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The Remodeling Of Bone Tissue Is A Function Of

The Remodeling Of Bone Tissue Is A Function Of

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Exercise, Nutrition, Hormones, And Bone Tissue

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By Addolorata Corrado Addolorata Corrado Scilit Google Scholar * , Daniela Cici Daniela Cici Scilit Google Scholar , Cinzia Rotondo Cinzia Rotondo Scilit Google Scholar , Nicola Maruotti Nicola Maruotti Scilit Francesco Google Scholar Paolo Cantatore Scilit Preprints .org Google Scholar

Received: April 30, 2020 / Revised: May 18, 2020 / Accepted: May 21, 2020 / Published: May 23, 2020

The Impact Of Immune Response On Endochondral Bone Regeneration

A decrease in bone mass leading to an increased risk of fracture is a common feature of age-related bone changes. The mechanisms underlying bone aging are very complex and involve systemic and local factors and are the result of a combination of several changes that occur at the cellular, tissue and structural levels; they include changes in bone cell differentiation and activity, oxidative stress, genetic damage and altered bone cell responses to various biological signals and mechanical loading. The molecular mechanisms responsible for these changes are still unclear and many data obtained from in vitro or animal studies appear contradictory and heterogeneous, possibly due to different experimental approaches; nevertheless, understanding the key physio-pathological processes that cause bone aging is important for the development of potential new therapeutic options to treat age-related bone loss. This article reviews current knowledge of the molecular mechanisms underlying the pathogenesis of age-related bone changes.

Bone is a complex, metabolically active and constantly remodeling tissue. Apart from the important mechanical properties that consist in the protection of internal organs, soft tissue support and movement, bone tissue has various metabolic functions [1], because it plays an important role in systemic mineral homeostasis and it is involved in hematopoiesis due to the close relationship between bone cells and hematopoietic bone marrow cells [2].

An overall decline in bone function is observed with aging, resulting in structural and geometric changes in the skeleton, reduced bone mass, reduced load-bearing capacity, altered responses to systemic humoral factors and decreased mineral content reserves. Taken together, these changes result in osteoporosis and an increased risk of fractures [3]. Osteoporosis is a systemic bone disease characterized by low bone mass and deterioration of the microarchitecture of bone tissue, leading to increased bone fragility and increased risk of fracture [4]. Depending on the underlying etiology, osteoporosis can affect all ethnic, gender and age groups, although it is most often observed in postmenopausal women and in the elderly of both sexes, and it is a major cause of morbidity and disability in the elderly population. [5]. Age is an independent risk factor for fracture: older subjects show up to a 10-fold increased risk of fracture over a ten-year period compared to younger subjects.

The Remodeling Of Bone Tissue Is A Function Of

Postmenopausal osteoporosis, in which the pathogenesis of estrogen deficiency plays an important role, mainly affects trabecular bone, while age-related bone changes occur in both trabecular and cortical bone. In trabecular bone, the main changes are represented by a reduction in the number of trabeculars, a decrease in trabecular thickness and an increase in trabecular distance, while in cortical bone, cortical thinning and expansion of the bone marrow cavity, due to increased endocortical absorption and increased bone formation in the bone. periosteal surface, observed (Figure 1). The mechanisms of age-related changes in bone tissue are very complex and involve systemic and local factors; the increased risk of fractures associated with bone aging is determined by a combination of changes that occur at the cellular, tissue and structural levels, the pathogenesis of which involves genetic factors, reduced cell differentiation, altered responses of bone cells to several biological signals and mechanical loading [ 6 , 7].

Bone Remodeling: An Operational Process Ensuring Survival And Bone Mechanical Competence

Bone is a composite tissue, consisting of inorganic mineral crystals and organic components represented by bone cells, bone marrow cells, extracellular matrix proteins, lipids and water. Bone cells are osteoblasts, osteocytes and osteoclasts that play an important role in maintaining bone homeostasis and bone remodeling processes; their metabolic activity is regulated by various local and systemic stimuli, including mechanical, hormonal and immunological factors.

Osteoblasts and osteocytes are derived from bone mesenchymal stem cells (BMSCs), while osteoclasts are derived from the monocyte/macrophage cell line of hematopoietic stem cells (Figure 2).

Bone cells produce and remodel a mineralized extracellular matrix, whose organic component is mainly represented by type I collagen and other collagen and non-collagen proteins, while the inorganic component is mainly composed of hydroxyapatite crystals [1]. Osteoblasts synthesize new bone matrix and control the mineralization process. Wnt signaling is a key pathway that promotes the differentiation, proliferation, maturation and activity of osteoblasts and it plays a fundamental role in bone development and repair. The Wnt pathway is involved in several biological processes, such as cellular proliferation and differentiation, tissue homeostasis and regeneration, embryonic development and stem cell commitment. It has been proven that dysregulation of Wnt signaling is involved in the pathogenesis of cancer, vascular disorders, autoimmune diseases and cell senescence. The Wnt signaling pathway has been classified into two main types, canonical Wnt signaling and non-canonical Wnt signaling, depending on the nature of the ligand and downstream events. The canonical Wnt pathway depends on the intracellular level of β-catenin and is mainly involved in the regulation of osteoblast differentiation, proliferation and metabolism, mineralization processes and in the modulation of bone formation. When canonical Wnt signaling is inactivated, intracellular β-catenin levels are low because it is embedded in the “destruction complex” which is an intracellular binding complex, composed of glycogen synthase kinase-3β (GSK3β), casein kinase I (CKI), adenomatous polyposis coli (APC ), and Axins. β-catenin is phosphorylated by GSK3 and then subjected to degradation via the ubiquitin-proteasome pathway. GSK3 and CKI inactivate cytosolic β-catenin through phosphorylation; Axin acts as a scaffold to the β-catenin destruction complex, promoting β-catenin degradation and thereby inhibiting Wnt signaling. Canonical Wnt signaling is activated by low-density lipoprotein receptor-related proteins (LRP)-5 and LRP-6 that complex by binding to the transmembrane Frizzled receptor and then stabilize cytosolic β-catenin blocking its phosphorylation and degradation thus allowing its translocation into the nucleus, where it promote the transcription of several target genes involved in osteoblast differentiation and bone formation [8, 9]. Several Wnt pathway antagonists, including Dickkopf-1 (Dkk-1) and sclerostin can suppress Wnt signaling in osteoblasts. Wnt signaling increases the expression of genes involved in the differentiation of BMSCs into osteoblasts, while it inhibits adipogenesis by stimulation of the Runt-related transcription factor 2 (Runx2) and inhibition of CCAAT-enhancer binding protein α (C/EBPα) [10]. ].

Osteoclasts are large multinucleated cells derived from mononuclear cell precursors of the monocyte/macrophage lineage found in the bone marrow, which function to resorb bone. In recent years, it has been shown that osteoclast recruitment, differentiation and activity are mainly regulated by the receptor activator of the NF-κB (RANK)/RANK (RANK-L)/osteoprotegerin (OPG) ligand system and by macrophage colonies. stimulatory factor (M-CSF). RANK-L, a member of the tumor necrosis factor (TNF) superfamily, is highly expressed in stromal/osteoblastic cells and activated T lymphocytes, directly inducing osteoclast differentiation by binding to its receptor RANK located on the surface of osteoclast precursors. Binding of M-CSF to the c-fms receptor located on the surface of osteoclast progenitors regulates the expression of RANK [11], thereby promoting osteoclastogenesis. OPG is a RANK-L decoy receptor that strongly inhibits osteoclast formation and activity by preventing interaction with the RANK receptor [12]. The RANK/RANKL/OPG and M-CSF/c-fms systems represent the main coupling mechanism between stromal/osteoblastic cells and osteoclast recruitment/activity and play an important role in regulating the balance between bone formation and resorption.

Bone Disorders: Pathology Review: Video & Anatomy

Osteocytes originate from quiescent osteoblasts; it is surrounded by a mineralized matrix and is a terminally differentiated osteolineage cell. Osteocytes, which represent up to 90% of bone cells and have a lifespan of 1 to 50 years [13], respond to mechanical loads and produce various factors involved in the regulation of bone metabolism.

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