PLATES
1. How is plate strength determined?
Plate strength is defined by the formula BH3. B is the width; H is height (or thickness). Therefore, the rigidity (bending stiffness) of the plate is proportional to the thickness of the plate to the power of 3.
2. What different functions can a plate provide?
-
- Bridging: In a comminuted fracture, the plate can bridge the fragment to allow restoration of length, rotation and alignment.
- Buttress: Generally used in the periarticular region. When placed at the apex of the fracture, they prevent displacement of the fracture by shear forces.
- Compression: This can be achieved in several manners:
- A lag screw through the plate.
- An eccentrically placed screw through the hole of a dynamic compression plate (DCP). There is a potential of 1.8 mm of glide when two holes are compressed, producing up to 600N of compression.
- An external compression device, for example, a Verbrugge clamp or AO articulated compression device.
- Overbending the plate so there is a small gap between the plate and the bone at the level of the fracture will achieve compression of both the near and far cortex and produce absolute stability.
- Neutralisation: This protects a lag screw from torsional, shear and bending forces.
- Tension band: A plate may be placed on the tension side of the bone to act as a tension band. When the bone is loaded, the plate converts tension into compression at the far cortex.
3. What type of bone healing will occur when a lag screw and neutralisation plate has been used?
Where there has been anatomical reduction and interfragmentary compression, this can achieve absolute stability (no motion between fracture surfaces under functional load). This will lead to direct bone healing (also known as primary bone healing) if the gap between bony fragments is less than 0.01 mm and interfragmentary strain is less than 2%.
Under these conditions, cutting cones are formed at the ends of the osteons closest to the fracture site. The tips of the cutting cones consist of osteoclasts, which cross the fracture line, generating longitudinal cavities at a rate of 50–100 μm/day.
These cavities are filled with blood vessels and osteoblasts, which lay down lamellar bone in the form of new osteons. This process may take many months and is difficult to see on a radiograph due to the lack of callus formation.
4. What type of bone healing will occur when a plate is used as a bridging plate?
When a plate is used as a bridging plate, bone healing will take the form of indirect (secondary) bone healing. This same form of bone healing occurs with cast treatment, IM nails and external fixation. There are four stages.
Stage 1 – Haematoma and Inflammation – Week 1
Haematoma from the ruptured blood vessels forms a fibrin clot. The clotting cascade and complement system are both activated. Macrophages, neutrophils and platelets release several cytokines, including PDGF, TNF-Alpha, TGF-Beta, IL-1, 6, 10, and 12.
There is angiogenesis and recruitment of fibroblasts, mesenchymal cells and osteoprogenitor cells as the haematoma is replaced by granulation tissue, which can tolerate the greatest strain before failure. Necrotic bone ends are resorbed by osteoclasts and other devitalised tissue is removed by macrophages.
Stage 2 – Soft Callus – Weeks 2–4
The granulation tissue formed during stage 1 is replaced by fibrous tissue due to the action of fibroblasts and chondroblasts which lay down cartilage (type II collagen). The mechanical environment drives differentiation of either osteoblastic (stable environment) or chondryocytic (unstable environment) lineages of cells. Cartilage production provides provisional stabilisation.
Stage 3 – Hard Callus – 1–4 months
Soft callus is resorbed by chondroclasts and osteoblasts produce osteoid, which is then mineralised to form woven bone (hard callus). The conversion of soft callus to hard callus is called endochondral ossification.
Stage 4 – Remodelling – Up to several years
Once the fracture has united, the hard callus (woven bone) is replaced with hard, dense lamellar bone by a process of osteoclastic resorption followed by osteoblastic bone formation. This is the same process seen during routine skeletal turnover. The bone assumes a configuration and shape based on stresses acting upon it (Wolff’s law).
Electric fields may play a role in Wolff’s law. The compression side is electronegative and stimulates osteoblast formation; the tension side is electropositive and simulates osteoclasts.