THE RELATIONSHIP OF GINGIVAL CREVICULAR FLUID SHORT-CHAIN CARBOXYLIC-ACID CONCENTRATION TO GINGIVAL INFLAMMATION

Short-chain carboxylic acids (SCCA; C less than or equal to 5; e.g., l actic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and ex hibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentration s, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingiva l inflammatory agents, gingival inflammation should increase with incr easing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an obje ctive quantitative assessment of gingival inflammation used. To accomp lish these tasks, sites within subjects were stratified by location an d pocket depth, and the following quantified: bacterial presence; SCCA . concentration; and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and c anines (all r greater than or equal to 0.47; all p less than or equal to 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation d id not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of thes e pathogens (-0.31 less than or equal to r less than or equal to 0.39; 0.08 less than or equal to p less than or equal to 0.75) for any of t he locations. Finally the SCCA concentration did not correlate with th e level of individual or groups of pathogens. These data, together wit h historical work and other preliminary data, support the hypothesis t hat SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, be gin to explain the apparent lack of a direct relationship between curr ent gingival inflammation and the prediction of bacterially-mediated p eriodontal attachment loss.