Percutaneous block and neurotomy of the medial branch of the spinal dorsal ramus has shown excellent results in treating facet joint-mediated low back pain. This study aimed to describe the clinical anatomy of the medial branch and its measurements.We dissected the lumbar spine of 12 adult cadavers (24 sides) and measured the distances between the medial branch and various anatomical landmarks. The distances were compared between L1 and L5 vertebrae.The distance between the dorsal ramus bifurcation and the superior border of the root of the transverse process was 3.52 ± 1.15 mm, 3.63 ± 1.36 mm, 3.46 ± 1.31 mm, 3.38 ± 1.24 mm, and 1.87 ± 0.88 for L1 to L5, respectively. The medial branch of the dorsal ramus is enclosed in a fibro-osseous canal bounded by the accessory process, the mammillary process, and the mammilloaccessory ligament.For the percutaneous treatment of block and neurotomy, the first choice of target is the medial branch fibro-osseous canal near to the accessory process. The accessory process is not displayed in x-ray films; therefore, the junction of the superior articular process and the root of the transverse process can be targeted.

Lumbar facet joint (LFJ) osteoarthritis (OA) is an important etiology of low back pain. Several animal models of LFJ OA have been established using intraarticular injection of various chemicals. This study aimed to establish a rat model of LFJ OA using urinary plasminogen activator (uPA). Sprague-Dawley rats were treated with intraarticular injection in the L5-L6 facet joints with uPA (OA group, n = 40) or normal saline (vehicle group, n = 40). Mechanical and thermal hyperalgesia in the ipsilateral hind paws were evaluated using von Frey hairs and a thermoalgesia instrument, respectively. Toluidine blue staining, hematoxylin-eosin staining, and immunohistochemical examination of the LFJ was performed. Treatment with uPA induced cartilage damage, synovitis, and proliferation of synovial cells in the fact joints. The OA group showed significantly higher hyperalgesia in the hind paws in comparison with the vehicle group and normal controls (P < 0.05). Expression of IL-1β, TNF-α, and iNOS in the LFJ cartilage in the OA group was significantly increased (P < 0.05). A rat model of LFJ OA was successfully established using intraarticular injection of uPA. This animal model is convenient and shows good resemblance to human OA pathology.