Researchers at Duke University Medical Center found that mice, in which the Type IX collagen (Col9a1) gene was inactivated developed premature osteoarthritis (OA) and degenerative disc disease (DDD).
OA and DDD are common, chronic musculoskeletal disorders, which cause joint pain, loss of function, and decreased quality of life.
In the study, the researchers aimed to determine the effect of Col9a1deficiency on functional ability in mice.
Led by Dr. Kyle Allen, the researchers compared the behavioural abilities of Col9a1 deficient mice to wild-type (WT) mice.
They selected mice of advanced age (9-11 months) because they represent an age at which there is histological evidence of OA and DDD.
Functional tests of reflexes, posture, strength, coordination, balance, sensorimotor skills, and gait were conducted to measure physical capabilities that could be impaired due to OA or DDD.
Symptomatic pain was assessed through mechanical and thermal withdrawal thresholds.
"We observed a pattern of behavioral changes in the collagen deficient mice that suggests a relationship to OA- and DDD-like degeneration," stated Dr. Allen. The data shows that mice deficient in Type IX collagen clearly displayed behavioral characteristics of pain and functional loss. These mice had delayed righting reflex (ability to regain footing from a back position), decreased sensorimotor skills, and altered gait compared with WT mice. Collagen deficient mice also had elevated levels of knee and intervertebral disc structural changes.
The study found that collagen deficient mice chose movements that limited peak joint forces and behaviours that reduced pain sensations.
"In future work, these measures may help track signs and symptoms as degeneration progresses. Further studies of the mouse model could provide useful data for evaluating the efficacy of therapeutic interventions for musculoskeletal disorders," said Allen.
Findings of this study appear in the September issue of Arthritis and Rheumatism, a journal of the American College of Rheumatology.