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Mandibular Appliance Modulates Condylar Growth through Integrins

¹ Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes 1524, CEP 05508-000, São Paulo, SP, Brazil; and
² Department of Internal Medicine, School of Medicine, State University of Campinas, R. Alexander Fleming 40, CEP 13083-970, Campinas, SP, Brazil

View larger version (145K): [in this window] [in a new window]   Figure 1. The propulsive appliance increased fibronectin expression and distribution in the condylar cartilage. (A) Fibronectin mRNA expression in the condylar cartilage of rats treated for 15 or 30 days and their age-matched controls. Results are presented as mean ± standard deviation of mRNA levels, expressed as fold-induction over the respective controls. Results were analyzed by ANOVA and Tukey’s post-test. *p < 0.01 (n = 6). (B) Immunohistochemical staining of fibronectin in the cartilage, showing the fibrous (f), proliferative (p), chondroblast (c), and hypertrophic (h) layers. (a-c) Control groups C5, C15, and C30, respectively. (d-f) Treated groups T5, T15, and T30, respectively. (g) Negative control, consisting of the omission of the primary antibody. Bar = 100 µm.

View larger version (15K): [in this window] [in a new window]   Figure 2. The orthopedic appliance increased 5 and v integrin subunits in the proliferative compartment of the rat condylar cartilage. Semi-quantitative analysis of immunoreactivity for v (A) and 5 (B) subunits in the proliferative compartment, absent (arbitrary value = 0), weak (arbitrary value = 1), medium (arbitrary value = 2), or strong (arbitrary value = 3) labeling intensity. The results are representative of all experiments and were plotted to show cyclical variations in integrin distribution and the effect of the appliance on this pattern. Four animals were analyzed per group, and there were at least 3–5 slides from each of them.

View larger version (145K): [in this window] [in a new window]   Figure 3. The propulsive appliance stimulated cell proliferation in the rat condylar cartilage. The number of proliferating cells was estimated based on immunoreactivity for PCNA. Results were expressed as % of labeled cells in the whole cartilage (A), or separately in the anterior (C), central (D), and posterior (E) cartilage regions. *P < 0.05, according to ANOVA and Tukey’s post-test (n = 4). (B) shows a reaction for PCNA in the anterior (d), central (e), and posterior regions (f) of the cartilage from rats that wore the appliance for 15 days, compared with their age-matched controls (a-c). Cells positively labeled are shown in blue. Bar = 100 µm.

View larger version (25K): [in this window] [in a new window]   Figure 4. Cyclic mechanical stretch regulated mRNA expression in cartilage-derived cells through RGD-binding integrins. Gene expression analyses of fibronectin (A), PCNA (B), IGF-I (C), and IGF-II (D) are shown in the non-stretched group (NS); the stretched group (S); the group stretched and treated with peptide containing RGE sequence (S+RGE); and the group stretched and treated with peptide containing RGD sequence (S+RGD). Data were normalized relative to the expression of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and presented as Mean ± Standard Deviation of fold-induction (n = 3 5). Control is arbitrarily set as 1. #p < 0.05 vs. NS; *p < 0.05 vs. S; +p < 0.05 vs. S+RGE (one-way ANOVA followed by Tukey’s procedure for multiple comparisons).

Journal of Dental Research, Vol. 87, No. 2, 153-158 (2008)
DOI: 10.1177/154405910808700210


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