title: Altered functional loading causes differential effects in the subchondral bone and condylar cartilage in the temporomandibular joint from young mice.
abstract: OBJECTIVE
  Altered loading is an important etiological factor for temporomandibular joint (TMJ) disorders. Studies examining altered loading of the TMJ have been done in rats but the response of the TMJ to altered loading in mice is largely unknown. Therefore, due to the potential usefulness of genetically engineered mice, the goal of this study was to develop a mouse TMJ altered functional loading model.
  
  
  METHODS
  One hundred and thirty four, 21-day-old CD-1 female mice were divided into two groups: (1) normal loading (hard pellet diet) for 2-6 weeks and (2) altered functional loading (incisor trimming every other day and soft dough diet) for 2-6 weeks. The mandibular condylar cartilage was evaluated by histology, the subchondral bone was evaluated by microcomputed tomography (micro-CT) analysis and gene expression was evaluated by real time polymerase chain reaction (PCR) analysis.
  
  
  RESULTS
  Altered functional loading for 2-6 weeks caused significant reduction in the thickness of the condylar cartilage whereas, only at 4 weeks was there a significant decrease in the bone volume fraction and trabecular thickness of the subchondral bone. Gene expression analysis showed that altered functional loading for 4 weeks caused a significant reduction in the expression of SRY-box containing gene 9 (Sox9), Collagen type X (Col X), Indian hedgehog (Ihh), Collagen type II (Col II) and Vascular endothelial growth factor (Vegf) and altered loading for 6 weeks caused a significant decrease in the expression of Sox9, Col II, Vegf and Receptor activator of NF-kappaB ligand (Rankl) compared to the normal loading group.
  
  
  CONCLUSIONS
  Altered functional TMJ loading in mice for 2-6 weeks leads to a loss of the condylar cartilage and a transient loss in the density of the mandibular condylar subchondral bone.
authors.affiliation: University of Connecticut Health Center, School of Dental Medicine, Department of Craniofacial Sciences, Division of Orthodontics, Farmington, CT 06030, United States.
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.forename: K P
authors.initials: KP
authors.lastname: Sorensen
authors.forename: T
authors.initials: T
authors.lastname: Gupta
authors.forename: T
authors.initials: T
authors.lastname: Kilts
authors.forename: M
authors.initials: M
authors.lastname: Young
authors.forename: S
authors.initials: S
authors.lastname: Wadhwa
mesh_terms: D000818:Animals; D001835:Body Weight; D015519:Bone Density / Q000502:physiology; D024043:Collagen Type II / Q000378:metabolism; D024121:Collagen Type X / Q000378:metabolism; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D051445:Fibrocartilage / Q000378:metabolism* / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D007180:Incisor; D008335:Mandibular Condyle / Q000473:pathology*; D008409:Mastication; D051379:Mice; D008852:Microradiography; D016133:Polymerase Chain Reaction; D053245:RANK Ligand / Q000378:metabolism; D055758:SOX9 Transcription Factor / Q000378:metabolism; D013314:Stress, Mechanical; D013704:Temporomandibular Joint; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D024043:Collagen Type II; D024121:Collagen Type X; D053245:RANK Ligand; D055758:SOX9 Transcription Factor; C527933:Sox9 protein, mouse; D042461:Vascular Endothelial Growth Factor A
references.citation: Arch Oral Biol. 1996 Jan;41(1):127-31
references.pmid: 8833602
references.citation: J Am Dent Assoc. 2003 Jun;134(6):705-14
references.pmid: 12839406
references.citation: J Dent Res. 2003 Aug;82(8):627-31
references.pmid: 12885848
references.citation: Bone. 2006 Nov;39(5):1043-1047
references.pmid: 16860618
references.citation: Arch Oral Biol. 1998 Jan;43(1):83-92
references.pmid: 9569994
references.citation: Trends Mol Med. 2006 Jan;12(1):17-25
references.pmid: 16356770
references.citation: Am J Anat. 1988 Jul;182(3):197-214
references.pmid: 3213819
references.citation: J Clin Invest. 2005 Jul;115(7):1734-42
references.pmid: 15951842
references.citation: Histochem J. 1996 Feb;28(2):99-107
references.pmid: 8737291
references.citation: Odontology. 2005 Sep;93(1):7-15
references.pmid: 16170470
references.citation: Microsc Res Tech. 2005 Aug 15;67(6):325-35
references.pmid: 16173089
references.citation: Acta Odontol Scand. 1994 Jun;52(3):129-34
references.pmid: 8091958
references.citation: J Orofac Pain. 1999 Fall;13(4):295-306
references.pmid: 10823044
references.citation: J Dent Res. 1994 Jun;73(6):1150-6
references.pmid: 8046103
references.citation: Acta Anat (Basel). 1986;125(3):145-51
references.pmid: 3962576
references.citation: Ann N Y Acad Sci. 2006 Apr;1068:1-13
references.pmid: 16831900
references.citation: Eur J Orthod. 2004 Feb;26(1):1-5
references.pmid: 14994876
references.citation: Arch Oral Biol. 1983;28(10):939-45
references.pmid: 6580850
references.citation: Acta Anat (Basel). 1988;131(2):136-9
references.pmid: 3369280
references.citation: Arch Oral Biol. 1995 Jul;40(7):677-80
references.pmid: 7575241
references.citation: Crit Rev Oral Biol Med. 1997;8(3):291-305
references.pmid: 9260045
references.citation: Dev Dyn. 2007 Feb;236(2):426-34
references.pmid: 17191253
references.citation: Osteoarthritis Cartilage. 2006 Aug;14(8):807-13
references.pmid: 16563813