Diagnosis:

Ruptured cranial cruciate ligament, which may be due to trauma / inconsistent exercise (chronic weight problem).

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The cranial cruciate ligament (CrCL) is a fibrous connective tissue that connects the femur to the tibia, and affords stability to the stifle joint.  Because the CrCL is within the (confined) joint space, its integrity and functionality is dependent upon conditions within the joint.   Unfavorable conditions may include effusion and inflammation, immune-mediated destruction of tissues, and direct trauma to the bone and/or supporting connective tissues. 


After the CrCL ruptured, increased joint laxity led to increased contact (excessive compressive forces) between the femur and tibia, resulting in changes to the layers of the articular cartilage.  These changes may be manifested by collagen and proteoglycan fragments released into the joint space.  The fragments are then phagocytized which initiates an inflammatory response.  The cartilage matrix responds to the loss of collagen by swelling.  Once the swelling occurs, a decreased capacity for force absorption is observed.


The pro-inflammatory mediators (cytokines TNF-alpha and IL-1beta, prostaglandins, etc.) are released by synoviocytes. In response to the inflammatory mediators, the synovial lining undergoes hypertrophy and hyperplasia, and is accompanied by increased synovial vasculature permeability.  Also, the inflammatory mediators attract neutrophils and monocytes to the joint space.  These inflammatory cells gain access to the joint space via the blood vessels lining the joint capsule, which explains the increased cell count in Bonnie's joint tap fluid.  RBC's may have also entered the joint space with the WBC's as a result of vascular leakage, however, iatrogenic hemorrhage (needle insertion), may also account for the reddish color of the modified transudate.  Synoviocytes themselves respond to the inflammatory mediators by increasing the production of low viscocity synovial fluid.  The subsynovial layer of the joint capsule will also thicken, due to activity of fibroblasts.  The body is attempting to stabilize the joint.  Distention of the joint capsule on either side of the patellar ligament was evident during physical exam.


Nociceptors, or pain receptors, are found within the subsynovial and fibrous layers of the joint capsule.  Increased joint fluid causes outward pressure on the joint capsule, to which nociceptors respond.  Also, inflammatory mediators further enhance the sensitivity of the pain receptors.  Bonnie's clinical presentation of having difficulty getting up and climbing stairs while still being able to ambulate with partial weight bearing once up correlates with pain response upon flexing the joint. Clinical signs of pain were not seen when Bonnie was walking, because she had the benefit of momentum, which allows the joint to stay in relative extension.


Obesity of an animal can predispose to degeneration / rupture of the CrCL.   While a sedentary lifestyle can decrease mechanical strength of the CrCL, Bonnie is obese despite her moderate activity.  The obesity may have contributed to an excessive force that led to breaking of the ligament during her activity.  In other words, hyperextension or excessive rotation of the stifle, in addition to the excessive weight load, may have led to rupture of Bonnie's CrCL.   


Age related changes, including loss of fibroblasts, loss of structural organization of collagen fibers and primary collagen bundles, destruction of the parallel ligament bundles and an increase in areolar tissue near the ligament's insertion are also known to contribute to decreased CrCL integrity.  These degenerative lesions may explain why 20-40% of dogs with unilateral CrCL suffer subsequent rupture of the opposite CrCL.  This may be a possibility with Bonnie, because she demonstrates a laxity in the right stifle (2mM), as well.  Although Bonnie is 6 years old and the owner reports regular exercise, some of these age-related changes may be contributing.

This is an acute rupture.  A lack of radiographic signs such as periosteal osteophyte formation along the trochlear ridge and caudal tibial plateau, subchondral bone sclerosis, narrowing of medial and/or lateral joint space, flattening of the articular surfaces, and valgus/varus deformities suggests that significant degenerative changes have not yet occurred for radiographic detection.  If left untreated, chronic instability and further degenerative changes would occur.

In summary, the role of the CrCL in maintaining the tibia in position explains the clinical findings of our case.  Excessive exercise, increased weight load, and age-related changes all may have predisposed to rupture of Bonnie's CrCL.  Once ruptured, abnormal movement of her tibia cranially, with respect to the femur, explains the cranial drawer sign.  CrCL rupture may also explain the difficulty Bonnie has with getting up and walking up stairs.