Cortical bone blocks height growth so it’s erosion is beneficial but only if coupled with replacement tissue(ideally cartilage).
Bone erosion in rheumatoid arthritis: mechanisms, diagnosis and treatment
“Bone erosion is a central feature of rheumatoid arthritis and is associated with disease severity and poor functional outcome. Erosion of periarticular cortical bone, the typical feature observed on plain radiographs in patients with rheumatoid arthritis, results from excessive local bone resorption and inadequate bone formation[so bone erosion occurs in everyone the balance is just switched in RA]. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines and receptor activator of nuclear factor κB ligand (RANKL), as well as antibodies directed against citrullinated proteins. Indeed, both cytokines and autoantibodies stimulate the differentiation of bone-resorbing osteoclasts, thereby stimulating local bone resorption. Although current antirheumatic therapy inhibits both bone erosion and inflammation, repair of existing bone lesions, albeit physiologically feasible, occurs rarely. Lack of repair is due, at least in part, to active suppression of bone formation by proinflammatory cytokines. This Review summarizes the substantial progress that has been made in understanding the pathophysiology of bone erosions and discusses the improvements in the diagnosis, monitoring and treatment of such lesions.”
“erosions can also be observed in forms of arthritis other than RA, such as gout, psoriatic arthritis, spondyloarthritis and even osteoarthritis,”
“bone erosions typically emerge at the site at which the synovium comes into direct contact with bone (known as bare areas), suggesting that anatomical factors render these areas of juxta-articular bone susceptible to erosion”
“Anatomical factors that predispose skeletal sites for erosions include: the presence of mineralized cartilage, a tissue particularly prone to destruction by bone-resorbing cells; the insertion sites of ligaments to the bone surface, which transduce mechanical forces to the bone and could induce microdamage; and inflamed tendon sheaths (termed tenosynovitis), which pass by the bone surface, and enable the spread of inflammation from the tendon to the articular synovium“<-maybe the transmission of mechanical forces via ligaments could be exploited to induce height gain.
“The small bone channels that penetrate cortical bone carry microvessels and bridge the outer synovial membrane and the inner bone marrow space; these channels are also prone to erosive change early in the course of RA. The microvessels located within these channels facilitate homing of osteoclast precursor cells to the bone, which, upon contact with bone and receipt of the appropriate molecular signals, differentiate into osteoclasts. Widening of cortical bone channels, as a result of osteoclast-mediated bone resorption, is a typical early change in animal models of arthritis”
“Osteoclasts, giant multinucleated cells derived from the monocyte lineage, are the only cells capable of resorbing bone in the body.2,3 Osteoclasts are designed to resorb bone by adhering tightly to the bone surface through interactions with both integrins and extracellular matrix proteins, as well as by assembling junctions, which seal the bone surface and the osteoclast and thereby separate bone from the surrounding extracellular space. Proton pumps along the osteoclasts’ ruffled border then create an acidic milieu, enabling solubilization of calcium from bone. Matrix enzymes synthesized by the osteoclast, including cathepsin K, matrix metalloproteinase 9 and tartrate-resistant acid phosphatase type 5 (TRAP), degrade the bone matrix”
“Development of osteoclasts occurs locally in the synovial tissue as a result of expression of the two essential osteoclastogenic mediators, macrophage colony-stimulating factor 1 (M-CSF)and receptor activator of nuclear factor κB ligand (RANKL; also known as TNF ligand superfamily member 11). This process involves the migration of monocyte-lineage cells from the bone marrow into the secondary lymphatic organs and finally into the joints. The differentiation step at which monocytes enter the joint is unclear. Indeed, monocytes could be already committed to a certain monocyte lineage, such as M1 or M2 macrophages, dendritic cells or osteoclast precursor cells when they enter the joint. Some data suggest that TNF, a key proinflammatory cytokine expressed in RA synovial tissue, stimulates the migration of osteoclast precursor cells from the bone marrow into the periphery. In addition, TNF stimulates expression of surface receptors such as osteoclast-associated immunoglobulin-like receptor before the precursor cells enter the joint, and these receptors facilitate differentiation. Once within the microenvironment of the joint, these cells are exposed to M-CSF and RANKL, and differentiate toward osteoclasts. Final differentiation into bone-resorbing osteoclasts is then achieved following contact with the bone surface.”
Inflammation plays a role in osteoclast formation.
