Bone Remodeling Research Paper

Osteopetrosis is a rare, genetic disease that causes extremely dense and brittle bones. This is because individuals affected with osteopetrosis do not have normal osteoclasts, which bones need to work correctly. Healthy bones require properly functioning osteoblasts and osteoclasts. Osteoblasts are responsible for making new bones and osteoclasts are bone cells that are responsible for bone resorption, which is the breaking down of bones and providing space for new bone marrow to grow. An individual with osteopetrosis has osteoclasts that do not function properly, therefore their bones are not healthy (Stocks, Wang, Thompson, Stocks, & Horwitz, 1998).

With my help, we are one step closer to figuring out the steps in the cellular pathway to bone

Haematopoietic stem cells (HSC) regulate the turnover of platelets, erythrocytes and all immune cells by changing between self-renewal and differentiation to a variety of specialised cells. Osteoblasts has a major role of secretion of mineralized bone matrix proteins and cells of the osteoblast lineage regulating osteoclast differentiation. (Purton & Scadden, 2008)

Bone is surrounded by a thin membranous layer of soft tissue called periosteum (Singh, 2017). When the bone breaks it bleeds from torn ends because of the disruption of the supplying blood vessels. And quite naturally the periosteum is also torn. A fracture hematoma forms and white blood cells march in to clean up the area that is injured. The periosteum is the primary source of osteoblasts, which plays a huge role in fracture healing (Singh, 2017). After the hematoma formation, the next step is callous formation with the formation of cartilage and bone and then the remodeling phase consisting of the osteoclasts and the osteoblasts reshaping the bone to its original state (Patton, 2012).

Over the years, advancements in healthcare have provided patients with an increased quality of life. Procedures such as kyphoplasty and vertebroplasty have provided such improvements with their introduction in healthcare only a few decades ago. There are several million people worldwide diagnosed with osteoporosis who suffer from vertebral compression fractures who now have the option to undergo one of these two minimally invasive procedures in order to experience immediate pain relief after conservative measures have failed.

Estrogen deficiency is a major factor of osteoporosis for both males and females, which contributes to its pathophysiology. Estrogen stimulates osteoprotegerin (OPG) production, which is a protein, in the osteoblast that causes it to exert anti-resorptive effects on the bone. It also goes together with parathyroid hormone (PTH) levels. Estrogen deficiency will cause the bones to become more sensitive due to PTH. We know that osteoclasts, osteoblasts, and osteocytes contribute to the building and the breaking of the bones. These three key bone cells provides support for future osteoclasts, T-cells, β-cells, and most other cells in the human bone marrow (Becker, 2008). The deficiency of estrogen levels leads to an activation of T-cells, which also contributes to the pathogenesis of osteoporosis. These T-cells produce proinflammatory cytokines, which are important in cell signaling. This can cause osteoblasts differentiation and apoptosis, which is a process that causes the premature death of osteoblasts. But there are other

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protects the organs and tissues of the body by providing a ‘cage’ around them and keeping the internal organs in their correct place. Strong bones e.g. the spine allow a person’s movement and they are able to stand straight without falling down. It also does a good job of supporting a person’s body mass which allows their muscles to function even if they are overweight. It holds the internal organs because of hollow spaces e.g. the skull does a good job of keeping the brain intact and holding it, whereas, the chest cavities forms a house around the heart and lungs.

Osteoblastogenesis takes place as a result of a number of signalling pathways such as the transforming growth factor-β (TGF-β), Wnt/β-catenin and mitrogen-activated protein kinase (MAPK) signalling. The TGF-β superfamily comprises of the TGF-βs and the bone morphogenetic proteins (BMPs), both of which play critical regulatory roles in bone tissue55,56. TGF-β presents in 3 isoforms namely TGF-β1, TGF-β2 and TGF-β3 with TGF-β1 in particular having a chemotactic effect on osteoblasts in order to promote bone formation55. TGF-β is initially expressed as an inactive complex which is made functional via one of three mechanisms: bond breaking between TGF-β and the latency associated peptide, degradation of the latency associated peptide or conformational change of the latency associated peptide itself55. Post-activation, the TGF-β binds to either type I or type II of the transmembrane serine/threonine receptors57.

Chen and Dragoo (2013) explain that bone healing starts following a crack in the bone with the creation of a hematoma and begin the swelling stage. Inflammatory agents and cytokines promote prostaglandin (PG) generation (Chen & Dragoo, 2013). Osteoblasts generate prostaglandins to boost the fracture callus, and PGE2 is the majority PG produced by osteoblasts to encourage and stimulate bone development and strengthens bone mass (Chen & Dragoo, 2013).

Cancellous bone is more active and is broken down and regenerated more quickly than compact bone. Because of this, cancellous bone is more likely to be affected when the break down and regeneration of bone are out of balance in osteoporosis. The cells that are responsible for the BMD to stay constant is osteoblasts and osteoclasts. The function of osteoblasts is that it produces new bone matrix in a process called ossification while osteoclasts are cells that remove and recycle bone matrix. For a normal bone, there is a balance between the action of osteoblasts and osteoclasts but in osteoporotic bone, the activity of the osteoclasts in removing bone matrix is faster than the osteoblasts can form a new bone matrix. This results in a net bone lose. Osteoporosis can also lead to thinning of both the compact bone and cancellous bone which makes bone more fragile to

The bones that are developed from endochondral ossification are referred to cartilaginous bones which occur in long bones and are essential during growth of lengthy bone. It proceeds via condensation of mesenchymal cells and gets differentiated into chondroblasts instead of osteoblasts. A cartilage template is produced by the activity of chondroblasts and serves as a template for the development of long bones such as femur and tibia. The cartilage template becomes surrounded by a membrane called perichondrium, which contains osteoprogenitor cells. As proliferation increases, the template begins to grow. The chondroblasts can secrete an extracellular matrix composed of collagen and proteoglycans. The chondroblasts

This paper summarizes the process and implications of bone remodeling as proposed by Svetalana V. Komarova, Robert J. Smith, S. Jeffrey Dixon, Stephan M Sims, and Lindi M. Wahl. Bone remodeling in the human body is an intricate process where osteoclasts resorb existing mineralized tissue and osteoblasts form new bone. Bone remodeling involves various interactions between different cells in the osteoclasts and osteoblasts. A problem occurs when these interactions are disturbed and can lead to numerous different bone disorders such as osteoporosis, osteoarthritis, or Paget’s disease. Manipulating Frost’s mechanostat theory, a theory that describes bone biology, and its corresponding biomechanical mathematical models of bone, Komoarova, Smith, Dixon, Sims, and Wahl were able to form their own model that allowed them to analyze how a change in interactions between cells can affect the bone remodeling process.

Trelles et al.1 examined the characteristics of bone repair using low energy laser after bone fracture fractures in the tibia of mice. histologically via controlling its reparation after exposure to 632 nm laser in doses of 2.4 Joules in one point was used. The radiation was directly applied to the area of fracture through the application of 12 treatments , they used a single treatment every second day, by optic microscope they observed, in the treated animals, a drastic increase in vascularisation and faster formation of osseous tissue with a dense trabecular net compared to the control group. that  presented only chondroid tissue and very poor vascularisation corresponding to an earlier stage of bone consolidation which  proves that

Osteoblasts are cells that form in the marrow of bones. These cells (Osteoblasts) are vital in the forming and developing of a foetus, as it grows to become a child. The bone cells don't stop working even once a person has reached adulthood, bone development occurs throughout your whole life. This continued development can be identified in the healing & repair of