In reply: Menopause, vitamin D, and oral health

In Reply: Dr. Mascitelli and colleagues bring up an excellent point regarding the role of vitamin D. Vitamin D deficiency (and insufficiency) is such a widespead problem that it deserves attention in both dental and medical circles, and to be fair, it deserves an article of its own. Low vitamin D has been associated with bone loss and an increased risk for certain cancers and other chronic diseases.¹ The literature also suggests that low levels of vitamin D are associated with periodontal disease,² and that supplementation with vitamin D (and calcium) leads to better periodontal health.^3,4 However, since vitamin D supplementation is not a recognized way to treat periodontitis, mentioning it with therapies adjudicated as treatment modalities (such as removal of biofilm, which we stressed in our paper) risks misinterpretation by clinicians less versed in periodontal and dental conditions in general.

Nevertheless, the comment brings to light that medical, dental, and nutritional colleagues are very interested in learning more about the pathophysiologic commonalities in the diseases we treat and in a common postmenopausal patient cohort. Our paper focused more closely on what periodontitis is, and on the more primary etiologic pathophysiology—what common resorptive pathways it shares with osteoporosis in the postmenopausal cohort, and biofilm, the primary etiology of periodontitis. But there is need for more discussion and research into bone development (during childhood and adolescence as well) and the role of nutrition during all stages of life.

In Reply: Dr. Mascitelli and colleagues bring up an excellent point regarding the role of vitamin D. Vitamin D deficiency (and insufficiency) is such a widespead problem that it deserves attention in both dental and medical circles, and to be fair, it deserves an article of its own. Low vitamin D has been associated with bone loss and an increased risk for certain cancers and other chronic diseases.¹ The literature also suggests that low levels of vitamin D are associated with periodontal disease,² and that supplementation with vitamin D (and calcium) leads to better periodontal health.^3,4 However, since vitamin D supplementation is not a recognized way to treat periodontitis, mentioning it with therapies adjudicated as treatment modalities (such as removal of biofilm, which we stressed in our paper) risks misinterpretation by clinicians less versed in periodontal and dental conditions in general.

Nevertheless, the comment brings to light that medical, dental, and nutritional colleagues are very interested in learning more about the pathophysiologic commonalities in the diseases we treat and in a common postmenopausal patient cohort. Our paper focused more closely on what periodontitis is, and on the more primary etiologic pathophysiology—what common resorptive pathways it shares with osteoporosis in the postmenopausal cohort, and biofilm, the primary etiology of periodontitis. But there is need for more discussion and research into bone development (during childhood and adolescence as well) and the role of nutrition during all stages of life.

In Reply: Dr. Mascitelli and colleagues bring up an excellent point regarding the role of vitamin D. Vitamin D deficiency (and insufficiency) is such a widespead problem that it deserves attention in both dental and medical circles, and to be fair, it deserves an article of its own. Low vitamin D has been associated with bone loss and an increased risk for certain cancers and other chronic diseases.¹ The literature also suggests that low levels of vitamin D are associated with periodontal disease,² and that supplementation with vitamin D (and calcium) leads to better periodontal health.^3,4 However, since vitamin D supplementation is not a recognized way to treat periodontitis, mentioning it with therapies adjudicated as treatment modalities (such as removal of biofilm, which we stressed in our paper) risks misinterpretation by clinicians less versed in periodontal and dental conditions in general.

Nevertheless, the comment brings to light that medical, dental, and nutritional colleagues are very interested in learning more about the pathophysiologic commonalities in the diseases we treat and in a common postmenopausal patient cohort. Our paper focused more closely on what periodontitis is, and on the more primary etiologic pathophysiology—what common resorptive pathways it shares with osteoporosis in the postmenopausal cohort, and biofilm, the primary etiology of periodontitis. But there is need for more discussion and research into bone development (during childhood and adolescence as well) and the role of nutrition during all stages of life.