Characterization of subchondral bone histopathology of facet joint osteoarthritis in lumbar spinal stenosis

Abstract

Facet joint osteoarthritis may be a cause of low back pain in degenerative spine diseases including lumbar spinal stenosis. Subchondral bone is regarded as a potential therapeutic target for osteoarthritis treatment. The goal of this study was to characterize subchondral bone histopathology in osteoarthritic facet joints from lumbar spinal stenosis patients. Fifteen patients with degenerative spinal stenosis scheduled for transforaminal lumbar interbody fusion surgery were recruited for this study. Osteoarthritis severity was graded on T1- and T2-weighted MRI images using Weishaupt scoring system. Dissected osteoarthritic facet joints were subjected to histological and immunohistochemistry analyses to study relative abundance of osteoblast, osteoclasts, and macrophages using van Gieson's, tartrate-resistant acid phosphatase and CD68-antibody staining, respectively. Presence of nerve fibers was evaluated by PGP9.5-antibody staining. Differential bone histopathology, independent from radiological osteoarthritis grade, was observed in facet joints. Extensive de novo bone formation was found in subchondral bone tissues of eight of fifteen specimens. Regions of bone formation showed high abundance of blood vessels and CD68-positive macrophages, but were devoid of multinucleated osteoclasts. Additional pathological changes in subchondral marrow spaces, including inflammatory infiltration and enhanced osteoclast activity, were characterized by macrophage-rich tissues. PGP9.5-positive nerve fibers were detected near arterioles, but not in regions displaying bone pathology. Individual histopathological parameters did not associate with clinical features or radiological osteoarthritis severity. Subchondral bone histopathology of facet joint osteoarthritis in lumbar spinal stenosis is characterized by marrow infiltration by macrophage-rich tissues and enhanced de novo bone formation. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1475-1480, 2016.

BMSCs‐Derived Exosomes Ameliorate Pain Via Abrogation of Aberrant Nerve Invasion in Subchondral Bone in Lumbar Facet Joint Osteoarthritis

“…However, BMSC‐exosomes could partially reverse the degenerated changes. Impairments of subchondral appear in parallel to the cartilage degeneration, which might accelerate cartilage damage as previously reported . While BMSCs‐exosomes simultaneously improve the reconstruction of cartilage and subchondral bone, supporting the notion that the cross‐talk between them maintains the physiological environment for articular in a synergistic approach.…”

Hypertrophy of the ligamentum flavum and expression of transforming growth factor beta

“… 9 The main pathologic changes include osteoproliferation of the lamina and facet joints, protrusion of the vertebral discs, and hypertrophy of the ligamentum flavum, with the last being the main cause of the spinal stenosis. 10 – 12 Repeated mechanical stretching due to instability of the degenerative lumbar spine is reportedly the main reason for injury to the ligamentum flavum, which leads to regional scar formation and hypertrophy of the ligament. 4 Suppression of the cauda equina by the ligamentum flavum is normally the cause of symptoms in patients with hypertrophy of the ligamentum flavum.…”

Comparative Analysis of Bone Structural Parameters Reveals Subchondral Cortical Plate Resorption and Increased Trabecular Bone Remodeling in Human Facet Joint Osteoarthritis

“…Both nociceptive nerve fibers and neuromodulators, such as substance P and nerve growth factor, have been identified in capsular tissues of degenerative facet joints. It has been shown that enhanced remodeling of subchondral bone and marrow tissues is a predominant feature in the trabecular compartment in FJOA [ 14 , 15 , 16 ]. Elevated active bone-forming osteoblasts accompanied by excessive collagen fiber deposition were indicative of a shift towards bone formation [ 14 ].…”