Periodontitis is a condition whereby the ligament supporting the alveolar bone (the bone containing the tooth sockets) becomes inflamed due to microbially induced inflammation. The result is a possible loss of teeth as the condition deteriorates the structures around the teeth. Systemic inflammation may be a contributory factor in periodontitis because those with other inflammatory disorders such as cardiovascular disease are at higher risk of periodontitis. The association between antioxidants and inflammatory conditions suggests that poor antioxidant status may be involved in the aetiology of periodontitis. Animal experiments also show that vitamin E is able to accelerate wound healing of the gingival tissue and may also protect from alveolar bone loss. However, the animal experiments to date were performed with very high concentrations of vitamin E. Epidemiological evidence to date has been inconsistent, with some studies showing no association between vitamin intake and tooth loss.
However, vitamin blood levels may be a better marker for vitamin E status that vitamin E intake. Also, dietary vitamin E is a measure of all forms of vitamin E, but some data shows that α-tocopherol may show the most protective effects in animals. When blood α-tocopherol is measured instead of estimating vitamin E intake, a protective effect for vitamin E may become apparent. For example, in one study1, researchers investigated the association between the serum levels of α-tocopherol, the most biologically active form of vitamin E, and the presence of mild, moderate or severe periodontitis. The results, taken from a study population of 4708 individuals, showed that serum α-tocopherol (adjusted to account for cholesterol levels, as lipoproteins number affects vitamin E levels) was inversely associated with both clinical attachment loss and probing pocket depth, two measures of periodontitis. In those with low levels of α-tocopherol, this relationship was linear, suggesting vitamin E may be protective.
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