerodontology 1984;3:5-15.

19. Beck JD, Hunt RJ. Oral health status in the United States: Problems of special patients. J Dent Educ 1985;49:407-426.

20. Sreebny LM, Schwartz SS. A reference guide to drugs and dry mouth. Gerodontology 1986;5:75-99.

21. Sreebny LM, et al. Xerostomia in diabetes mellitus. Diabetes Care 1992;15:900-904.

22. Matthews DC. The relationship between diabetes and periodontal disease. J Can Dent Assoc 2002;68:161-164.

23. Moore PA. Type 1 diabetes mellitus and oral health: Assessment of periodontal disease. J Periodontol 1999;70:409-417.

24. Haber J, et al. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol 1993;64:16-23.

25. Shaw JH. Sugars in dental caries. In: Horowitz AM, ed. Dental Caries Prevention in Public Health Programs. Bethesda, MD: National Institutes of Health; 1981:1119-1137. DHHS Publication No. (NIH) 81-2235.

26. Owens BM, et al. Perimylolysis of the permanent teeth in an adolescent. J Tenn Dent Assoc 1997;77:26-29.

27. Smart RJ, Rosemberg M. Methamphetamine abuse: Medical and dental considerations. J Mass Dent Soc 2005;54:44-48.

28. Dean HT. Domestic water and dental caries V. Additional studies of the relation of fluoride in domestic waters to dental caries experience in 4425 white children aged 12-14 years of 13 cities in 4 states. Public Health Rep 1942;57:1155-1179.