Drug Therapy Attenuates Progression of Osteoarthritis in the Temporomandibular Joint

Objectives:
The objective of this study is to obtain data in support of the hypothesis that a chemical block in the form of drug therapy will ameliorate the inflammatory signaling pathway of Tgf-ß1 observed during osteoarthritic (OA) progression in the temporomandibular joint (TMJ) using a genetic mouse model.
Methods:
A murine OA model developed in our laboratory displaying the heterozygous chondrodysplasia gene (cho/+), a Col11a1 mutation, was used in the current experiment. The animals were divided into two groups, i.e., drug treatment (n=6) and vehicle control (n=6). Under IACUC protocol #150901 the experimental animals were administered the drug via their drinking water which was replaced weekly. Animals were monitored for weight gain and drinking behavior throughout the study. Following the seven-month treatment period animals were euthanized and the TMJs were collected and analyzed for histopathological discrepancies between treatment and control groups. Briefly, tissues were fixed in 4% paraformaldehyde, decalcified, embedded in paraffin, sectioned, and stained with Safranin O to visualize proteoglycans found in the condylar cartilage. Tissues were counterstained with Fast Green. Using the Modified Mankin and OARSI scoring systems, the degree of staining and OA progression was evaluated comparing treatment and control groups. Further, immunofluorescence microscopy was used in selected tissue samples to evaluate differences in expression of the inflammatory mediator Tgf-ß1.
Results:
Results of the current investigation will be presented testing the hypothesis that, relative to the control group, heterozygous animals receiving drug therapy showed diminished degeneration of condylar cartilage, confirmed by a statistically lower histopathology score and decreased expression of Tgf-ß1 in the TMJ.
Conclusions:
Via drug therapy, this study aims to improve treatment of OA in the TMJ by targeting the membrane receptor thereby blocking Tgf-ß1, a key molecular intermediate in the progression of the disease.