Juxta-articular fractures are fractures occurring near the joint surface. They may be intra- or extra-articular. Intra-articular
fractures include Salter III and IV fractures as well as humeral and femoral supracondylar fractures. Most juxta-articular
fractures occur in skeletally immature dogs. These fractures are challenging because of the short length of one of the bone
segments, the potentially small size of the bone, the relative softness of bone and because of the presence of articular surfaces
near the fracture site or involved in the fracture.
Juxta-Articular fractures are fractures result in the disruption of the articular cartilage, underlying subchondral bone and usually some portion of
the epiphyseal, metaphyseal or diaphyseal bone. These fractures can alter joint morphology immediately affecting joint stability,
cause pain, and disrupt the effective motion of the joint. Therefore, treatment of articular fractures is aimed at anatomic
reconstruction of the fracture and articular cartilage, rigid internal compression and stabilization of the fracture fragments
and early mobilization of the joint. The aims in treatment are to restore joint stability and congruity, to minimize degenerative
articular changes and maintain joint function.
Small bone fragment size either including or near the joint surface can limit methods of stable fixation. Recommendations
for plating of a fracture include at least 6 cortices on either side of the fracture site. Juxta-articular fractures are often
not amenable to conventional plating methods due to the small and inadequate number of screws that can be placed in the fracture
fragment and resultant tenuous fixation. The development of L-plates and T-plates changes the configuration and placement
of the screws in a fracture fragment allowing for increased screw placement and stability of the fracture fixation. These
plates still require a specific fracture configuration. Other alternatives for fixation include cross-pinning with k-wires,
and lag screw fixation. These repairs may also not result in a rigid fracture fixation. External skeletal fixation awards
the ability to place pins are wires at different angles to maximize purchase within a small fragment. External fixators can
be constructed in either a uniplanar, biplanar or bilateral fashion with connecting bars or free form when using epoxy connecting
bars. Circular external fixators using small transfixation wires require minimal fragment size for stabilization.
Despite appropriate reduction, stabilization of small fragments may not be adequate to allow weight bearing and joint motion
without adjunctive stabilization. This can be achieved with either external coaptation with splinting, rigid external skeletal
fixation or hinged transarticular external fixation. External coaptation is relatively unexpensive and can be atraumatic.
Downfalls of bandaging include weekly bandage changes, pressure sores from a slipped or inappropriately placed bandage, or
wounds secondary to a wet bandage. Rigid transarticular external fixation precludes the need for weekly bandage changes and
possible pressure sores, however, pin tract infections are a common sequelae to external fixators and diligent cleaning of
the pin tracts is required. Both rigid fixation and splinting prevent joint range of motion which is detrimental to the health
of the articular cartilage, joint range of motion, limb muscle mass and overall limb function. If adjunctive fixation is warranted,
hinged transarticular external skeletal fixation is the only means of protecting the primary repair while allowing range of
motion and ambulation.
Articular cartilage fractures result in disruption of the matrix and cellular components of hylaline cartilage. These changes can be irreversible. The
composition of hyaline cartilage does not incite spontaneous healing due to its complexity and inability for chondrocytes
to migrate to the site of injury, the overall low number of chondrocytes present within the hyaline cartilage matrix, and
the lack of vascularity of hyaline cartilage which results in an absence of an inflammatory response and induction of healing.
Although chondrocytes close to the site of injury will replicate and increase matrix formation, their response is limited
and insufficient to restore the defect to its pre-injury condition.
Defects in articular cartilage and damage to the underlying subchondral bone induces hematoma formation and a reparative matrix
produced by chondrocytes close to the site of injury and undifferentiated mesenchymal cells derived from the underlying bone.
The hematoma formation and resulting cellular infiltrate organizes into a fibrin clot apposing the cartilage wound edges.
This reparative fibrous tissue differs from the original cartilage in its predilection for cartilage type I collagen formation
rather than type II collagen formation found in hyaline cartilage. This fibrocartilage has ineffectual bonds between water
and the proteoglycans compared to the original hyaline cartilage, fibrocartilage lacks the mechanical properties and durability
of hyaline cartilage and will eventually degenerate.