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The effect of subclinical ascorbate deficiency on periodontal health in nonhuman primates
Author(s) -
Alvares Olav,
Altman Leonard C.,
Springmeyer Steven,
Ensign Wayne,
Jacobson Kerry
Publication year - 1981
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1981.tb01001.x
Subject(s) - ascorbic acid , subclinical infection , periodontitis , ascorbic acid deficiency , gingivitis , periodontium , medicine , physiology , endocrinology , biology , dentistry , food science
The aim of this study was to evaluate the effects of chronic subclinical ascorbic acid deficiency on periodontal health in a nonhuman primate model. Young adult Macaca fascicularis monkeys were fed an ascorbic acid free diet for nine weeks followed by a diet with a suboptimal level of ascorbic acid for an additional sixteen weeks. During the 25‐week period, a pair fed control group was fed a nutritionally adequate diet in amounts equivalent to that consumed by the experimental group. From the second week onward, whole blood ascorbic acid levels in the experimental animals but not in pair fed controls were significantly reduced. Experimental animals did not develop clinical signs of ascorbate deficiency, and there was little evidence of spontaneous gingivitis or periodontitis in either group between weeks 0 and 23. At week 23, plaque‐associated periodontitis was experimentally induced to evaluate the response of the periodontal tissues to the underlying subclinical ascorbate deficiency. Gingival index scores and pocket depth measurements were significantly greater in the ascorbate deficient animals than in controls. Preliminary studies of leukocyte function suggested that this susceptibility to periodontitis might be related to impaired polymorphonuclear leukocyte chemotaxis and phagocytosis. This study indicates that the periodontium is vulnerable to chronic inflammation as a consequence of subclinical ascorbic acid deficiency.