Saturday, December 19, 2009

Recombinant AAV-mediated VEGF gene therapy induces mandibular condylar growth

A B M Rabie , J Dai, and R Xu: Recombinant AAV-mediated VEGF gene therapy induces mandibular condylar growth. Gene Therapy 14, 972–980 (1 June 2007).

Craniofacial anomalies resulting from impaired growth of mandibular condyles require multidisciplinary interventions, which impose a substantial burden on patients and their families. So far, correcting such deformities with an alternative strategy – gene therapy – is still an uncharted territory. Here, we established an effective in vivo gene delivery system with recombinant adeno-associated virus (rAAV)-mediated vascular endothelial growth factor (VEGF) to enhance mandibular condylar growth. With in situ hybridization, RT-PCR, immunostaining and Western blot, transgene expression was clearly detected in the mandibular condyles during the whole experiment periods. At defined time points, specific osteogenetic markers (alkaline phosphatase and osteocalcin) and chondrogenetic markers (collagen type II and collagen type X) were assessed by means of biochemical analysis and their expression significantly changed from day 30. Proliferation index by proliferating cell nuclear antigen staining showed also a significant increase in cell proliferation. Morphological measurement identified that the size of mandibular condyle significantly increased from day 30. Taken together, rAAV-VEGF was successfully established as an efficient delivery system to induce mandibular condylar growth, which provides the basis for future gene therapy to treat patients with craniofacial deformities. Gene Therapy (2007) 14, 972–980; doi:10.1038/sj.gt.3302943; published online 26 April 2007

Wednesday, December 16, 2009

Subjective reactions to intervention with artificial interferences in

YRSA LE BELL, PAIVI M. NIEMI, TAPIO JAMSA , MERVI KYLMALA & PENTTI ALANEN: Subjective reactions to intervention with artificial interferences in
subjects with and without a history of temporomandibular disorders. Institute of Dentistry, Department of Teacher Education, and Department of Statistics, University of Turku, Turku, Finland. Acta Odontologica Scandinavica, 2006; 64: 59-63.

In a previous double-blind randomized controlled study, subjects with a history of temporomandibular disorder (TMD) reacted to artificial interference with more signs of TMD than did subjects with no TMD history. In the present study, we analysed the subjective reactions of these individuals on several symptom scales. Every day during the 2-week follow-up period, the subjects rated the intensity of their symptoms on 9 VAS scales (occlusal discomfort, chewing difficulties, tender teeth, fatigue in the jaws, headache, facial pain, opening difficulty, bruxism, ear symptoms). Subjects with a history of TMD and true interferences reported stronger symptoms than subjects with no TMD history and placebo interferences.

The most prominent symptoms were occlusal discomfort and chewing difficulties. The difference in outcome between the groups with and without a TMD history suggests that there are individual differences in vulnerability to occlusal interferences. It is likely that the etiological role of occlusal interferences in TMD has not been correctly addressed in previous studies on artificial interferences.

Functional malocclusion that induces posterior condylar displacement

Purisa Cholasueksa, DDSa; Hiroyuki Warita, DDS, PhDb; Kunimichi Soma, DDS, PhDc.: Alterations of the Rat Temporomandibular Joint in FunctionalvPosterior Displacement of the Mandible. Angle Orthod 2004;74:677–683.

Abstract: Functional malocclusion that induces posterior condylar displacement may affect the remodeling processes of the temporomandibular joint structures. We tested the hypothesis that intermittent posterior condylar displacement due to functional malocclusion traumatizes condylar cartilage and joint innervated nerve fibers. Thirty-nine eight-week-old Wistar rats were used. To induce functional posterior condylar displacement, guiding appliances were attached to maxillary incisors of 24 rats for four, seven, and 14 days. Fifteen normal rats served as controls. Sections were stained with hematoxylin and eosin or processed for immunohistochemistry of protein gene product 9.5 and growth-associated protein-43 (GAP- 43). Functional posterior condylar displacement led to a diminution in proliferative cells, reduction in cartilage width, and re-expression of GAP-43–immunoreactive nerve fibers. These results indicate that intermittent posterior condylar displacement due to functional malocclusion causes dysfunctional remodeling of condylar cartilage and nerve injury.

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