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Fracture healing can be conveniently divided, based on the biologic event taking place, into the following four stages#$. Hematoma formation in%ammation! and angiogenesis.&. cartilage formation with subsequent calcication.'. cartilage removal and bone formation.(. Bone remodelin.

)nitially, there is hematoma formation followed by an in%ammatory phase characteri"ed by an accumulation of mesenchymalcell around the fracture site. this mesenchymal cells di*erentiate into chondrocytes or osteoblast. growth factors and

cytokines derived mainly from platelets are essential for angiogenesis, cellular chemotaxis, proliferation, and di*erentiation.growth factor induce mesenchymal cells and osteoblast to produce type & collagen and proteoglycans. pratelet+derivedgrowth factor -F! reqruits infammatory cells at the fracture site. bone morphogenetic proteins B/s! are osteoinductivemediators inducing metaplasia of mesenchymal cells into osteoblasts. interleukin )0!+$ and )0+1 reqruit in%ammatory cells tothe fracture site. periosteum has been compromised, stem cells originate from the circulation and the surrounding softtissues.

0ow oxygen tension, low pH, and movement favor the di*erentiation into chondrocytes2 high oxygen tension, high pH, andstability predispose toward osteoblast stimulation. in the presence of mechanical instability, fracture heal by the process of

endochondral ossication bony callus formation is preceded by a cartilaginous template.

chondrocytes and broblasts produce a semi rigid soft callus that is able to provide a mechanical support to the fracture, aswell as act as a template for the bony callus that will later supersede it. the most active stage of osteogenesis, also known asprimary bone formation is charateri"ed by high levels of osteoblast activity and the formation of minerali"ed bone matrix,which arises directly in the peripheral callus in areas of stability. minerali"ation causes chondrocyte degeneration, hipertrophy,and nnlay apoptosis.the phase of mineralli"ed callus leads to a state in which the fracture site is enveloped in apolymorphous mass of minerali"ed tissues consisting of calcied cartilage, woven bone made from cartilage, and wovenbone formed directly. the woven bone minerali"ed callus has to be replaced by lamellar bone arranged in osteonal system toallow the bone to resume its normal function. in order for bridging new hard callus to form, the insecure soft callus is gradually

removed, concomitant with revasculari"ation. the new bone is know as hard callus, and it is typically, irregular andunderremodeled.

the nal stage of fracture repair, also re*ered to as secondary bone formation, encompasses the remodeling of the wovenbone hard callus into original cortical and trabescular bone conguration. the key cell type involved with the resorption ofminerali"ed bone is the osteoclast, which is a large, multinucleated cell formed by fussion of monocytes. osteoblasts aremononuclear and are responsible for the accretion of bone.

macrophage colony stimulating factor /+34F! and receptor activator of nuclear factor b ligand 56780! are two principalcytokines secreted by osteoblasts that are critical for the induction, survival, and comptency of osteoclasts.

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enyembuhan tulang

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9ulang

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rimer

4ekunder

:ika ter;adiksasi rigid

:ika tidakter;adiksasi rigid

Hematoma

Formation