The effect of BMP-2, BMP-4 and BMP-6 on bone destruction of cholesteatoma presence

Oger, M.; Alpay, Hayrettin Cengiz; Orhan, İsrafil; Onalan, Ebru Ethem; Yanilmaz, Muhammed; Sapmaz, Emrah

doi:10.1016/j.amjoto.2013.06.007

Cited by 7 publications

(5 citation statements)

References 10 publications

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“…Incubation of these fibroblasts with cholesteatoma tissue caused the transcription of BMP-2 [123]. Moreover, another prospective more recent study was conducted by Oger et al [124] to investigate gene expression of BMPs, BMP2, BMP4, and BMP6 in 80 patients with chronic OM with and without cholesteatoma. The cholesteatoma group showed higher expression of BMPs, BMP2, and BMP6.…”

Section: Mechanisms Of Bone Resorption In Cholesteatomamentioning

confidence: 99%

“…Furthermore, BMPs positivity was significantly related with the bone destruction of all ossicles. Thus, it can be used as a marker for cholesteatoma activity in bone destruction [124]. …”

Section: Mechanisms Of Bone Resorption In Cholesteatomamentioning

confidence: 99%

“…These factors can be used as predictors for aggressiveness and recurrence of cholesteatoma and hence can be useful in determining the necessity and timing of intervention before occurrence of complications. These factors include TNF-alpha [103,106], IL-1α [102,106], MMP 9 and tenascin [111], amphiregulin [83], MIB1 [82], and BMPs [124]. Finally, RANKL/OPG ratio was considered to be a reliable index for bone erosion in cholesteatoma [68] (Table 2).…”

Section: Predictors For Severity Of Bone Resorptionmentioning

confidence: 99%

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Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives

Hamed

Nakata

Sayed

et al. 2016

Clin Exp Otorhinolaryngol

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Cholesteatoma is a cystic non tumorous lesion of the temporal bone that has the ability to destroy nearby structures by its power to cause bone resorption and as a result, fatal complications prevail. We aimed to conduct a comprehensive review for pathogenesis of acquired cholesteatoma, bone resorption mechanisms, and offer a future vision of this serious disease. We have reviewed different theories for pathogenesis of acquired cholesteatoma including the most relevant and updated ones with special emphasis on the mechanisms of bone resorption through Medline/PubMed research using the keywords ‘aetiopathogenesis, bone resorption, acquired cholesteatoma, temporal bone, and cytokines.’ In order to strengthen our study, we searched the reference lists of identified reviews. Cholesteatoma is a subject of debate among otolaryngologists since it was prescribed firstly. Over many decades, several theories were postulated for aetiopathogenesis of cholesteatoma with a tendency to follow more than one theory to explain the proper nature of that disease. Until now, the mechanism of bone resorption has yet to be more clarified. In the last century, a leap has occurred in the field of biomolecular cholesteatoma research which improved our knowledge about its pathophysiology and bone destructive mechanism. However, surgery is still the only available treatment. We conclude that discovery of new therapeutic choices for cholesteatoma other than surgery by the use of anti-growth, anti-proliferative, apoptotic agents as well as medications that antagonize osteoclastogenesis should be the main concern in the future clinical and experimental research work. Also, searching for predictors of the aggressiveness of cholesteatoma can affect the timing of intervention and prevent occurrence of complications.

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Section: Mechanisms Of Bone Resorption In Cholesteatomamentioning

confidence: 99%

“…Furthermore, BMPs positivity was significantly related with the bone destruction of all ossicles. Thus, it can be used as a marker for cholesteatoma activity in bone destruction [124]. …”

Section: Mechanisms Of Bone Resorption In Cholesteatomamentioning

confidence: 99%

Section: Predictors For Severity Of Bone Resorptionmentioning

confidence: 99%

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Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives

Hamed

Nakata

Sayed

et al. 2016

Clin Exp Otorhinolaryngol

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“…Additionally, some molecules were found to be related to the bone resorption capacity of cholesteatoma and therefore, could predict its behavior. Of these molecules are tumor necrosis factor-α, interleukin-1α, epidermal growth factor [ 13 ], matrix metaloproteinase-9, tenascin [ 14 ] and bone morphogenic proteins [ 15 ]. This knowledge has improved our understanding of this serious disease and also paved the way for alternative therapeutic strategies other than surgical intervention [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Cytokeratin 13, Cytokeratin 17, and Ki-67 Expression in Human Acquired Cholesteatoma and Their Correlation With Its Destructive Capacity

Hamed

Nakata

Shiogama

et al. 2017

Clin Exp Otorhinolaryngol

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Objectives Cholesteatoma is a nonneoplastic destructive lesion of the temporal bone with debated pathogenesis and bone resorptive mechanism. Both molecular and cellular events chiefly master its activity. Continued research is necessary to clarify factors related to its aggressiveness. We aimed to investigate the expression of Ki-67, cytokeratin 13 (CK13) and cytokeratin 17 (CK17) in acquired nonrecurrent human cholesteatoma and correlate them with its bone destructive capacity.Methods A prospective quantitative immunohistochemical study was carried out using fresh acquired cholesteatoma tissues (n=19), collected during cholesteatoma surgery. Deep meatal skin tissues from the same patients were used as control (n=8). Cholesteatoma patients were divided into 2 groups and compared (invasive and noninvasive) according to a grading score for bone resorption based upon clinical, radiologic and intraoperative findings. To our knowledge, the role of CK17 in cholesteatoma aggressiveness was first investigated in this paper.Results Both Ki-67 and CK17 were significantly overexpressed in cholesteatoma than control tissues (P<0.001 for both Ki-67 and CK17). In addition, Ki-67 and CK17 were significantly higher in the invasive group than noninvasive group of cholesteatoma (P=0.029, P=0.033, respectively). Furthermore, Ki-67 and CK17 showed a moderate positive correlation with bone erosion scores (r=0.547, P=0.015 and r=0.588, P=0.008, respectively). In terms of CK13, no significant difference was found between cholesteatoma and skin (P=0.766).Conclusion Both Ki-67 and CK17 were overexpressed in cholesteatoma tissue and positively correlated with bone resorption activity. The concept that Ki-67 can be a predictor for aggressiveness of cholesteatoma was supported. In addition, this is the first study demonstrating CK17 as a favoring marker in the aggressiveness of acquired cholesteatoma.

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“…Characterized by constant keratinized epithelial proliferation2 and temporal bone destruction3, human acquired cholesteatoma can erode ossicles and temporal bone and destroy inner structures, such as vascular, neural and adjacent central nervous system structures4. This disease causes hearing loss, labyrinthitis, facial paralysis and even brain abscess5.…”

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confidence: 99%

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

Jiang

et al. 2016

Sci Rep

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Triggering receptor expressed on myeloid cells (TREM) has been broadly studied in inflammatory disease. However, the expression and function of TREM-2 remain undiscovered in acquired cholesteatoma. The expression of TREM-2 was significantly higher in human acquired cholesteatoma than in normal skin from the external auditory canal, and its expression level was positively correlated with the severity of bone destruction. Furthermore, TREM-2 was mainly expressed on dendritic cells (DCs). In human acquired cholesteatoma, the expression of proinflammatory cytokines (IL-1β, TNF-α and IL-6) and matrix metalloproteinases (MMP-2, MMP-8 and MMP-9) were up-regulated, and their expression levels were positively correlated with TREM-2 expression. Osteoclasts were activated in human acquired cholesteatoma. In an animal model, TREM-2 was up-regulated in mice with experimentally acquired cholesteatoma. TREM-2 deficiency impaired the maturation of experimentally acquired cholesteatoma and protected against bone destruction induced by experimentally acquired cholesteatoma. Additional data showed that TREM-2 up-regulated IL-1β and IL-6 expression via TLR4 instead of the TLR2 signaling pathway and promoted MMP-2 and MMP-8 secretion and osteoclast activation in experimentally acquired cholesteatoma. Therefore, TREM-2 might enhance acquired cholesteatoma-induced bone destruction by amplifying the inflammatory response via TLR4 signaling pathways and promoting MMP secretion and osteoclast activation.

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The effect of BMP-2, BMP-4 and BMP-6 on bone destruction of cholesteatoma presence

Cited by 7 publications

References 10 publications

Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives

Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives

Cytokeratin 13, Cytokeratin 17, and Ki-67 Expression in Human Acquired Cholesteatoma and Their Correlation With Its Destructive Capacity

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

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