The role of immune cells in modulating chronic inflammation and osteonecrosis

Abstract

Osteonecrosis occurs when, under continuous stimulation by adverse factors such as glucocorticoids or alcohol, the death of local bone and marrow cells leads to abnormal osteoimmune function. This creates a chronic inflammatory microenvironment, which interferes with bone regeneration and repair. In a variety of bone tissue diseases, innate immune cells and adaptive immune cells interact with bone cells, and their effects on bone metabolic homeostasis have attracted more and more attention, thus developing into a new discipline - osteoimmunology. Immune cells are the most important regulator of inflammation, and osteoimmune disorder may be an important cause of osteonecrosis. Elucidating the chronic inflammatory microenvironment regulated by abnormal osteoimmune may help develop potential treatments for osteonecrosis. This review summarizes the inflammatory regulation of bone immunity in osteonecrosis, explains the pathophysiological mechanism of osteonecrosis from the perspective of osteoimmunology, and provides new ideas for the treatment of osteonecrosis.

Talar Neck Fractures With Associated Ipsilateral Foot and Ankle Fractures Have a Higher Risk of Avascular Necrosis

“…In animal studies, inflammatory markers and osteoclast activity were shown to be elevated in mice with multiple fractures compared with single fractures. 23,24 Hildebrand et al 25 explored the relationship between concomitant fractures and bone healing, which demonstrated the deleterious effects of systemic inflammation on local fracture site healing and the negative association between increased gene expression of proinflammatory signaling molecules and fracture stability.…”

Emerging factors affecting peri‐implant bone metabolism

“…228 T cells can modify bone metabolism because they are able to secrete OPG or RANKL and can regulate the local inflammatory environment. 228,229 There are three types of T cells, and their contribution to bone metabolism is different; regulatory T cells (Tregs) mainly contribute to lowering inflammation levels, while T helper cells (Th) and cytotoxic lymphocytes (CTLs) mainly promote inflammation. 228 Treg secretion of the anti-inflammatory cytokines IL-4, IL-10, and TGF-B initiates the arrest of inflammation and reduces osteoclast activity and osteolysis.…”

“…228,229 There are three types of T cells, and their contribution to bone metabolism is different; regulatory T cells (Tregs) mainly contribute to lowering inflammation levels, while T helper cells (Th) and cytotoxic lymphocytes (CTLs) mainly promote inflammation. 228 Treg secretion of the anti-inflammatory cytokines IL-4, IL-10, and TGF-B initiates the arrest of inflammation and reduces osteoclast activity and osteolysis. 229 In contrast, some types of Th cells, such as Th-2, Th-9, and Th17 cells, can release IL-9, IL-17, and other enzymes that trigger inflammation and tissue damage.…”

“…229 In contrast, some types of Th cells, such as Th-2, Th-9, and Th17 cells, can release IL-9, IL-17, and other enzymes that trigger inflammation and tissue damage. 228,230 Moreover, excessive infiltration of CTLs is related to osteonecrosis 228,231 and these cells can increase osteoclast activity due to cytotoxic T lymphocyte-associated protein 4 (CTLA-4). 232 B cells participate in adaptive humoral responses and can produce and release antibodies while presenting antigens to T cells.…”

“…228 Some papers have reported that between 40% and 64% of the bone marrow production of OPG depends on B cells. 228,234 When B cells become activated under inflammatory conditions, they release RANKL and increase bone catabolic effects. 228,235,236 Osteoblast-and B-lineage cells are the main sources of physiological OPG, and when aging reduces production by osteoblasts, B cells gain importance in OPG production to compensate for the RANK-RANKL-OPG quotient and counteract age-associated bone resorption.…”