Abstract

Bone is a mineralized and elastic connective tissue that provides fundamental functions in the human body, including mechanical support to the muscles and joints, protection of vital organs and storage of minerals. Bone is a metabolically active organ that undergoes continuous remodeling processes to maintain its architecture, shape, and function throughout life. One of the most important medical discoveries of recent decades has been that the immune system is involved in bone remodeling. Indeed, chronic inflammation has been recognized as the most significant factor influencing bone homeostasis, causing a shift in the bone remodeling process toward pathological bone resorption. Bone osteolytic diseases typified by excessive bone resorption account for one of the greatest causes of disability worldwide, with significant economic and public health burdens. From this perspective, we discuss the recent findings and discoveries highlighting the cellular and molecular mechanisms that regulate this process in the bone microenvironment, in addition to the current therapeutic strategies for the treatment of osteolytic bone diseases.

Highlights

  • Bone is a highly vascu larized and mineralized tissue that naturally maintains its mass, microarchitecture, shape, and function through an orchestrated process called bone remodeling

  • Disruption of the bone remodeling process frequently occurs during inflammation, which plays a major role in skewing this balanced process toward bone resorption through promoting osteoclast activity [3]

  • There is a growing body of evidence to suggest that the accumulation of senescent cells such as myeloid cells, osteocytes and osteoblasts facilitates the development of a proinflammatory environment in bone tissues, leading to osteoporosis [46,123,124]

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Summary

Introduction

Bone is a highly vascu larized and mineralized tissue that naturally maintains its mass, microarchitecture, shape, and function through an orchestrated process called bone remodeling This process requires tight coordination between four types of cells, all of which reside in the bone. A1 (AnxA1), and cardiotrophin-like cytokine factor 1 (CLCF1) act as negative regulators of osteoclastogenesis and act by blocking the activation of transcription factors needed for cell differentiation [31,32,33,34,35,36] These extremely important findings highlight the importance of inflammatory pathways as critical targets in both the prevention and therapy of bone osteolytic diseases

Cellular and Signaling Networks Linking Inflammation and Pathological
Inflammation and the Regulatory Functions of Osteoblasts and Osteocytes
Potential Contribution of Osteal Macrophages to Bone Remodeling
Inflammation and Bone Osteolytic Diseases
Osteoporosis
Rheumatoid Arthritis
Aseptic Loosening
Osteoarthritis
Osteomyelitis
Other Mechanisms Involved in Inflammation-Induced Pathological
Findings
Conclusions and Future Prospects

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