enhanced by motion and is inhibited by rigid fixation.

Fracture healing can be conveniently divided, based on the biologic event taking place, into the following four stages:
1. Hematoma formation (inflammation) and angiogenesis.
2. cartilage formation with subsequent calcification.
3. cartilage removal and bone formation.
4. Bone remodelin.
Initially, there is hematoma formation followed by an inflammatory phase characterized by an accumulation of mesenchymal
cell around the fracture site. this mesenchymal cells differentiate into chondrocytes or osteoblast. growth factors and
cytokines derived mainly from platelets are essential for angiogenesis, cellular chemotaxis, proliferation, and differentiation.
growth factor induce mesenchymal cells and osteoblast to produce type 2 collagen and proteoglycans. pratelet-derived
growth factor (PDGF) reqruits infammatory cells at the fracture site. bone morphogenetic proteins (BMPs) are osteoinductive
mediators inducing metaplasia of mesenchymal cells into osteoblasts. interleukin (IL)-1 and IL-6 reqruit inflammatory cells to
the fracture site. periosteum has been compromised, stem cells originate from the circulation and the surrounding soft
tissues.
Low oxygen tension, low pH, and movement favor the differentiation into chondrocytes; high oxygen tension, high pH, and
stability predispose toward osteoblast stimulation. in the presence of mechanical instability, fracture heal by the process of
endochondral ossification bony callus formation is preceded by a cartilaginous template.
chondrocytes and fibroblasts produce a semi rigid soft callus that is able to provide a mechanical support to the fracture, as
well as act as a template for the bony callus that will later supersede it. the most active stage of osteogenesis, also known as
primary bone formation is charaterized by high levels of osteoblast activity and the formation of mineralized bone matrix,
which arises directly in the peripheral callus in areas of stability. mineralization causes chondrocyte degeneration, hipertrophy,
and finnlay apoptosis.the phase of minerallized callus leads to a state in which the fracture site is enveloped in a
polymorphous mass of mineralized tissues consisting of calcified cartilage, woven bone made from cartilage, and woven
bone formed directly. the woven bone mineralized callus has to be replaced by lamellar bone arranged in osteonal system to
allow 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 revascularization. the new bone is know as hard callus, and it is typically, irregular and
underremodeled.
the final stage of fracture repair, also reffered to as secondary bone formation, encompasses the remodeling of the woven
bone hard callus into original cortical and trabescular bone configuration. the key cell type involved with the resorption of
mineralized bone is the osteoclast, which is a large, multinucleated cell formed by fussion of monocytes. osteoblasts are
mononuclear and are responsible for the accretion of bone.
macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor b ligand (RANKL) are two principal
cytokines secreted by osteoblasts that are critical for the induction, survival, and comptency of osteoclasts.

Penyembuhan tulang
Penyembuha
n
Tulang

Primer

Jika terjadi
fiksasi rigid

Tahap

Hematoma
Formation &
Angiogenesis
Cartilage
Formation

Sekunder

Jika tidak
terjadi
fiksasi rigid

Cartilage
Removal and
Bone Fomation
Bone
Remodeling

Tahap penyembuhan
tulang
Inflama
si

Reparatif

Remodeli
ng