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Menopause, vitamin D, and oral health

To the Editor: Buencamino and colleagues1 reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.2 In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.3

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.4 The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.5 This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

References
  1. Buencamino MC, Palomo L, Thacker HL. How menopause affects oral health, and what we can do about it. Cleve Clin J Med 2009; 76:467475.
  2. Dietrich T, Joshipura KJ, Dawson-Hughes B, Bischoff-Ferrari HA. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr 2004; 80:108113.
  3. Krall EA, Wehler C, Garcia RI, Harris SS, Dawson-Hughes B. Calcium and vitamin D supplements reduce tooth loss in the elderly. Am J Med 2001; 111:452456.
  4. Amano Y, Komiyama K, Makishima M. Vitamin D and periodontal disease. J Oral Sci 2009; 51:1120.
  5. Timms PM, Mannan N, Hitman GA, et al. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM 2002; 95:787796.
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Luca Mascitelli, MD
Comando Brigata Alpina “Julia” Medical Service, Udine, Italy

Francesca Pezzetta, MD
Cardiology Service, Ospedale di Tolmezzo, Tolmezzo, Italy

Mark R. Goldstein, MD, FACP
Fountain Medical Court, Bonita Springs, FL

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Luca Mascitelli, MD
Comando Brigata Alpina “Julia” Medical Service, Udine, Italy

Francesca Pezzetta, MD
Cardiology Service, Ospedale di Tolmezzo, Tolmezzo, Italy

Mark R. Goldstein, MD, FACP
Fountain Medical Court, Bonita Springs, FL

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Luca Mascitelli, MD
Comando Brigata Alpina “Julia” Medical Service, Udine, Italy

Francesca Pezzetta, MD
Cardiology Service, Ospedale di Tolmezzo, Tolmezzo, Italy

Mark R. Goldstein, MD, FACP
Fountain Medical Court, Bonita Springs, FL

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To the Editor: Buencamino and colleagues1 reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.2 In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.3

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.4 The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.5 This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: Buencamino and colleagues1 reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.2 In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.3

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.4 The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.5 This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

References
  1. Buencamino MC, Palomo L, Thacker HL. How menopause affects oral health, and what we can do about it. Cleve Clin J Med 2009; 76:467475.
  2. Dietrich T, Joshipura KJ, Dawson-Hughes B, Bischoff-Ferrari HA. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr 2004; 80:108113.
  3. Krall EA, Wehler C, Garcia RI, Harris SS, Dawson-Hughes B. Calcium and vitamin D supplements reduce tooth loss in the elderly. Am J Med 2001; 111:452456.
  4. Amano Y, Komiyama K, Makishima M. Vitamin D and periodontal disease. J Oral Sci 2009; 51:1120.
  5. Timms PM, Mannan N, Hitman GA, et al. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM 2002; 95:787796.
References
  1. Buencamino MC, Palomo L, Thacker HL. How menopause affects oral health, and what we can do about it. Cleve Clin J Med 2009; 76:467475.
  2. Dietrich T, Joshipura KJ, Dawson-Hughes B, Bischoff-Ferrari HA. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr 2004; 80:108113.
  3. Krall EA, Wehler C, Garcia RI, Harris SS, Dawson-Hughes B. Calcium and vitamin D supplements reduce tooth loss in the elderly. Am J Med 2001; 111:452456.
  4. Amano Y, Komiyama K, Makishima M. Vitamin D and periodontal disease. J Oral Sci 2009; 51:1120.
  5. Timms PM, Mannan N, Hitman GA, et al. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM 2002; 95:787796.
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