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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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