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material upon the tooth, where normally smooth, non-irritating cuticle exists, soon causes inflammation; at first only microscopic in extent. Minute and microscopic quantities of inflammatory exudate and pus cells are poured out through the inflamed tissue into the gingival crevice, and these tend to promote the growth of microorganisms and increase of the concretion. As the foreign material on the tooth increases and advances further into the gingival crevice, the soft tissues attached to the tooth are forced back by the accompanying inflammation and ulceration. Gradually and almost imperceptibly a larger and larger portion of the tooth is exposed as the gingival margin moves further away from the occlusal level. The gum "recedes."

Many factors influence the progress of the lesions at different locations about a given tooth, about different teeth in the same individual and in different individuals. For our present purpose of prevention of the disease (lesions) and prevention of further progress of lesions that already exist, it is only necessary to adopt and direct effective measures against the conditions at and within the gingival crevice. The disease process involving the more remote tissues—periodontal membrane, alveolar bone—rapidly subsides as soon as the local lesions consisting of inflamed, suppurating and broken surface of the epithelial tissue of the gum within the crevice, subside and disappear.

Fig. 10. Proximal of extracted tooth stained with crystal violet showing biconcave disc of bacterial material surrounding contact area, and heavy film which extended from the gingival border (gingival crevice) occlusalward. Contact point (1). Disc of bacterial film material surrounding contact point (2). Heavy bacterial material on area protected from functional friction (3). Epithelial cells remaining attached to tooth (4). Location of cemento-enamel junction (5). Some epithelial attachment tissue retained on tooth (6).

 

From the earliest stage and continuously as the lesion progresses, the tooth surrounded by this concretion and bacterial material adhering to it within the gingival crevice is, in effect, a foreign body infected with many different kinds of bacteria. It is a suppurating lesion constantly exposed to invasion by any and all of the many different kinds of bacteria within the mouth which are capable of growing in such an environment.

This foreign body effect was recognized and emphasized as the cause of periodontoclasia more than seventy years ago by Dr. John W. Riggs.l6 He supported his claims by the marked benefit and control of the disease he secured by removing this foreign material from the surface of the tooth and polishing it so it no longer caused the constant irritation and suppuration characteristic of the disease. The treatment had to be repeated frequently as the material soon reformed. How different it would have been if he and those who followed him could have had their patients carry out the personal oral hygiene procedure we now know to be possible and essential, thereby preventing the recurrence of the local conditions which originally caused and promoted the disease!

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