Although there is no doubt that gingivitis can develop in the absence of supragingival calculus, it is not clear to what extent the presence of mineralized deposit enhances gingival inflammation. Partial inhibition of plaque mineralization can be accomplished by chemical agents, but there has been no demonstration in humans of a reduction in gingivitis. It remains to be established what level of inhibition (if any) is required to have more than a cosmetic effect. Since the accepted scenario is that apical growth of supragingival plaque precedes the formation of subgingival calculus, there is no longer an issue of whether subgingival calculus is the cause or the result of periodontal disease. Subgingival mineralization results from the interaction of subgingival plaque with the influx of mineral salts that is part of the serum transudate and inflammatory exudate. This chronology, however, should not be the basis for relegating calculus to the ash heap. Morphologic and analytical studies point to the porosity of calculus and retention of bacterial antigens and the presence of readily available toxic stimulators of bone resorption. When coupled with the increased build up of plaque on the surface of the calculus, the combination has the potential for extending (beyond that of plaque alone) the radius of destruction and the rate of displacement of the adjacent junctional epithelium. The centrality of thorough scaling and root planing in the successful maintenance of periodontal health supports the view that subgingival calculus contributes significantly to the chronicity and progression of the disease, even if it can no longer be considered as responsible for initiation.