Duke University Medical Center LogoOsteoarthritis (OA) and degenerative disc disease (DDD) are known to be ordinary, chronic musculoskeletal disorders. It was estimated that both diseases caused joint pain, loss of function, and decreased quality of life for approximately more than 27 million OA and 59 million DDD suffers in the US.

Researchers at Duke University Medical Center discovered that mice with the Col9a1 gene seem to have inactivated prematurely in order to develop OA and DDD. They conducted a study on the mice in order to determine the effect of Type IX collagen (Col9a1) deficiency on functional ability.

According to a 2003 Medical Expenditure Panel Survey, arthritis such as OA seems to costs the U.S. economy nearly $128 billion each year in medical care. Also, indirect expenses appear to include lost wages and productivity.

Lead researcher, Kyle Allen, PhD along with other researchers selected mice of an advanced age. The mice were between 9 to 11 months. Supposedly, this age group represents an age at which there is histological evidence of OA and DDD. Later, they compared the behavioral abilities of Col9a1 deficient mice to wild-type (WT) mice.

Functional tests of reflexes, posture, strength, coordination, balance, sensorimotor skills, and gait were noted to have been conducted in order to measure the physical capabilities which could be impaired due to OA or DDD. Furthermore, symptomatic pain appears to have been evaluated 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,” says Dr. Allen.

The findings revealed that mice deficient in Type IX collagen evidently exhibited behavioral characteristics of pain and functional loss. These mice seem to have delayed righting reflex, decreased sensorimotor skills and altered gait in contrast to WT mice.

Righting reflex is the ability to recover footing from a back position. Additionally, collagen deficient mice were observed to have higher levels of knee and intervertebral disc structural changes.

Dr. Allen further stated that, “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.”

The study claims that collagen deficient mice selected movements which limited peak joint forces and behaviors that reduced pain sensations.

The findings of the study will be published in Arthritis & Rheumatism, a journal of the American College of Rheumatology.