BONE-RESORPTION CAUSED BY 3 PERIODONTAL PATHOGENS IN-VIVO IN MICE IS MEDIATED IN PART BY PROSTAGLANDIN

Gingival inflammation, bacterial infection, alveolar bane destruction, and subsequent tooth loss are characteristic features of periodontal disease, but the precise mechanisms of bone loss are poorly understood . Most animal models of the disease require injury to gingival tissues or teeth, and the effects of microorganisms are thus complicated by h ost responses to tissue destruction. To determine whether three putati ve periodontal pathogens, Porphyromonas gingivalis, Campylobacter rect us, and Fusobacterium nucleatum, could cause localized bone resorption in vivo in the absence of tissue injury, we injected live or heat-kil led preparations of these microorganisms into the subcutaneous tissues overlying the calvaria of normal mice once daily for 6 days and then examined the bones histologically. We found that all three microorgani sms (both live and heat killed) stimulated bone resorption and that th e strain off. nucleatum based appeared to be the strongest inducer of osteoclast activity. Treatment of the mice concomitantly with indometh acin reduced but did not completely inhibit bone resorption by these m icroorganisms, suggesting that their effects were mediated,in part, by arachidonic acid metabolites (e.g., prostaglandins). Our findings ind icate that these potential pathogens can stimulate bone resorption loc ally when placed beside a bone surface in vivo in the absence of prior tissue injury and support a role for them in the pathogenesis of bone loss around teeth in periodontitis.