Bone Physiology Flashcards
Describe the Internal Structure of Bone
Cortical Bone is made up of sub-units termed Osteons. At the centre of each osteon is the Haversian canal containing blood vessels. Around the canal are concentric rings (lamellae) of Bone matrix containing Osteocytes. Adjacent Osteons communicate via Volkmann’s Canals, also containing blood vessels.
Osteons are tightly arranged and overlap, providing cortical bone with its high density. They are arranged along the lines of force, usually parallel to the long axis of the bone. Where osteons overlap they intercommunicate via canaliculi (gap junctions within channels), they spread out from the central canal like spokes on a wheel. At the edge of each osteon lie cement lines, areas with no collagen fibres or canaliculi, they are areas of relative weakness where cracks may propagate.
In the Diaphysis the cortical bone surrounds a medullary canal containing a central nutrient artery, bone marrow and cancellous bone.
In the Metaphysis the cortex is thin and the architecture comprises a delicte trabeculae of woven bone/cancellous bone. Cancellous bone has 8 times the turnover rate of cortical bone. It is less dense, less strong and less elastic than cortical bone. Haversian systems are not present in cancellous bone.
Describe the Periosteum
The periosteum lies on the outer surface of the cortex. It is a layer of specialised connective tissue. An inner Cambial Layer contains progenitor cells (giving ability for osteogenesis) and is highly vascular. Then a much tighter outer fibrous layer, which is structural, less cellular and is continuous with joint capsules. As the periosteum is vital for osteogenesis it tends to be much thicker in Children. On the inner aspect of the cortex is a similar membrane called the Endosteum.
What determines which mode of Bone Healing occurs?
Perren’s Strain Theory determines what type of fracture healing occurs.
- Fracture Gap strain measures the extent a fracture moves. It is defined as the Fracture Length Gap (DL) divided y the original Fracture Gap (DL).
If strain is > 10% then Granulation Tissue occurs.
If strain is 2-10% then Fibrocartilage can form (initiating Secondary Healing).
If strain < 2% then Bone forms (Primary Healing).
Immediately following a fracture strain is high, granulation tissue occurs increasing the stability and reducing the strain, then fibrocartilage may form, thus further increasing stability then allowing bone to form (soft callus progressing to hard callus = secondary healing).
For primary bone healing you need anatomical reduction (minimal strain) and absolute stability, this is only achieved through open reduction internal fixation. If the reduction is not perfect ie > 2% strain, but the fixation is rigid. Then the gap may be too large for the cutting cones to bridge the gap, but there may not be enough movement (lack of strain) for callus to form, thus predisposing to non-union.
Describe Primary Bone Healing
In states of absolute stability (<2% strain across fracture site) and anatomical reduction, primary bone healing may occur. There needs to be Interfragmentary compression to achieve absolute stability. Full congruence between the fracture ends is never achieved, but there needs to be sufficient contact between the fragments to allow healing without callus. Therefore techniques involving absolute stability can only be applied to simple fracture patterns.
There will be contact zones and gaps e.g. compression applied to tranverse fracture results in compression of fragments on side of plate and small gap on contralateral cortex. In contact healing, bone union and remodelling occur simultaneously whereas in gap healing they occur as sequential steps.
In the first few days following surgery, there is development of new blood vessels which grow into any gaps (gap healing). Mesenchymal cells differentiate into OsteoBlasts which lay down Lamellar Bone in areas of small gaps and Woven Bone in Big Gaps.
Subsequently, OsteoClasts form Cutting Cones which travel through areas of direct contact or minute gaps, creating a path for Blood Vessels and Osteoblasts to follow in their wake, which in turn creates Lamellar Bone, in the form of new Osteons. This process is essentially the same as stage IV of Secondary Healing - Remodelling.
Primary Bone Healing is term Haversian healing as it only involves remodelling of the cortical bone and no Callus formation.
Describe Secondary Bone Healing
Stage I; Haematoma and Inflammation (up to 1 week)
- Damaged blood vessels cause a Haematoma made up of Fibrin Clot.
- Damaged tissue and degranulated platelets release signalling molecules, growth factors and cytokines (IL-1, IL-6), leading to Migration of Inflammatory Cells.
- Proliferation, Differentiation and Matrix synthesis as Haematoma is replaced by Granulation tissue.
- There is Angiogenesis, recruitment of Fibroblasts, Mesenchymal Cells and Osteoprogenitor Cells (Periosteum is important in this).
- At the necrotic bone ends, osteoclasts resorb bone and macrophages remove tissue debris.
Stage II; Regeneration (1 - 4 weeks)
- Increased cellularity, mesenchymal cells produce fibrous Connective Tissue and Cartilage resulting in Soft Callus formation.
- IntraMembranous Ossification occurs peripherally to the callus with Osteoprogenitor Cells in the Cambium Layer of Periosteum produce woven bone is an early response of the callus.
- Endochondral Callus occurs centrally across the fracture site. Mechanism = multipotent stem cells differentiate into fibroblasts and chondrocytes. Fibroblasts produce Type II Collagen creating a cartilagenous soft callus, then chondrocytes calcify it.
- Endochondral ossification then occurs by Chondroclasts resorbing the soft callus and new blood vessels forming bringing with them Osteoblasts who lay down Type 1 (Osteoid) Collagen and the Hard Callus forms. This typically occurs at 1 to 4 months.
Remodelling (up to Several Years); Osteoclasts create a cutting cone which resorbs the Trabeculated Woven Bone creating a space for Osteoblasts to follow laying down Compact Lamellar Bone. This is the same as Primary Bone Healing.
What causes Hypertrophic Non-Union at a Fracture site?
Hypertrophic non-union (appears as excessive callus then s clearly visible fracture line suggesting non-union) occurs when there is excessive strain ie too much movement. This can occur for example when a tibial shaft fracture is IM nailed alongside an unstable fibula fracture which is left untreated.
