Healing of Bones
Healing of bones resembles dermal healing with some notable differences and specific terms.
| Phase | Process | Nota bene |
|---|---|---|
| Hematoma and Inflammation | Accumulation of blood, devitalized soft tissue, dead bone and necrotic marrow at the fracture site → Breakdown and liquefaction of non-viable elements at the fracture site → new blood vessels from the adjacent bone grow into the fracture site (analogous to granulation tissue) | Characterized by pain, swelling, and erythema |
| Formation of soft callus (proliferation) | A soft tissue scaffolding forms uniting the fragments and preventing damage to blood vessels | Marked by the end of pain and inflammation |
| Formation of hard callus (maturation) | The soft callus undergoes mineralization and converts to bone | Complete bony union occurs in 2-3 months. The bone is strong enough to bear weight and appears healed on radiograph |
| Remodelling of bone | Resorption of excessive callus and recanalization of the marrow cavity | Remodelling allows physical forces to be correctly transmitted and restores the conture of bone |
Healing of Cartilage
Cartilage has the same phases of wound healing as the dermis. However, it is prone to poor healing since it is relatively avascular. Healing requires the presence of a hypervascular perichondrium and injuries to this may result in permanent defects.
| Depth of injury | Healing | Nota bene |
|---|---|---|
| Superficial cartilagenous injury | Less blood supply to cartilage → less inflammation → slow synthesis of collagen and proteoglycans → slow healing and persistent structural defects | The cauliflower ear is an acquired deformity due to trauma to the ear following boxing, rugby, etc. Trauma shears tissue causing a hematoma to form which disrupts the blood supply to the perichondrium and cartilage of the ear. Cartilage dies and is replaced with fibrosis causing the ear to take on the characteristic appearance. Treatment involved draining the hematoma so that the blood vessels can heal and supply the perichondrium and cartilage. |
| Deep cartilagenous injury | Damage to soft tissue and bone in addition to cartilage exposed blood vessels → follows the typical phases of healing → restoration of structure and function of cartilage |
Healing of tendons and ligaments
Tendon and ligament also have the same phases of healing as the dermis. However, regeneration is slow and results in a fibrous scar at the point of union. Furthermore, collagen fibres orient along the lines of stress. The degree of vascularization is essential in determining healing. Hypovascular tendon and ligaments heal with less motion and more scar than those with better blood supply.
Healing of Nerves
In the CNS, neurons cannot be regenerated. Healing is by proliferation of glial cells which form a glial scar.
Peripheral nerves contain axons, schwann cells and other non-neuronal cells, and extracellular matrix. Injury to nerves occur in 3 degrees (Seddon’s classification of nerve injury), listed below from mild to severe:
| Type of injury | Description | Function loss | Full recovery |
|---|---|---|---|
| Neuropraxia | Focal demyelination with no loss of nerve continuity | Motor disruption. Minimal sensory or autonomic disruption. | Results from transient pressure, and once this pressure is resolved the injury resolves |
| Axonotmesis | Interruption of axon with preserved perineurium and epineurium. | Motor, sensory, and autonomic disruption | Depends on the length of involved segment and how quickly compression is relieved |
| Neurotmesis | Complete transection of the nerve | Motor, sensory, and autonomic disruption | Rare |
For peripheral nerves to recover function:
- Cell bodies of the neuron must survive
- The axon has to regenerate, grow across the transected nerve and reach the distal stump. Phagocytes remove degenerating axons and myelin from the distal stump (Wallerian degeneration). Axons sprout from the proximal stump and probe distal stump and surrounding tissue. Schwann cells ensheath and help remyelinate regenerating axons.
- Regenerating nerve ends have to connect to the appropriate nerve ends or organ targets to create a functional unit
Recovery from surgical re-approximation of divided nerves is better in younger patients, in pure motor/sensory nerves, and in injury where the site is closer to the target organ. The rate of regeneration is 1mm per day so that the more proximal the damage, the more time must elapse before the functional result can be assessed.
Healing of muscle
| Muscle | Healing properties |
|---|---|
| Skeletal muscle | Has some regenerative ability if the cell membrane (sarcolemma) is intact. Severe injury heals by fibrosis. |
| Smooth muscle | Limited regenerative ability. Heals by fibrosis. |
| Cardiac muscle | No regenerative ability. Heals by fibrosis (permanent scar) |
Healing of the gastrointestinal tract
The GIT undergoes the same phases as dermal healing. The serosa and mucosa heal without scar formation. However, during the first week, there is decreased anastomotic strength due to collagenase activity. Collagenolysis precedes collagen syntheis. It begins day 3-5 while collagen synthesis takes several days to begin.
| Layer of the GIT | Role |
|---|---|
| Submucosa | Has the greatest tensile strength and suture-holding ability |
| Serosa | Healing forms a watertight seal. Highlighted by higher leak rates seen in extraperitoneal tissue (esophagus and rectum) |
Full thickness injury of bowel is common in surgery. Repair begins with surgical reapproximation. To maximize healing, anastomosis should:
- Be tension free
- Have adequate blood supply
- Receive good nutrition
- Be free of sepsis
Post-op over-administration of fluid can affect anastomosis by causing third-spacing (edema of the bowel wall) and increasing intra-abdominal pressure which compromises blood flow to the anastomosis.
