THURSDAY, Sept. 3 (HealthDay News) -- Mice with a defective gene that impairs collagen production needed for joint maintenance may provide a model for the investigation of the pathogenesis and treatment of osteoarthritis and degenerative disc disease (DDD), according to a study in the September issue of Arthritis & Rheumatism.

Kyle D. Allen, Ph.D., of Duke University Medical Center in Durham, N.C., and colleagues observed and examined mice with the Col9a1^−/− gene defect, that do not form functional type IX collagen molecules. The Col9a1^−/− mice were compared to wild-type mice to identify symptomatic changes that may be associated with the premature development of osteoarthritis and DDD among the mutant mice. The researchers studied functional impairment, sensorimotor skills, reflexes, mechanical and thermal sensitivity, and gait. After the mice were harvested, blood samples were analyzed for hyaluronan, and their knees and spines were examined for cartilage degeneration.

The researchers found that the Col9a1^−/− mice had impaired physical ability, heightened mechanical sensitivity, and exhibited compensatory gait changes compared to wild-type mice. They also had elevated blood levels of hyaluronan and increased cartilage and intervertebral disc degeneration.

"The observed pattern of behavioral changes suggested a relationship to osteoarthritis- and DDD-like degeneration in mutant mice, such that the Col9a1^−/− mouse model may provide the potential to study interventions and their effects on the behavioral features of osteoarthritis and DDD," the authors conclude.

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