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Elevated temperature is one of 4 cardinal inflammatory signs. Previous work indicates that subgingival temperature assessments are accurate and re- liable, and provide objective, quantitative information over a broad 10 degrees C range, in small 0.1 degrees C increments with a direct, immediate report on the inflammatory status at the pocket base. However, complicating the use and interpretation of subgingival temperature assessments are its 3 forms: actual subgingival temperature, sublingual temperature minus subgingival temperature (temperature differential), and a temperature indicator light. We reasoned that if one could determine which of the temperature assessments reflected the periodontal condition, and which were independent variables, they would provide new and unique information about the inflammatory status of the periodontium. We also reasoned that by providing objective, quantitative data over a broad range, subgingival temperature should reduce the sample size required to obtain significance in clinical trials. Therefore, the purpose of this study was 2-fold: (1) to determine whether the 3 subgingival temperature assessments could differentiate between clinically defined periodontal health and disease; (2) to determine whether the 3 assessments were dependent or independent clinical variables. The data indicated that all 3 subgingival temperature assessment methods differentiated between clinically-defined periodontal health and disease (all p<0.02). All 3 assessments also correlated significantly (all p<0.03), but modestly (all r>0.49), with bleeding on probing. Based on scatter-plot matrices and common factor analysis, the data indicated that only actual subgingival temperature and temperature differential were independent variables. Taken together, this data indicates that subgingival temperature and temperature differential provide unique information about the periodontal inflammatory state. Power calculations indicated that the temperature differential may significantly reduce the subject number required to achieve significance in clinical trials examining gingival inflammation. Because of the body's rapid temperature response, these assessments may also significantly reduce the time required for gingival inflammation trials.

Pulpal and periodontal diseases are bacterial infections which result in local connective tissue and bone destruction. Effective host resistance to these infections is primarily mediated by neutrophils and other phagocytic cells. PGG glucan (poly-beta 1-6-glucotriosyl-beta 1-3-glucopyranose glucan) is a biological response modifier which stimulates the production of neutrophils and upregulates their phagocytic and bactericidal activity. In the present studies, the effect of PGG glucan on infection-stimulated alveolar bone resorption was tested in an in vivo model. Periapical bone resorption was induced in Sprague-Dawley rats by surgical pulp exposure and subsequent infection from the oral environment. Animals were administered PGG glucan (0.5 mg/kg) or saline (control) subcutaneously the day before and on days 2, 4, 6, 9, 11, 13, 16, and 18 following the pulp exposure procedure. PGG glucan enhanced the number of circulating neutrophils and monocytes and increased neutrophil phagocytic activity approximately two-fold. PGG glucan-treated animals had significantly less infection-stimulated periapical bone resorption than control animals, as determined radiographically (-48.0%; p < 0.001) and by histomorphometry (-40.8% and -42.4% for first and second molars, respectively; p < 0.001). PGG glucan-treated animals also had less soft tissue destruction, as indicated by decreased pulpal necrosis. Only 3.3% of the first molar pulps from PGG glucan-treated animals exhibited complete necrosis, as compared with 40.6% of pulps from controls. Finally, PGG glucan had no effect on either PTH- or IL-1-stimulated bone resorption in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)