REDUCTION OF INFECTION-STIMULATED PERIAPICAL BONE-RESORPTION BY THE BIOLOGICAL RESPONSE MODIFIER PGG GLUCAN

Pulpal and periodontal diseases are bacterial infections which result in local connective tissue and bone destruction. Effective host resist ance to these infections is primarily mediated by neutrophils and othe r phagocytic cells. PGG glucan (poly-beta 1-6-glucotriosyl-beta 1-3-gl ucopyranose glucan) is a biological response modifier which stimulates the production of neutrophils and upregulates their phagocytic and ba ctericidal activity. In the present studies, the effect of PGG glucan on infection-stimulated alveolar bone resorption was tested in an in v ivo model. Periapical bone resorption was induced in Sprague-Dawley ra ts by surgical pulp exposure and subsequent infection from the oral en vironment. 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 enhance d the number of circulating neutrophils and monocytes and increased ne utrophil phagocytic activity approximately two-fold. PGG glucan-treate d 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 < 0.01). PGG glucan-treated animals al so had less soft tissue destruction, as indicated by decreased pulpal necrosis. Only 3.3% of first molar pulps from PGG glucan-treated anima ls exhibited complete necrosis, as compared with 40.6% of pulps from c ontrols. Finally, PGG glucan had no effect on either PTH- or IL-1-stim ulated bone resorption in vitro. These findings support the concept th at a biological response modifier which enhances endogenous antibacter ial mechanisms in neutrophils can decrease infection-stimulated alveol ar bone and soft tissue destruction in vivo.