arm pathology
Five Stages of Fracture Healing
Stage 1: Haematoma Formation
Mechanism: A fracture results in the breaking of blood vessels crossing the fracture line. This leads to bleeding in the fractured bone, the medullary cavity, and the periosteum.
Timing: A fracture haematoma, or blood clot, forms between the ends of the bone fragments, in the medullary cavity, and under the periosteum approximately hours after the fracture occurs.
Necrosis: Bone and periosteal cells die at the fracture site because torn blood vessels are unable to deliver nutrients to that specific area of the bone.
Fibrin Network: The haematoma serves as a fibrin network that facilitates two critical processes:
Angiogenesis (formation of new blood vessels).
Invasion of cells.
Stage 2: Cellular Proliferation and Inflammation
Inflammatory Response: This stage involves an influx of inflammatory cells and cellular invasion.
Cell types: Neutrophils and macrophages arrive at the site.
Phagocytic Activity: An influx of phagocytic cells removes debris from the fracture site.
Cytokines and Growth Factors involved in the Inflammation/Granulation Tissue stage:
Platelets: Release , , , , and .
Neutrophils: Release , , , , , , and .
Macrophages: Release , , , , , , , , and .
Involved Cells: Mesenchymal Stem Cells (MSCs), NK Cells, and the formation of capillary buds.
Stage 3: Callus Formation
Differentiation: Mesenchymal stem cells differentiate into chondrocytes and fibroblasts.
Product: These cells produce a fibrocartilaginous callus, also known as a procallus. This stage consists of cartilage and osteoid.
Duration: This stage lasts approximately weeks.
Immune Interaction: T-Lymphocytes are active here, releasing , , , , and .
Stage 4: Ossification
Bone Deposition: Osteoblasts invade the area and deposit new bone tissue.
Replacement: The fibrocartilaginous callus is mineralized and replaced with woven bone (primary bone).
Duration: This stage lasts up to approximately weeks.
Immune Interaction: B-Lymphocytes release and .
Stage 5: Remodelling
Process: Cellular proliferation decreases. Osteoclasts dissolve excess bone tissue to smooth out irregularities and reorganize the bone.
Bone Types: Osteoblasts lay down lamellar bone.
Structural Alignment: The reorganization of newly formed bone occurs along the lines of mechanical stress.
Cycles: Continuous cycles of resorption and formation occur until the bone regains its normal appearance.
Duration: Remodelling can take months to years.
Supracondylar Fracture
Epidemiology and Mechanism: This fracture is common in children, typically occurring around years of age. It is often caused by a Fall On Outstretched Hand (FOOSH).
Anatomy:
Typically extra-articular in children, involving the thin bone between the coronoid fossa and the olecranon fossa.
In adults, these fractures may be intra-articular.
The fracture line usually angles from an anterior distal point to a posterior proximal site.
Gartland Classification:
Type I: Undisplaced fracture.
Type II: Displaced fracture with an intact posterior cortex. This may (Type IIb) or may not (Type IIa) include a rotational deformity.
Type III: Characterized by complete displacement.
Complications:
Malunion or misalignment (such as cubitus varus).
Volkmann’s contracture.
Nerve damage.
Humeral Shaft Fracture
Mechanisms and Fracture Patterns:
Bending Force: Produces a transverse fracture of the shaft.
Torsion Force: Results in a spiral fracture.
Bending + Torsion: Leads to an oblique fracture, which may or may not include a butterfly fragment.
Compression Forces: Typically fracture either the proximal or distal ends of the bone.
Specific Types:
Short Oblique Fractures: Displaced fractures through the distal shaft are difficult to reduce and maintain in a reduced position. These may be associated with delayed healing.
Long Spiral Fractures: These include spiral, comminuted, and oblique fractures, which tend to heal rapidly.
Potential Issues:
Muscle Interposition: If a displaced fracture has a gap that does not close when rotational alignment is restored, muscle tissue may be trapped between fragments.
Atrophic Nonunion: If there is good alignment but a significant gap remains between fracture fragments, the injury will likely develop into an atrophic nonunion.
Proximal Humeral Fracture
Anatomical Neck Fracture:
The fracture plane passes through the anatomical neck rather than the surgical neck.
Significant chondral defects and minimally separated fragments may not be visible on plain films.
There is a much higher incidence of Avascular Necrosis (AVN) compared to surgical neck fractures.
Even if soft tissue is detached from the humeral head, undisturbed blood supply transmitted through the tuberosities may prevent osteonecrosis of the articular segment.
Surgical Neck Fracture:
The most common type of fracture of the proximal humerus.
It is extracapsular and usually maintains an adequate blood supply, resulting in a relatively low incidence of AVN.
Deformity: The upper fragment is usually abducted and externally rotated by muscles inserting onto the greater tubercle. The lower fragment is adducted and internally rotated by the internal rotator muscles.
Greater Tuberosity (GT) Fractures:
Commonly associated with anterior shoulder dislocations.
Isolated, displaced GT fractures account for less than of proximal humeral fractures.
Displaced fractures of the GT are associated with longitudinal rotator cuff tears.
Hill-Sachs Lesion:
The magnitude of a fracture defect in the humeral head can be over-estimated if a Hill-Sachs lesion is present but unrecognized.
Definition: A fracture in the posterolateral head of the humerus caused by impaction against the glenoid rim.