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Ossification and osteogenesis are two processes deemed necessary in bone. Bone growth, maintenance, repair and remodelling are a continuous process, even throughout early adulthood. Compact bone tissue provides support and protection in attempt to resists the stressors we place upon them. As we grow or encounter a traumatic experience our bones deteriorate allowing new bone tissue to be replaced (McGee-Lawrence, & Westendorf, 2010).
The metaphysis (mature bone region) is where the bone shaft and the distal or proximal ends of the bone join. A layer of hyaline cartilage is within each growing bone to allow the diaphysis (long bone) to grow in length (Walker, Lovejoy, Bedfford & Yee, 2006). When the length of the bone has fulfilled its length, the cartilage is replaced by a bony epiphyseal (bony structure). With its thin layer the articular cartilage reducing resistance to absorb joints that have free movement. The repair of articular cartilage is minimal because it lacks irregular tissue, perichondrium (McGee-Lawrence, & Westendorf, 2010).
If the articular cartilage is not covering bone surface, the periosteum is put in replacement. The periosteum, acting as a tough sheath of dense irregular tissue is able to serve as an attachment point for ligaments and tendons. This gives them the ability to also assist in bone tissue nourishment and assist in fracture repair (Tortora, 2005).
The extracellular matrix is where cells, collagen fibre and crystallised mineral salts are held. Crystallisation is where minerals combine to create the tissue hardness, the beginning of bone formation (McGee-Lawrence, & Westendorf, 2010). Within the microscopic spaces of collagen fibres, an abundant amount of inorganic mineral salts such as calcium phosphate, magnesium hydroxide, fluoride and sulphate are deposited. An amalgamation of minerals allows crystallisation to occur within the framework formed by collagen fibres, initiated by osteoblasts. This is the process of calcification. A profuse amount of mineral crystals surround the collagen fibre creating the hardness and characteristics of bone. The hardness of a bone is dependent on the crystallisation formation whereas collagen fibres are responsible for the flexibility (Walker et al., 2006).
Mesenchyme stem cells are the foundation of bone formation during embryonic development and have the capability of transformation into a range of cells: osteogenic, osteoblasts, osteocytes and osteoclasts cells. Osteogenic cells are located within the periosteum and within bone containing blood vessels. Their only role is to undergo cell division resulting in osteoblasts (McGee-Lawrence, & Westendorf, 2010).
Osteoblasts synthesize and secrete collagen fibres in combination with organic components to build extracellular matrix of bone tissue, also responsible for calcification (Tortora, 2005). Plasma proteins bring new bone formation via the synthesis of osteoid, a non-mineralised bone matrix. When osteoblasts trap themselves with an excess amount of extracellular matrix, they are then called osteocytes. Within the Osteoblasts, many receptors are found in bone marrow assisting in regulating osteoclastic bone remodelling. The amount of osteoclast formation is determined by the level of receptor activator of nuclear factor KB-ligand (RANKL). If there is a defect of RANKL, a patient may suffer Paget Disease. This is when bone abnormality can occur; both resorption and formation (Walker et al., 2006).
Osteocytes, also known as mature bone because of their function are located in a hardened bone matrix (lacuna). They are the key cell in bone tissue, maintaining daily metabolism (exchange nutrients and waste in blood) and secrete protein such as sclerostin to reduce bone formation (McGee-Lawrence, & Westendorf, 2010). They have the capability to communicate with each other to exchange nutrients from capillaries containing nutrient-rich fluids. Osteocytes also communicate with osteoblasts and osteoclasts, signalling both when and where to resorb and form new bone (McGee-Lawrence, & Westendorf, 2010).
Osteoclasts are the major resorptive white blood cells containing lysosomes or digestive vacuoles filled with hydrolytic enzymes. The release of enzymes digests protein and mineral components in the extracellular matrix of bone, as part of the maintenance, repair and growth of bone. This process is called resorption. Once completed, they revert to their parent cell or become inactive (Walker et al., 2006).
Bone remodelling is an ongoing procedure from new bones at with to healing period of fractures. The strength of a bone is determined by the stressors placed upon it whilst in the remodelling phase. The most common fractures paramedics face on road is:
· Compressed – most common in old age, osteoporosis
· Spiral – ragged break, mostly seen in sports injuries
· Depressed – pressed inwards, skull fracture
· Greenstick – Incomplete break, most common in children
First action to take place in a fracture is formation of hematoma. Blood vessels are broken, resulting in a leakage from the torn ends (Walker et al., 2006). A blood clot around the site of the fracture usually within 6 to 8 hours following the injury is called hematoma. As clotting continues and fracture hematoma forms, blood flow to the site of injury becomes minimal, causing bone cells to die. Swelling and inflammation is the result of dead bone cells, producing additional cellular debris. This allows phagocytes and osteoclasts to eliminate damaged tissue. This process should take 2 to 3 weeks to conclude (Tortora, 2005).
The help of new blood capillaries in the fracture helps growing connective tissue called procallus. Fibroblasts (producing collagen fibres) and osteogenic cells attack the procallus to assist in connecting ends of the broken bones. Osteogenic cells transform into chondroblasts where healthy bone cartilage are developing and become fibrocartilage. Within 3 weeks, signs of bone tissue repair begin to show. This action is successful when the procallus is transformed into a fibrocartilaginous. Whiles this is occurring, phagocytes continue to remove any debris surrounding the fracture (McCance, Heuther, Brashers & Rote, 2010).
Osteogenic cells are later converted into osteoblasts to produce spongy bone trabeculae, a microscopic tissue. Trabeculae join the living and dead portions of the bone. After 3-4 months, Fibrocartilage changes into bony callus, a spongy bone (McCance et al, 2010).
The final phase of bone repair is remodelling. Osteoclasts gradually resorb original fragments of broken bones as compact bone replaces spongy bone. If all cells are working in a healthy patient, detection of fracture line under radiograph is unseen. As the stressor on the bone increases, signs of thickness may later show (McCance et al, 2010).
Bone remodelling is a slow process of removing old tissue and producing new bone tissue. As we grow, bone tissue goes through maintenance, repair and development in order to cope with the stressors. The remodelling of bone tissue only occurs when a patient has gone through a traumatic injury; this is where the housekeeping phagocytes are active and inflammation to ensure bacteria do not enter blood vessels, causing further damage.
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