Vitamin D and Tooth Loss in the ElderlyHave We Seen the Light?
Vitamin D and Tooth Loss in the ElderlyHave We Seen the Light?
By Susan T. Marcolina, MD, FACP. Dr. Marcolina is a board-certified internist and geriatrician in Issaquah, WA; she reports no financial relationship to this field of study.
Although osteoporosis and osteopenia occur in persons of all ages, they most commonly affect institutionalized long-term care and community-dwelling elderly patients, the same population segments with the highest risk of tooth loss and periodontal disease. Periodontal disease (PD) is a chronic infectious/inflammatory disorder that affects the tissues (gums and periodontal ligaments) that support and anchor teeth into the alveolar bone of the mandible and maxilla. It represents a significant public health problem because it is the leading cause of tooth loss in the elderly and has been shown to be a risk factor for poor health beyond the oral cavity in several studies.1,2
Calcium and vitamin D are important nutrients for bone health. Calcium is a primary mineral component of hydroxyapatite, present throughout the bony skeleton, and vitamin D has important hormonal regulatory effects on bony metabolism as well as immunomodulatory effects. Given that osteoporosis, periodontal disease, and tooth loss are preventable conditions and that dietary supplementation with calcium and vitamin D is a relatively inexpensive, well-tolerated, and effective treatment for both conditions, it is important for primary care physicians to recommend these dietary nutrients to vulnerable elderly patients and their families in conjunction with other lifestyle and pharmacological therapies.
Prevalence of Tooth Loss in Elders
According to data from the National Institute of Dental and Craniofacial Research (NIDCR) of the National Institutes of Health (NIH), 24% of U.S. senior citizens aged 65-74 and 31% of U.S. senior citizens age 75 or older are edentulous. Additional risk factors for the edentulous state are summarized in Table 1.3
![]() |
Sequelae of Tooth Loss in Elderly Patients
Edentia (complete loss of native teeth) in non-institutionalized elders doubled the risk of significant weight loss in one year after adjustment for age, gender, baseline weight, and income.4 Periodontitis, the most common cause of tooth loss in geriatric patients, has a prevalence of roughly 60-90% in studies of geriatric patients from various countries when it is defined as at least one tooth site with 4 mm of attachment loss (calibrated probe depth measurement of distance in millimeters from the free gum margin to the bottom of the periodontal pocket between the tooth and gum; it is a cumulative measure of periodontitis and is abnormal when it is 2 mm or greater in depth).5-8
Tooth loss results in diminished chewing ability and nutritional intake, and impaired speech, sequelae associated with diminished quality of life and increased mortality in geriatric patients.9
Classification of Periodontal Disease
Periodontal disease is broadly categorized as either gingivitis or periodontitis. Periodontitis is distinguished from gingivitis by the presence of alveolar bone destruction that does not occur in gingivitis. Gingivitis is characterized by the presence of redness, swelling, and toothbrushing- or flossing-provoked bleeding of the gums. The transition from gingivitis to the more severe periodontitis is significantly variable between individuals and can be from weeks to years.10
Pathophysiology of Tooth Loss in Geriatric Patients
Periodontitis and osteoporosis are chronic diseases, which can influence tooth loss independently and synergistically. Common risk factors are outlined in Table 2.11,12
![]() |
Whether intraoral PD and alveolar bone resorption occur as a result of and concomitantly with systemic extracranial osteoporosis has been controversial. The association has been substantiated in some studies,13,14 but not in others.15,16 A substudy of 58 postmenopausal women from the Women's Health Initiative (WHI) has, however, shed some light on the relationship between extracranial osteoporosis, alveolar bone loss (ABL), and periodontal disease. In this three-year longitudinal oral bone ancillary study, women with osteoporosis had more than three times the amount of ABL compared to women without osteoporosis, regardless of whether they had active PD. Certainly, this confirms the fact that the same risk factors responsible for the imbalance of bone resorption relative to bone formation apply to bone metabolism throughout the body. In addition, alveolar bone, unlike extracranial bone, is uniquely affected by periodontal disease that occurs in the oral cavity. Indeed, the women who experienced the greatest amount of ABL in the WHI substudy were those with both PD and osteoporosis.11
Microbiology and Pathobiology of Periodontal Disease
Bacterial infection, primarily involving gram-positive anaerobes such as Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum cause adult periodontal disease.17 These bacteria inhabit the plaque or sticky biofilm, which adheres to the supragingival (above gum) and subgingival (below gum) surfaces of the teeth. The host immune response incited by the bacterial biofilm is an important mechanism whereby the soft-tissue attachment (gum and periodontal ligament) is eroded and alveolar bone (mandibular and maxillary bony substrate in which teeth are implanted) is resorbed. As part of this process, there is an influx of tissue monocytes to these pockets of bacterial infection. Such monocytes secrete cell proteins known as cytokines, which modulate local and systemic inflammatory responses by cellular signaling. Specific cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-a) have osteoclastic signaling activity, which is responsible for alveolar bone resorption.18,19 IL-1, TNF-a, and IL-6 are all expressed in inflamed gingival tissues and several investigators have documented increased levels in the crevicular (pocket between the tooth and gum) fluid from patients with periodontitis.19,20 These cytokines stimulate osteoclast formation and bone resorption.21 The vascularity of the oral cavity facilitates hematogenous transmission of infection and inflammatory mediators systemically, potentially contributing to cardiovascular and cerebrovascular complications.
Immunomodulatory Effects of Vitamin D
Vitamin D receptors (VDRs) are ubiquitous in periodontal tissue and several associations between various vitamin D receptor polymorphisms and periodontal disease have been described.22
Many tissues (prostate, breast, colon, and cytokine-producing immune cells) that express the VDR also contain 25(OH)D-1-alpha hydroxylase, which catalyses the conversion of 25(OH)D to 1,25(OH)2D (calcitriol) locally. In vitro studies show that 1,25(OH)2D can block the synthesis of macrophage mRNA for IL-1, IL-6, and TNF-a, thus modulating the inflammatory cascade and mitigating tissue and bone damage.23 The concentrations of such locally elaborated calcitriol are not as tightly regulated as the renally produced hormone, but are dependent upon an adequate depot supply of 25(OH)D.24,25
Data from the third National Health and Nutrition Examination Survey (NHANES III) suggest that serum 25(OH)D levels greater than 85.6 nmol/L or 34 ng/mL are associated with less attachment loss in patients 50 years of age and older.26
One study involving a population with chronic severe congestive heart failure demonstrated elevated levels of IL-10 (anti-inflammatory cytokine) and decreased concentrations of the pro-inflammatory cytokine TNF-a, with an increase in serum levels of 25(OH)D (to a mean level of 125 nmol/L, or 50 ng/mL) after supplementation with 2,000 IU daily of vitamin D3 (cholecalciferol) plus 500 mg calcium for nine months.27 Such results are in agreement with experimental data that demonstrated the ability of vitamin D to suppress the release of TNF-a and to enhance IL-10 synthesis.28 Of note is the fact that a previous study by Witte et al using a vitamin D dosage of 400 IU/d did not affect cytokine concentrations. Thus, it appears that there is a threshold dosage necessary for the immunomodulatory effects as well as the skeletal effects of vitamin D.29
Clinical Studies of Vitamin D, Periodontal Disease, and Tooth Loss
In a three-year, randomized, placebo-controlled trial of 145 healthy ambulatory adults 65 years and older, Krall et al demonstrated that adults supplemented with 500 mg of calcium plus 700 IU of cholecalciferol (vitamin D3) had a lower odds ratio (OR) of tooth loss that was significantly different from the placebo group (OR = 0.4; P < 0.05).30
Dietrich et al analyzed NHANES III data from more than 77,000 teeth in 6,700 nonsmokers ages 13-90+ to evaluate the anti-inflammatory effects of vitamin D in humans. They found an inverse association between the serum concentrations of 25(OH)D levels and the presence of chronic gingivitis (early manifestation of inflammatory soft tissue-only oral disease), as manifested by probe-induced gum bleeding. This association was consistent across racial and ethnic groups and was independent of age, sex, income, calculus, body mass index (BMI), vitamin C intake, diabetes, use of hormone replacement therapy or oral contraceptives, and frequency of dental visitation, and linear across the range of serum 25(OH)D values in this study (highest value was 114 nmol/L, or 46 ng/mL).31
Optimal Vitamin D Target Serum Levels
Serum levels of 25(OH)D for persons living in the proximity of the equator or consistently exposed to sunlight for long periods of time (outdoor workers) typically are in the 100-160 nmol/L range (40-64 ng/mL). Such serum levels have been regarded by experts as being the upper limit for safe levels. Additionally, when 25(OH)D levels are 80-100 nmol/L (32-40 ng/mL), there is optimal intestinal calcium absorption as well as minimal parathyroid hormone (PTH) secretion.32
Importance of Daily Oral Hygiene
The most important factor for the prevention of periodontitis is the maintenance of a regular oral hygiene regimen of twice-daily toothbrushing and pre-bedtime flossing in conjunction with a well-balanced diet low in refined sugars and carbonated beverages. These practices are important to remove the bacterial biofilm from the surface of the teeth. Should the biofilms be allowed to accumulate on the teeth over 36 hours, they become calcified there as a result of the mineral content of the saliva and must be removed by professional dental scaling and cleaning.33
Challenges for Elderly Persons with Oral Care
Daily oral hygiene measures can present challenges to geriatric patients who may have cognitive impairment secondary to dementing illnesses, diminished eyesight, or compromised manual dexterity secondary to arthritis and neuromuscular disease. Furthermore, many geriatric patients receive medications that decrease salivary flow. Table 3 lists several common types of medications that can cause xerostomia.
![]() |
Under normal circumstances, saliva functions as an acid buffer, lubricant, and a cleanser for the oral cavity. It contains bacteriostatic compounds such as lysozyme, lactoferrin, lactoperoxidase, and secretory immunoglobulins. The secretory immunoglobins, primarily IgA, are important for the prevention of bacterial adherence to tooth surfaces. Medication-, radiation-, or inflammation- induced hyposalivation can cause permanent or temporary reductions in salivary flow, which dramatically alter the natural oral bacterial ecosystem, resulting in an increase in oropharyngeal colonization with gram-negative bacteria and other pathogens that exacerbate PD and tooth decay and serve as a reservoir for serious pulmonary infections. Wide handled battery-powered toothbrushes can facilitate the necessary daily dental cleansing and specially formulated toothpastes and moisturizing gels such as Biotene® and Oral Balance® Mouth Moisturizing gel, which contain some salivary components, help offset some of these problems.35
Recommendations for Intake
The Institute of Medicine recommends 1,000-1,300 mg/d of elemental calcium for adults. Consumers can use the Calcium Calculator to track their daily calcium intake (www.iofbonehealth.org/patients-public/calcium-calculator.html).36 Since vitamin D is produced in the skin via exposure to ultraviolet radiation from the sun, many people receive adequate vitamin D by cutaneous synthesis. However, for persons infrequently or inconsistently exposed to sunlight such as homebound or institutionalized elderly, dietary intake of at least 800-1,000 IU is essential to supplement endogenous production and to maintain 25(OH)D levels within the normal recommended range of 30-40 ng/mL (75-100 nmol/L). For patients whose depot vitamin D levels are insufficient (20-30 ng/mL) or deficient (< 20 ng/mL), more aggressive supplementation has been recommended with follow-up serum levels of 25(OH)D after three months to assess adequacy of body stores.32
Conclusion
Vitamin D and calcium supplementation have ancillary benefits, in conjunction with daily oral hygiene and professional dental care, for the prevention and treatment of periodontal diseases and tooth loss, both of which have significant and costly ramifications for geriatric patients in terms of increased cardiovascular and cerebrovascular risk, diminished nutritional status, and overall decreased general medical health. This is another reason to screen susceptible patients in a general medical practice for vitamin D deficiency and general oral health.
Recommendation
During routing office visits, primary care physicians should screen geriatric patients for vitamin D adequacy, which has been found to be in the range of 30-40 ng/mL (75-100 nmol/L) and supplement according to guidelines to achieve this goal. It is equally important to evaluate their cognitive and physical abilities to properly perform oral hygiene measures with a toothbrush and floss. If a basic oral examination reveals gingival inflammation, bleeding, supragingival calculus, dental mobility, or peridental suppuration, prompt referral to a dental professional is indicated.
References
1. Joshipura KJ, et al. Periodontal disease, tooth loss, and incidence of ischemic stroke. Stroke 2003;34:47-52.
2. Joshipura KJ, et al. Possible explanations for the tooth loss and cardiovascular disease relationship. Ann Periodontol 1998;3:175-183.
3. National Institute of Dental and Craniofacial Research, National Institutes of Health. Tooth Loss in Seniors Age 65 and Older. Available at:www.nidcr.nih.gov/DataStatistics/FindDataByTopic/ToothLoss/ToothLossSeniors65andOlder.htm. Accessed March 26, 2009.
4. Ritchie CS, et al. Oral health problems and significant weight loss among community-dwelling older adults. J Gerontol A Biol Sci Med Sci 2000;55:M366-M371.
5. Krustrup U, Erik Petersen P. Periodontal conditions in 35-44 and 65-74-year-old adults in Denmark. Acta Odontol Scand 2006;64:65-73.
6. Levy SM, et al. the prevalence of periodontal disease measures in elderly adults, aged 79 and older. Spec Care Dentist 2003;23:50-57.
7. Mack F, et al. Caries and periodontal disease of the elderly in Pomerania, Germany: Results of the Study of Health in Pomerania. Gerodontology 2004;21:27-36.
8. Hirotomi T, et al. Longitudinal study on periodontal conditions in healthy elderly people in Japan. Community Dent Oral Epidemiol 2002;30:409-417.
9. Soikkonen K, et al. Radiographic periodontal attachment loss as an indicator of death risk in the elderly. J Clin Periodontol 2000;27:87-92.
10. Burt B; Research, Science and Therapy Committee of the American Academy of Periodontology. Position paper: Epidemiology of periodontial diseases. J Periodontol 2005;76:1406-1419.
11. Geurs NC, et al. Osteoporosis and periodontal disease progression. Periodontol 2000 2003;32:105-110.
12. Genco RJ. Current view of risk factors for periodontal disease. J Periodontol 1996;67(10 Suppl):1041-1049.
13. Persson RE, et al. Assessment of periodontal conditions and systemic disease in older subjects. I. Focus on osteoporosis. J Clin Periodontal 2002;29:796-802.
14. Wactawski-Wende J, et al. The role of osteopenia in oral bone loss and periodontal diseases. J Periodontol 1996; 67:1076-1084.
15. Hildebolt CF, et al. Attachment loss with postmenopausal age and smoking. J Periodontal Res 1997;32:619-625.
16. Elders PJ, et al. The relation between periodontitis and systemic bone mass in women between 46 and 55 years of age. J Clin Periodontol 1992;19:492-496.
17. Adriaens LM, et al. Does pregnancy have an impact on the subgingival microbiota? J Periodontol 2009;80:72-81.
18. Offenbacher S. Periodontal diseases: Pathogenesis. Ann Periodontol 1996;1:821-878.
19. Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol 2003;74:391-401.
20. Boch JA, et al. Interleukin 1 signal transductioncurrent concepts and relevance to periodontitis. J Dent Res 2001; 80:400-407.
21. Horowitz J, Lorenza JA. Local regulators of bone: IL-l, TNF-alpha, lymphotoxin, interferon-gamma, IL-8, IL-10, IL-4, the LIF/IL-6 family and additional cytokines. In: Bilezikian JP, et al. Principles of Bone Biology. 2nd ed. San Diego, CA: Academic Press; 2002:961-978.
22. Hennig BJ, et al. Association of a vitamin D receptor gene polymorphism with localized early-onset periodontal disease. J Periodontol 1999;70:1032-1038.
23. Scharla SH, et al. Alfacalcidiol vs plain vitamin D in inflammation induced bone loss. J Rheumatol Suppl 2005;76:26-32.
24. Holick MF. Vitamin D: The underappreciated D-lightful hormone that is important for skeletal and cellular health. Curr Opin Endocrinol Diabetes 2002;9:87-98.
25. Bouillon R. Vitamin D: From photosynthesis metabolism, and action to clinical applications. In: DeGroot LJ, Jameson JL. Endocrinology. Philadelphia, PA: W.B. Saunders; 2001:1009-1028.
26. Dietrich T, et al. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr 2004;80:108-113.
27. Schleithoff SS, et al. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: A double-blind, randomized, placebo-controlled trial. Am J Clin Nutr 2006;83:754-759.
28. Zhu Y, et al. Calcium and 1 alpha,25-dihydroxyvitamin D3 target the TNF-alpha pathway to suppress experimental inflammatory bowel disease. Eur J Immunol 2005;35: 217-224.
29. Witte KK, Clarke AL. Chronic heart failure and multiple micronutrient supplementation: Realistic hope or idealistic conjecture? Heart Fail Monit 2005;4:123-129.
30. Krall EA, et al. Calcium and vitamin D supplements reduce tooth loss in the elderly. Am J Med 2001;111:452-456.
31. Dietrich T, et al. Association between serum concentrations of 25-hydroxyvitamin D and gingival inflammation. Am J Clin Nutr 2005;82:575-580.
32. Dawson-Hughes B. Treatment of vitamin D deficient states. In: Official Topic Review from UpToDate® Clinical Information Service. Accessible at:www.uptodate.com/home/store/index.do.
33. American Dental Association. How do I floss my teeth? Available at:www.ada.org/public/topics/cleaning_faq.asp. Accessed March 22, 2009.
34. Screenby LM, Schwartz SS. A reference guide to drugs and dry mouth. Gerodontology 1986;5:75-99.
35. Beck JD, Hunt RJ. Oral health status in the United States. Problems of special patients. J Dent Educ 1985;49:407-426.
36. International Osteoporosis Foundation. Patients and public: IOF Calcium Calculator. Available at:www.iofbonehealth.org/patients-public/calcium-calculator.html. Accessed March 20, 2009.
Although osteoporosis and osteopenia occur in persons of all ages, they most commonly affect institutionalized long-term care and community-dwelling elderly patients, the same population segments with the highest risk of tooth loss and periodontal disease.Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.