Bone Resorption Factors in Chronic Otitis Media

1984 ◽  
Vol 92 (3) ◽  
pp. 322-328 ◽  
Author(s):  
Hiroshi Moriyama ◽  
Cheng Huang Chun ◽  
Maxwell Abramson ◽  
Michimasa Kato

Collagenase was identified within naturally occurring rat chronic otitis media by the use of an immunohistochemical technique with peroxidase-antiperoxidase to stain the paraffin. Collagenase was found in fibroblasts, mononuclear cells, and osteoclast cells in the bone-resorbing area. Collagenase was found only in fibroblasts in contact with epithelial basal cells. Macrophages from rat peritoneum were cultured with different concentrations of a lipopolysaccharide. The prostaglandin E2 level reached a maximum during the 12-to 24-hour period in the presence of endotoxin. This prostaglandin E2 was confirmed by immunofluorescent staining. The endotoxin-activated macrophage produced an insignificant amount of collagenase. These findings suggest that activated macrophages may be able to stimulate fibroblast collagenase production through the chemical mediator prostaglandin E2. Also, the interaction between fibroblasts and epidermal cells appears to encourage and enhance the biochemical events resulting in bone resorption in chronic otitis media.

1980 ◽  
Vol 88 (3) ◽  
pp. 316-323 ◽  
Author(s):  
Timothy T.K. Jung ◽  
Douglas M. Smith ◽  
S.K. Juhn ◽  
Jonathan M. Gerrard

Prostaglandins (PG) are naturally occurring, cyclic, unsaturated fatty acids that possess a wide range of potent biologic activities. Prostaglandins have been found in human middle ear effusions and may have implications for understanding the inflammation and, possibly, the bone resorption seen in chronic otitis media. In the study presented, PGs were measured by radioimmuno-assay in middle ear effusions from experimentally induced serous and purulent otitis media in chinchillas. The ability of chinchilla middle ear mucosa to synthesize PGs from 14C-arachidonic acid was also demonstrated. The authors suggest an active role for PGs in the inflammation and the bone resorption seen in otitis media.


1985 ◽  
Vol 100 (1-2) ◽  
pp. 72-80 ◽  
Author(s):  
Gilead Berger ◽  
Michael Hawke ◽  
J. Kenneth Ekem

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10898
Author(s):  
Hailong Wang ◽  
Jinqiao Li ◽  
Zihan Xu ◽  
Feng Wu ◽  
Hongyu Zhang ◽  
...  

Osteocalcin (OCN) was the most abundant noncollagen protein and considered as an endocrine factor. However, the functions of Undercarboxylated osteocalcin (ucOCN) on osteoclast and bone resorption are not well understood. In the present study, preosteoclast RAW264.7 cells and bone marrow mononuclear cells (BMMs) were treated with ucOCN purified from prokaryotic bacteria. Our results showed that ucOCN attenuated the proliferation of RAW264.7 cells with a concentration dependant manner by MTS assay. Scrape wounding assay revealed the decreased motility of RAW264.7 cells after ucOCN treatment. RT-qPCR results manifested the inhibitory effects of ucOCN on the expression of osteoclastic marker genes in RAW264.7 cells during inducing differentiation of RANKL. It was also observed that ucOCN inhibited the formation of multinucleated cells from RAW264.7 cells and BMMs detected by TRAP staining. The number and area of bone resorb pits were also decreased after treatment with ucOCN during their osteoclast induction by toluidine blue staining. The formation and integrity of the osteoclast actin ring were impaired by ucOCN by immunofluorescent staining. Time dependant treatment of ucOCN during osteoclastic induction demonstrated the inhibitory effects mainly occurred at the early stage of osteoclastogenesis. Signaling analysis of luciferase activity of the CRE or SRE reporter and ERK1/2 phosphorylation showed the selective inhibitor or siRNA of Gprc6a (a presumptive ucOCN receptor) could attenuate the promotion of ucOCN on CRE-luciferase activity. Taken together, we provided the first evidence that ucOCN had negative effects on the early differentiation and bone resorption of osteoclasts via Gprc6a.


ORL ◽  
2002 ◽  
Vol 64 (2) ◽  
pp. 95-107 ◽  
Author(s):  
Jae Y. Jung ◽  
Richard A. Chole

1988 ◽  
Vol 97 (6) ◽  
pp. 661-666 ◽  
Author(s):  
Richard A. Chole

Bone resorption and remodeling are characteristic of chronic otitis media with and without cholesteatoma and otosclerosis. The consequences of this remodeling process may be hearing loss, repeated infection, vestibular disturbance, or intracranial complications. Evidence of osteoclastic bone resorption was found in surgical specimens of 11 of 24 cases of cholesteatoma, two of three cases of chronic otitis media, and three of ten cases of otosclerotic stapes; all three spongiotic lesions had osteoclasts. With careful serial sectioning these cells are almost always multinucleate and have the typical appearance of osteoclasts with ruffled borders. Some specimens had evidence of bone erosion in the absence of osteoclasts; this finding represents an inactive phase of the remodeling process. Since the osteoclast plays an important role in the resorption and remodeling of bone in these middle ear diseases, the source, physiology, and local control of these cells are of prime importance in investigating the pathophysiology of these diseases. At the present time, the local control of activation and recruitment of osteoclasts, as well as their chemotactic responses, is poorly understood.


1981 ◽  
Vol 6 (3) ◽  
pp. 179-186 ◽  
Author(s):  
J. THOMSEN ◽  
P. BRETLAU ◽  
M. BALSLEV JØRGENSEN

1979 ◽  
Vol 88 (5) ◽  
pp. 693-700 ◽  
Author(s):  
Bruce J. Gantz ◽  
Jerry Maynard ◽  
Robert M. Bumsted ◽  
Cheng Chun Huang ◽  
Maxwell Abramson

Bone resorption is an important aspect of chronic otitis media contributing to many complications of this disease. It is postulated that the mechanism of this localized destructive process is chemical in origin. Collagenase, lysosomal enzymes, prostaglandins, and other cell mediators are thought to induce bone resorption, but the site of action and cellular origin of these substances remains unclear. In this report, we demonstrate the location and attempt to delineate the cellular origin of two enzymes, collagenase and the lysosomal enzyme acid phosphatase in guinea pig temporal bones and human ossicles from ears containing chronic otitis media. Tissue localization of these enzymes identifies sites of active bone resorption and demonstrates the cells initiating this process. Using immunohistochemical and immunocytochemical techniques, collagenase was seen surrounding mononuclear inflammatory cells of granulation tissue at bone resorbing margins and at the periphery of osteocyte lacunae adjacent to resorbing areas. Electron microscopic data suggests that collagenase is an extracellular enzyme found at the periphery of osteocytes. In addition, abundant acid phosphatase activity was seen in the same cells that exhibited collagenase staining, lending credence to the destructive function of these cells. The chronic inflammatory reaction found in chronic otitis media appears to activate bone destruction through the dynamic activity of mononuclear inflammatory cells and stimulates bone cells to increase their destructive biochemical functions.


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