Role of apoptosis in pathogenesis and treatment of bone-related diseases

Abstract

In this article, bone cells and their intercellular communications have been reviewed. Gap junctions and hemichannels are the main routes of interactions in bone tissue. They play a substantial role in survival and cell death, since pro-apoptotic signals can propagate through them. Different adhesion molecules are required for apoptosis, particularly caspase family as well as noncaspase proteases. The disruption outcome of apoptosis could result in bone-related diseases such as osteonecrosis. Anti-apoptotic strategies include inhibition of caspase, poly [ADP-ribose] polymerase (PARP), and Bcl-2 proteins as well as induction of the PKB/Akt pathway and inhibitors of apoptosis (IAP) family of proteins. Thus, understanding the mechanism of apoptosis gives detailed insights of anti-apoptotic molecular targets. Based on these targets, different treatments were designed and produced such as estrogen replacement therapy, administration of different bisphosphonates, raloxifene, calcitonin, sodium fluoride, calcium, and vitamin D. As a result, new applicable drugs for treatment of related bone problems can be proposed for clinical approach especially in the early stage of diseases.

Effect of the three Enterococcus faecalis strains on apoptosis in MC3T3 cells

“…Inflammatory bone destruction in persistent apical periodontitis (PAP) is widely considered as an imbalance of bone remodelling that is sophisticatedly regulated by osteoclasts and osteoblasts (Chen et al., ). Apoptosis is a process of programmed cell death and a necessary component in bone turnover (Mollazadeh, Fazly Bazzaz, & Kerachian, ). About 60%–80% of osteoblasts assembling at the bone resorption pit are found to die by apoptosis (Moriishi et al., ).…”

Pleiotropic roles of Ca+2/calmodulin-dependent pathways in regulating cadmium-induced toxicity in human osteoblast-like cell lines

“…We previously reported that cadmium induces apoptosis in human osteoblasts via extracellular signal-regulated protein kinase (ERK) activation, increasing oxidative stress, and activating caspase-3 (Coonse et al, 2007; Smith et al, 2009; Arbon et al, 2012). Since apoptosis is an integral component of bone remodeling, disruption of the apoptotic signaling cascades in osteoblasts may contribute to net bone loss, leading to a bone disease state (Mollazadeh et al, 2015). …”

The effect of adrenocorticotropic hormone on alpha‐2‐macroglobulin in osteoblasts derived from human mesenchymal stem cells

“…The leading aetiology in destruction of femoral head called ‘ANFH’ is apoptosis of femoral head's bone. It has been shown that patients suffering from ANFH have obstructed blood vessels . Reduction in shear stress due to declined blood flow could cause apoptosis of endothelial cells, which can eventually contribute to plaque erosion and thrombus formation .…”