Expression of chondromodulin-1 in the temporomandibular joint condylar cartilage and disc.
BACKGROUND
The temporomandibular joint (TMJ) cartilage consists of condylar cartilage and disc and undergoes continuous remodeling throughout post-natal life. To maintain the integrity of the TMJ cartilage, anti-angiogenic factors play an important role during the remodeling process. In this study, we investigated the expression of the anti-angiogenic factor, chondromodulin-1 (ChM-1), in TMJ cartilage and evaluate its potential role in TMJ remodeling.


METHODS
Eight TMJ specimens were collected from six 4-month-old Japanese white rabbits. Safranin-O staining was performed to determine proteoglycan content. ChM-1 expression in TMJ condylar cartilage and disc was determined by immunohistochemistry. Three human perforated disc tissue samples were collected for investigation of ChM-1 and vascular endothelial growth factor (VEGF) distribution in perforated TMJ disc.


RESULTS
Safranin-O stained weakly in TMJ compared with tibial articular and epiphyseal cartilage. In TMJ, ChM-1 was expressed in the proliferative and hypertrophic zone of condylar cartilage and chondrocyte-like cells in the disc. No expression of ChM-1 was observed in osteoblasts and subchondral bone. ChM-1 and VEGF were both similarly expressed in perforated disc tissues.


CONCLUSIONS
ChM-1 may play a role in the regulation of TMJ remodeling by preventing blood vessel invasion of the cartilage, thereby maintaining condylar cartilage and disc integrity.
Fang
Wei
W
Key Laboratory of Oral Biomedical Engineering of Ministry of Education, Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei Province, PR China.
Friis
Thor Einar
TE
Long
Xing
X
Xiao
Yin
Y
D020533:Angiogenesis Inhibitors / Q000032:analysis*; D000818:Animals; D016723:Bone Remodeling / Q000502:physiology; D002358:Cartilage, Articular / Q000033:anatomy & histology* / Q000473:pathology; D049109:Cell Proliferation; D019902:Chondrocytes / Q000166:cytology; D004396:Coloring Agents; D004838:Epiphyses / Q000033:anatomy & histology; D005260:Female; D006801:Humans; D006984:Hypertrophy; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis*; D008335:Mandibular Condyle / Q000033:anatomy & histology*; D008565:Membrane Proteins / Q000032:analysis*; D010006:Osteoblasts / Q000166:cytology; D010619:Phenazines; D011509:Proteoglycans / Q000032:analysis; D011817:Rabbits; D051381:Rats; D011917:Rats, Inbred Lew; D013704:Temporomandibular Joint / Q000033:anatomy & histology*; D019224:Temporomandibular Joint Disc / Q000033:anatomy & histology* / Q000473:pathology; D013705:Temporomandibular Joint Disorders / Q000473:pathology; D013977:Tibia / Q000033:anatomy & histology; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
D020533:Angiogenesis Inhibitors; C489407:Cnmd protein, rat; D004396:Coloring Agents; D036341:Intercellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D010619:Phenazines; D011509:Proteoglycans; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C068675:CNMD protein, human; C009195:safranine T