Background Osteoarthritis (OA) of the spine is typically characterized by OA changes within the facet joints. Radiographically, OA of the facet joints appears similar to appendicular synovial joints; however, the specific mechanisms associated with facet joint cartilage degeneration in spine OA are unknown.

Objectives In this study, we obtained facet joint cartilage from patients with facet joint OA undergoing lumbar surgery for neurogenic claudication due to spinal stenosis and cartilage from young patients with imaging (MRI) normal facets joints undergoing microdiscectomy for intervertebral disc herniation (control group). By comparing two groups, we determine the expression of (a) inflammatory markers (b) catabolic markers (c) anabolic factors (d) cell death (apoptosis) markers and (e) cartilage homeostasis (autophagy) markers to identify specific mechanisms associated with the degeneration of facet cartilage during spine OA.

Methods Facet cartilage was collected from 12 patients (mean age =68.1±11.4 years) with facet joint OA and 7 young patients (mean age =29.0±3.9 years) with intervertebral disc herniation. Tissues were obtained from L4 to S1 facet joints (medial aspect) and the expression of inflammatory (IL-1β, TNF-α, IL-6, COX-2 and MCP-1), catabolic (MMP-3, MMP-13 and ADAMTS-5), anabolic (aggrecan and type II collagen), cell death (PARP-1 and caspase-3) and cellular survival and homeostasis markers (LC3B, ULK-1, mTOR) were determined using quantitative real time PCR.

Results Our results showed increased expression of inflammatory (IL-1β, TNF-α, IL-6, COX-2 and MCP-1) and catabolic (MMP-3, MMP-13 and ADAMTS-5) factors as well as a decrease in the expression of key cartilage extracellular matrix components including aggrecan and type II collagen in facet joint OA cartilage compared to younger controls (p<0.05). We have previously shown that mTOR (master negative regulator of autophagy) is responsible for shutting down autophagy signaling in knee articular cartilage resulting in decreased chondroprotection and enhanced cartilage degeneration. Indeed, in spine OA facet joints compared to disc herniation control group, we observed significant (p<0.05) increase in mTOR expression and decrease in the expression of chondroprotective autophagy markers including LC3 and ULK1 as well as enhanced expression of cell death (apoptosis) markers including PARP-1 and caspase-3. These results clearly show enhanced catabolic/inflammatory activity in facet joint cartilage associated with disrupted cartilage homeostasis in spine OA facet cartilage.

Conclusions To our knowledge, this is the first study showing high catabolic/inflammatory activity and dysregulated homeostatic status of facet joint OA compared to imaging normal facet joints from young patients with intervertebral disc herniation. Our unique use of control facet specimens from otherwise normal young patients with herniated disc enables stepwise exploration of the endogenous mechanisms responsible for initiating facet joint degeneration in spine OA.

Disclosure of Interest None declared