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Infection and Immunity, September 1998, p. 4158-4162, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Bone Resorption Caused by Three Periodontal Pathogens In Vivo in Mice Is Mediated in Part by Prostaglandin

Yuval Zubery,1 Colin R. Dunstan,2 Beryl M. Story,2 Lakshmyya Kesavalu,1 Jeffrey L. Ebersole,1,* Stanley C. Holt,3 and Brendan F. Boyce2

Departments of Periodontics,1 Pathology,2 and Microbiology,3 University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284-7894

Received 1 December 1997/Returned for modification 2 February 1998/Accepted 10 June 1998

Gingival inflammation, bacterial infection, alveolar bone 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 host responses to tissue destruction. To determine whether three putative periodontal pathogens, Porphyromonas gingivalis, Campylobacter rectus, and Fusobacterium nucleatum, could cause localized bone resorption in vivo in the absence of tissue injury, we injected live or heat-killed 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 microorganisms (both live and heat killed) stimulated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer of osteoclast activity. Treatment of the mice concomitantly with indomethacin reduced but did not completely inhibit bone resorption by these microorganisms, suggesting that their effects were mediated, in part, by arachidonic acid metabolites (e.g., prostaglandins). Our findings indicate that these potential pathogens can stimulate bone resorption locally 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.

* Corresponding author. Mailing address: Department of Periodontics, School of Dentistry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284-7894. Phone: (210) 567-3591. Fax: (210) 567-6858. E-mail: EBERSOLE{at}UTHSCSA.EDU.

Infection and Immunity, September 1998, p. 4158-4162, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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