Fractures

Sequence of events for fracture healing

 

1. Immediately after fracture a haematoma forms. The clotted blood provides a fibrin mesh which seals off the fracture site and creates a framework for the influx of inflammatory cells and ingrowth of fibroblasts and new capillaries.Platelets and inflammatory cells release TGF-b, PDGF and FGF which activate osteoprogenitor cells and stimulate to the production of osteoblastic and osteoclastic cells. These remodel the ends of the fractured bone resulting in the formation of soft tissue callous (or pro-callous) which provides some anchorage for the two bone ends but no structural rigidity

 

2. Bony callous is formed by osteoprogenitor cells which lay down woven bone. Mesenchymal cells close to the fracture line can also differentiate into chondroblasts and produce fibrocartilage and hyaline cartilage. This can then undergo endochondral ossification. As the fractured ends are bridged by a bony callous and it mineralises then the strength increases until the point is reached when some controlled weight bearing can be tolerated

 

3. In the early stages of callous formation, excess fibrous tissue, cartilage and bone are formed and if the bones are not aligned the volume of callous is greatest in the concave portion of the fracture site. As the callous matures and transmits weight bearing forces, the portions that are not physically stressed are reabsorbed until the shape of the bone is re-established

 

 

Impairment of fracture healing

 

• Displaces or comminuted (when the bone is splintered) fractures frequently result in some deformity
• The deviated fragments of splintered bone require reabsortion which delays healing and enlarges the callous
• Inadequate immobilisation permits constant movement of the fracture so that the normal callous constituents don’t form. This results in instability and delayed union or non union
• If a non union allows too much motion along the fracture gap, the central portion of the callous can undergo cystic degeneration and the luminal suface can become lined with synovial –like cells forming a false joint or pseudoarthrosis
• Infection prevents fracture healing
• Bone repair is also hindered by;
  • Calcium, phosphate and vitamin deficiencies
  • Systemic infections
  • Diabetes
  • Vascular insufficiency

 

Osteonecrosis (Avascular necrosis)

 

• Mechanisms that induce ischemia;
  • Fracture
  • Corticosteroids
  • Infection
  • Thrombosis and embolism e.g. nitrogen bubbles in dysbarism
  • Vessel injury secondary to vascultitis or radiation
  • Increased interosseous pressure and vascular compression
  • Venous hypertension
• Aside from fracture most cases are idiopathic or result from corticosteroid administration
• Infarcts may be subchondral or medullary
• Subchondral infarcts are chronically painful and can result in severe secondary osteoarthritis.
• Medullary infarcts can be clinically silent except for vbery large ones associated with Gaucher’s disease (lysosomal storage disorder), dysbarism and hemoglobulinopathies