Lateral functional shift of the mandible: Part II. Effects on gene expression in condylar cartilage.
There is considerable evidence that proliferation and growth in the mandibular condylar cartilage (MCC) might be altered after a change in the postural position of the mandible. However, almost nothing is known about the molecular basis of this response. Using semiquantitative reverse-transcription polymerase chain reaction, we examined the expression of insulin-like growth factor-1 (Igf-1), fibroblast growth factor-2 (Fgf-2), and their receptors (Igf-1r, Fgfr1, Fgfr2, and Fgfr3) in the MCC of 28 day-old rats at 3, 7, and 14 days after placing intraoral appliances designed to produce a lateral functional shift of the mandible. This shift resulted in a transverse rotation of the mandible so that the condyle on the side away from the shift was distracted anteriorly (ie, protruded) from the glenoid fossa, while the contralateral condyle remained in place or moved slightly posteriorly (ie, nonprotruded). Gene expression for 5 of the 6 genes studied was significantly different (P <.05) between the protruded and the nonprotruded sides. In nearly every instance at the 3- and 7-day intervals, mRNA expression on the protruded side compared with age-matched controls was altered in the opposite direction from the nonprotruded side. Especially on the protruded side, the most pronounced differences from the control were evident at 3 and 7 days. In general, the changes in gene expression preceded the alterations in proliferative activity documented previously. These data suggest that alterations in the mRNA expression of Igf-1, Fgf-2, and their receptors might underlie in part changes in MCC proliferative activity after alteration in mandibular posture.
Fuentes
Maria Angeles
MA
Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M University System Health Sciences Center, 3302 Gaston Avenue, Dallas, TX 75246, USA.
Opperman
Lynne A
LA
Buschang
Peter
P
Bellinger
Larry L
LL
Carlson
David S
DS
Hinton
Robert J
RJ
D000818:Animals; D002356:Cartilage / Q000254:growth & development / Q000378:metabolism*; D016022:Case-Control Studies; D002455:Cell Division; D016222:Fibroblast Growth Factor 2 / Q000235:genetics; D005786:Gene Expression Regulation / Q000235:genetics*; D006132:Growth Plate / Q000254:growth & development / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D008297:Male; D008310:Malocclusion / Q000235:genetics / Q000503:physiopathology*; D008335:Mandibular Condyle / Q000254:growth & development / Q000378:metabolism*; D009967:Orthodontic Appliances; D011505:Protein-Tyrosine Kinases; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics; D051496:Receptor, Fibroblast Growth Factor, Type 1; D051497:Receptor, Fibroblast Growth Factor, Type 2; D051498:Receptor, Fibroblast Growth Factor, Type 3; D017526:Receptor, IGF Type 1 / Q000235:genetics; D017468:Receptors, Fibroblast Growth Factor / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012399:Rotation; D018709:Statistics, Nonparametric; D013997:Time Factors
D012333:RNA, Messenger; D017468:Receptors, Fibroblast Growth Factor; D016222:Fibroblast Growth Factor 2; D007334:Insulin-Like Growth Factor I; C496350:Fgfr1 protein, rat; C496356:Fgfr2 protein, rat; D011505:Protein-Tyrosine Kinases; D020794:Receptor Protein-Tyrosine Kinases; D051496:Receptor, Fibroblast Growth Factor, Type 1; D051497:Receptor, Fibroblast Growth Factor, Type 2; D051498:Receptor, Fibroblast Growth Factor, Type 3; D017526:Receptor, IGF Type 1