Background: Severe and chronic back pain often originates from degenerated intervertebral discs, probably from lesions in the outer posterior anulus. Unlike the nucleus, the outer anulus has a high cell density and adequate metabolite transport. The outer annulus can heal after injury in small and young experimental animals, but little is known about the healing potential of adult human discs.

Purpose: We seek evidence that healing of the human outer anulus follows the three stages of tendon healing: inflammation, repair, remodelling. If so, then manual therapy and self-treatment techniques known to facilitate tendon healing could be adapted to treat discogenic back pain.

Methods: Anulus tissue was removed at surgery (usually posteriorly) from 14 patients with discogenic back pain. Tissue was paraffin embedded and sectioned at 5 μm for histology and immunohistochemistry. Apoptosis was detected using an antibody for caspase-3.

Results: Fissures in the peripheral posterior annulus, and herniated tissue fragments, were associated with blood vessels, inflammatory cells, and with focal loss of proteoglycans. Cell density decreased with distance from fissures from the disc periphery. Overall cell density decreased with age. Apoptosis was greater in the nucleus than in the annulus, and was particularly associated with cell clusters, and with anulus fissures.

Conclusion: These preliminary results suggest an inflammatory healing response in the outer anulus, strongly associated with radial fissures. Loss of proteoglycan from fissure margins may facilitate the ingrowth of capillaries and nerves, which then stimulate local healing in the vicinity of the fissures.

Conflicts of Interest: None

Source of Funding: BackCare

Apoptosis of articular chondrocytes may play an important role in the pathogenesis of osteoarthritis (OA). The aim of this study was to investigate the incidence of chondrocyte apoptosis in equine articular cartilage (AC) specimens and examine the relationship between the process of cell death and the degree of cartilage degradation.

The study comprised 2 populations of equine cartilage taken from the left forelimb. Population 1 (n=10) consisted of full depth cartilage from weight-bearing regions of equine metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints. Population 2 (n=9) comprised cartilage from 6 different regions of the MCP joint: dorsomedial, dorsolateral, centromedial, centrolateral, palmarome-dial and palmarolateral areas. Cartilage from each horse for each of the joints and joint regions was not always available. Seven micrometre cryostat sections were obtained. Haematoxylin and Eosin with Safranin-O stained sections were used to score structural differences between samples for features of cartilage pathology using a ‘modified’ Mankin scoring system. Two methods were used to quantify apoptotic chondrocytes: a direct method in which chondrocytes were assessed for morphological features of apoptosis using a light microscope and an immunohistochemical staining technique to detect the expression of active caspase-3 using a commercially available monoclonal antibody.

Apoptosis assessed by the direct method did not show any association with increasing severity of OA (r=0.11, p=0.7205). Overall there was a positive correlation between caspase-3 expression and cartilage damage (r= 0.44, p=0.0043). Caspase-3 expression was found to increase linearly with increasing severity of OA in the superficial, middle and deep zones of AC (r=0.36, p=0.0198; r=0.49, p=0.0011 and r=0.37, p=0.0237 respectively). Moreover, caspase-3 expression was higher in the superficial and middle zones than in the deep zone (p< 0.001). In the superficial, middle and deep zones the expression of caspase-3 was higher in the MCP joint than the PIP joint (p< 0.05, p< 0.01 and p< 0.05 respectively).

The significant positive correlation between disease severity and chondrocyte apoptosis, suggests that this process plays an important role in the pathogenesis of OA. The differences in the extent of apoptosis observed in different joints could be explained by the biomechanical environment of the joints.