We report generation and characterization of
pain-related behavior in a minimally invasive facet joint degeneration (FJD) animal model in rats. FJD was produced by a non-open percutaneous
puncture-induced injury on the right lumbar FJs at three consecutive levels. Pressure
hyperalgesia in the lower back was assessed by measuring the vocalization response to pressure from a force transducer. After
hyperalgesia was established, pathological changes in lumbar FJs and alterations of intervertebral foramen size were assessed by histological and imaging analyses. To investigate treatment options for lumber FJ
osteoarthritis-induced
pain, animals with established
hyperalgesia were administered with
analgesic drugs, such as
morphine, a selective
COX-2 inhibitor, a non-steroidal anti-inflammatory drug (
NSAID) (
ketorolac), or
pregabalin. Effects were assessed by behavioral
pain responses. One week after percutaneous
puncture-induced injury of the lumbar FJs, ipsilateral primary pressure
hyperalgesia developed and was maintained for at least 12 weeks without foraminal
stenosis. Animals showed decreased spontaneous activity, but no secondary
hyperalgesia in the hind paws. Histopathological and microfocus X-ray computed tomography analyses demonstrated that the percutaneous
puncture injury resulted in
osteoarthritis-like structural changes in the FJs cartilage and subchondral bone. Pressure
hyperalgesia was completely reversed by
morphine. The administration of
celecoxib produced moderate
pain reduction with no statistical significance while the administration of
ketorolac and
pregabalin produced no
analgesic effect on FJ
osteoarthritis-induced
back pain. Our animal model of non-open percutanous
puncture-induced injury of the lumbar FJs in rats shows similar characteristics of
low back pain produced by human facet
arthropathy.