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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Sci+Rep
2017 ; 7
(ä): 46322
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Elevation of pro-inflammatory cytokine levels following anti-resorptive drug
treatment is required for osteonecrosis development in infectious osteomyelitis
#MMPMID28387378
Morita M
; Iwasaki R
; Sato Y
; Kobayashi T
; Watanabe R
; Oike T
; Nakamura S
; Keneko Y
; Miyamoto K
; Ishihara K
; Iwakura Y
; Ishii K
; Matsumoto M
; Nakamura M
; Kawana H
; Nakagawa T
; Miyamoto T
Sci Rep
2017[Apr]; 7
(ä): 46322
PMID28387378
show ga
Various conditions, including bacterial infection, can promote osteonecrosis. For
example, following invasive dental therapy with anti-bone resorptive agents, some
patients develop osteonecrosis in the jaw; however, pathological mechanisms
underlying these outcomes remain unknown. Here, we show that administration of
anti-resorptive agents such as the bisphosphonate alendronate accelerates
osteonecrosis promoted by infectious osteomyelitis. Potent suppression of bone
turnover by these types of agents is considered critical for osteonecrosis
development; however, using mouse models we found that acceleration of bone
turnover by teriparatide injection did not prevent osteonecrosis but rather
converted osteoclast progenitors to macrophages expressing inflammatory
cytokines, which were required for osteonecrosis development. In fact, we
demonstrate that TNF?-, IL-1?/?- or IL-6-deficient mice as well as wild-type mice
administered a TNF?-inhibitor were significantly resistant to development of
osteonecrosis accompanying infectious myelitis, even under bisphosphonate
treatment. Our data provide new insight into mechanisms underlying osteonecrosis
and suggest new ways to prevent it.
|Alendronate/adverse effects
[MESH]
|Animals
[MESH]
|Bisphosphonate-Associated Osteonecrosis of the Jaw/etiology/*metabolism/pathology
[MESH]
|Bone Density Conservation Agents/adverse effects
[MESH]