title: Histopathological changes in collagen and matrix metalloproteinase levels in articular condyle of experimental model rats with jaw deformity.
abstract: OBJECTIVE
  To investigate the dynamics of the cartilage matrix in the articular condyle after removal of a side shift plate; Emergence of type I, II, and III collagen in the matrix as well as changes in levels of matrix metalloproteinase (MMP)-1, -8, and -13 that degrade collagen were studied histopathologically and immunohistochemically.
  
  
  METHODS
  Lateral displacement of the mandible was achieved by attaching a side shift plate to the anterior teeth of the maxilla in male rats at 6 weeks. The wearing period of the side shift plate was 8 weeks. Observations were made at 0, 1, 2, 4 and 8 weeks after removal.
  
  
  RESULTS
  In histopathological findings, the timing of proliferation of the layer of hypertrophy varied between the bilateral sides. In immunohistochemical findings a significant decline in the expression of type II collagen in the displacement side was observed immediately after removal. Moreover, the expressions of MMPs were elevated in both sides on 0 weeks. At 1 week after removal, a significant elevated in the expression of type II collagen, MMPs was decline in both sides.
  
  
  CONCLUSIONS
  After removal, the levels of MMP-1, -8, and 13 were reduced and the emergence of type II collagen increased. Thus, cellular outgrowth was initiated to trigger intracartilaginous ossification to restore the cartilage matrix.
authors.affiliation: Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan. watanabe.aya40@nihon-u.ac.jp
authors.forename: A
authors.initials: A
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: T
authors.initials: T
authors.lastname: Utsunomiya
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Kasai
mesh_terms: D000818:Animals; D001862:Bone Resorption / Q000473:pathology; D002358:Cartilage, Articular / Q000473:pathology; D002454:Cell Differentiation; D049109:Cell Proliferation; D003094:Collagen / Q000032:analysis*; D024042:Collagen Type I / Q000032:analysis; D024043:Collagen Type II / Q000032:analysis; D024061:Collagen Type III / Q000032:analysis; D003238:Connective Tissue / Q000473:pathology; D006984:Hypertrophy; D008297:Male; D008310:Malocclusion / Q000473:pathology*; D008335:Mandibular Condyle / Q000473:pathology*; D020781:Matrix Metalloproteinase 1 / Q000032:analysis; D053509:Matrix Metalloproteinase 13 / Q000032:analysis; D020784:Matrix Metalloproteinase 8 / Q000032:analysis; D020782:Matrix Metalloproteinases / Q000032:analysis*; D010012:Osteogenesis / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D024042:Collagen Type I; D024043:Collagen Type II; D024061:Collagen Type III; D003094:Collagen; D053509:Matrix Metalloproteinase 13; D020782:Matrix Metalloproteinases; C507083:Mmp13 protein, rat; D020784:Matrix Metalloproteinase 8; D020781:Matrix Metalloproteinase 1