Calcium and periodontitis: clinical effect of calcium medication.

In contrast to the generally held concept that periodontal disease is caused by microorganisms, Henriksson (1968) suggested that a nutritional deficiency of calcium might be the cause. He elicited secondary hyperparathyroidism in beagles from a low calcium/high phosphorus diet and found that the osteolytic demineralization of bone that followed seemed to involve alveolar bone more than other bones. In a report on 10 persons with advanced periodontal disease, Krook et al. (1972) stated that the disease was reversed when they were given 1 g Ca/day for 180 days. These results have been disputed. The present study is an attempt to repeat the experiment performed by Krook et al. (1972) under more stringent conditions. The hypothesis that calcium supplementation reverses destructive periodontal disease is tested. 66 persons referred to our clinic for periodontal problems were prescribed at random calcium (1 g) or placebo tablets daily during a trial period of 180 days. Their periodontal status was examined at day 0 and at day 180. The parameters used for comparison were Plaque Index, Gingival Index, probing depth, mobility and furcation involvement. The radiographically registered level of alveolar bone was also recorded, but subsequently discarded since no change could be ascertained. The patients were interviewed as to their consumption of calcium via milk and cheese at days 90 and 180. This was in order to estimate roughly whether or not their dietary calcium consumption was adequate. The recommended allowance of 800 mg/day was used as a reference. During the trial period 7 persons withdrew -- 2 from the test group and 5 from the control group. This was due mainly to digestive disorders, reported by the patients. A comparison at day 0 between the 31 test and 28 control patients revealed no statistical differences concerning the periodontal parameters studied. At day 180 both groups showed a slight improvement in Plaque Index, Gingival Index and probing depth; however, there was still no statistical difference between them. The dietary analysis established a low calcium consumption among 1/3 of the patients. Even in these cases calcium supplementation had no effect. It is concluded that calcium supplementation for 180 days does not influence the periodontal status of patients with moderate to advanced periodontal disease. Secondly, patients on a low calcium diet do not differ from those receiving an adequate supply. Finally, the study cannot support the hypothesis that calcium deficiency is a main cause of destructive periodontal disease.