Canine Cranial Cruciate Disease: Updating Our Knowledge about Pathogenesis & Diagnosis

James K. Roush, DVM, MS, Diplomate ACVS

Cranial cruciate ligament rupture is not only the most common cause of hindlimb lameness in dogs, it is also the most common misdiagnosed or overlooked cause of canine lameness. This article addresses pathogenesis and diagnosis in a handy question and answer format; a future article will discuss the latest innovations in therapy.

Cranial cruciate ligament rupture (CrCLR) is the most common cause of hindlimb lameness in dogs and, in my experience, the most common misdiagnosed or overlooked cause of canine lameness. Of 369 dogs referred to a teaching hospital for treatment of hip dysplasia, 32% had CrCLR as the primary cause of hindlimb lameness.¹

In most dogs, undiagnosed or untreated CrCLR results in rapid advancement of osteoarthritis (OA). Radiographs taken within 6 weeks of acute cruciate rupture often display signs of OA, including peripatellar and peritrochlear osteophytes, joint effusion, and joint space collapse. Timely, accurate diagnosis and treatment of CrCLRs are likely very important to minimize progression of OA and optimize surgical outcomes.²

DIAGNOSIS OF CRANIAL CRUCIATE DISEASE

Why Is CrCLR Underdiagnosed So Frequently?

Veterinary school instruction has traditionally emphasized teaching subtle and difficult manipulative physical examination procedures, such as cranial drawer sign and cranial tibial thrust, to definitively diagnose CrCLR. Cranial tibial thrust is the stifle vector force created by the dog when weight-bearing, which results in cranial translation of the tibia with each step in a dog with CrCLR. The correct performance of either test is a learned skill, mastered only after much experience and practice on healthy dogs as well as those with partial or complete CrCLRs.

Immature dogs are often misdiagnosed with CrCLR because they have greater than expected cranial drawer sign due to normal puppy laxity. Lameness in immature dogs is rarely due to CrCLR because young ligaments are often stronger than bone physes and fracture occurs first. CrCLR can occur in young dogs but the history usually includes severe trauma, such as vehicular trauma.
Even with 25 years of experience as a veterinary orthopedic surgeon, I would estimate that examination with the cranial drawer sign or tibial thrust allows me to diagnose CrCLR in only about 80% of the dogs that subsequently undergo surgery, even though virtually 100% of these dogs have visible cruciate damage at arthrotomy.

How Can Clinical Detection Be Improved?

Hindlimb Lameness. A diagnosis of CrCLR should be considered in any dog with hindlimb lameness until proven otherwise. This is due to the fact that a high percentage of hindlimb lameness in dogs is caused by CrCLR, especially in patients with recent or sudden development or worsening of hindlimb lameness.

Extension & Range of Motion. Dogs with CrCLR often show pain during extension of the hip: it is a common error to inadvertently extend the stifle while extending the hip, resulting in stifle pain misattributed as hip pain. On the other hand, many dogs with CrCLR are not overtly painful during non–weight-bearing stifle range of motion or palpation, further complicating lameness localization.

Medial Buttress Sign. All veterinarians should learn and recognize the appearance of the medial buttress sign. Shortly after CrCLR, most, if not all patients, develop a distinct, firm swelling over the proximo-medial tibia in the region of insertion of the medial collateral ligament (Figure 1).

Is a reliable clinical sign of cruciate rupturePalpation of a medial buttress over the proximal tibia of the affected leg:

• Occurs rapidly after ligament rupture in most dogs
• Provides ample indication for surgical joint exploration even in the absence of a cranial drawer sign.

Figure 1. Medial buttress is a firm swelling palpable on the medial aspect of the proximal tibia; presence of medial buttress is a characteristic clinical sign of CrCLR.

This swelling can be best detected by simultaneously palpating the medial tibial plateau of both hindlimbs, comparing the swelling of the lame limb to lack of swelling in the normal limb. My preference is to position myself at the caudal aspect of a standing dog, with my hands simultaneously wrapped around from the cranial to the medial aspect of both hindlimbs (Figure 2).

Figure 2. To evaluate medial buttress, the dog should be standing and the examiner should simultaneously reach around the cranial aspect of both stifles and palpate the proximal-medial tibia.

In patients with suspected bilateral CrCLR, remain aware that a bilateral medial buttress will be present and must be considered during diagnosis.

What Role Does Radiography Play in Diagnosis?

On orthogonal stifle radiographs, the following findings are highly suggestive of CrCLR (Figure 3):

• Joint effusion (characterized by compression of infrapatellar fat pad)

• Peripatellar or peritrochlear osteophyte formation.

Figure 3. Radiographic signs of stifle OA secondary to CrCLR include periarticular osteophytes on the patella (white arrows) and trochlear ridge (green arrow) and a compressed infrapatellar fat pad (circled). These radiographic signs strongly suggest stifle instability in dogs without other evidence of septic arthritis or visible trauma.

Either finding alone is sufficient indication for joint arthrocentesis, arthroscopy, or arthrotomy for further diagnosis and treatment.

Increasing severity of radiographic signs of OA is an even stronger indication for further diagnostic attention and treatment. Other less frequent causes of joint pathology, such as septic arthritis, distal femoral osteochondritis dissecans, or chronic fracture, can cause similar radiographic changes; however, their relative rarity and differing clinical histories make inadvertent surgery of these conditions unlikely.

Severity of OA is not of value in treatment determinations because OA scores are not related to kinetic gait parameters and lameness in dogs.⁴

PATHOGENESIS OF CRANIAL CRUCIATE DISEASE

Are Certain Breeds Predisposed to CrCLR? 

Our understanding of CrCLR remains a chicken-or-egg-first quandary. Recent information suggests that CrCLR disease is heritable as a recessive trait in certain breeds, such as Newfoundlands, in which there is an identified heritability index of 0.27.⁵

Bilateral CrCLR is present at initial diagnosis in up to 30% of large breed dogs presented for CrCLR. Bilateral disease in small breeds is much less frequent than in large breed dogs.

How Does a Rupture Develop?

In small breed dogs, CrCLR is often associated with long-standing patella luxation or acute trauma. In large breed dogs, CrCLR occurs as 2 distinct disease types:

1. A small percentage of large breed dogs acutely develop CrCLR, with no preexisting evidence of OA and often during strenuous activity in which the cruciate rupture occurs as a result of hyperextension and/or excessive strain on the cranial cruciate ligament.
2. The majority of large breed dogs, however, have preexisting radiographic OA at the time of complete CrCLR, suggesting that an unknown etiology causes slow degeneration of the ligament before functional failure occurs.

What Are the Risk Factors for CrCLR?

Risk factors for increased prevalence of cranial cruciate ligament (CCL) injury include:⁶

• Obesity
• Neutering

Degeneration of the CCL is associated with:⁷

• Aging
• Excessively straight hindlimb conformation
• Immune-mediated arthropathies.

In some studies^8,9 but not others,^10,11 degeneration of the CCL has also been associated with:

• Increased tibial plateau angle (TPA)
• Excessive patellar ligament-plateau angle.

How Likely Is Rupture of the Contralateral CCL?

In one study, 48% of Labrador retrievers ruptured the contralateral CCL within a median time of 5.5 months.¹² Therefore, it is prudent to warn owners of large breed dogs with unilateral CrCLR that these dogs have a high probability of contralateral CrCLR.

TPA is not a useful predictor of contralateral CrCLR in dogs with existing unilateral CrCLR.¹³ Consequently, any measures that decrease stress on the remaining intact ligaments are important therapy additions, including careful weight management of the patient and exercise restriction.

What Is the Focus of Current Research Efforts?

After CrCLR, there are:

• Increased matrix turnover with increased collagen and glycosaminoglycan synthesis¹⁴
• Increased matrix metalloproteinases and changes in proteinase location within the ligament and synovial membrane^15-17
• Histologic changes, including decreased typical fibroblasts and increased chondroid cells in the ruptured ligament core.¹⁸

A great degree of research effort has been directed at understanding and comparing changes in the extracellular matrix of ruptured ligaments and cytokines in stifles affected by CrCLR versus intact ligaments, but few findings have been relevant to prevention or treatment of ligament rupture.

Findings of recent in-depth summaries^19,20 on the pathogenesis of CCL disease and those of future studies may ultimately lead to better anti-inflammatory joint therapies and shed some light on disease progression and prevention. Surgical intervention after CrCLR will still be a necessary part of therapy for the foreseeable future.

State-of-the-art treatment considerations for CrCLR will be discussed in the second article in this series, Canine Cranial Cruciate Disease: Updating Our Knowledge about Therapy & Prognosis.

CCL = cranial cruciate ligament; CrCLR = cranial cruciate ligament rupture; OA = osteoarthritis; TPA = tibial plateau angle; TPLO = tibial plateau leveling osteotomy; TTA = tibial tuberosity advancement

References

1. Powers MY, Martinez SA, Lincoln JD, et al. Prevalence of cranial cruciate ligament rupture in a population of dogs with lameness previously attributed to hip dysplasia: 369 cases (1994-2003). JAVMA 2005; 227:1109-1111.
2. Hulse D, Beale B, Kerwin S. Second look arthroscopic findings after tibial plateau leveling osteotomy. Vet Surg 2010; 39:350-354.
3. Wilke VL, Robinson DA, Evans RB, et al. Estimate of the annual economic impact of treatment of cranial cruciate ligament injury in dogs in the United States. JAVMA 2005; 227:1604-1606.
4. Gordon WJ, Conzemius MG, Riedesel E, et al. The relationship between limb function and radiographic osteoarthrosis in dogs with stifle osteoarthrosis. Vet Surg 2003; 32:451-454.
5. Wilke VL, Conzemius MG, Kinghorn BP, et al. Inheritance of rupture of the cranial cruciate ligament in Newfoundlands. JAVMA 2006; 228:61-64.
6. Slauterbeck JR, Pankratz K, Xu KT, et al. Canine ovariohysterectomy and orchiectomy increases the prevalence of ACL injury. Clin Orthop Rel Res 2004; 429:301-305.
7. Shultz K. Diseases of the joints and stifle. In Fossum TW (ed): Small Animal Surgery, 3rd ed. Philadelphia: Mosby Elsevier, 2007, pp 1254-1300.
8. Wilke VL, Conzemius MG, Besancon MF, et al. Comparison of tibial plateau angle between clinically normal Greyhounds and Labrador Retrievers with and without rupture of the cranial cruciate ligament. JAVMA 2002; 221:1426-1429.
9. Schwandt CS, Bohorquez-Vanelli A, Tepic S, et al. Angle between the patellar ligament and tibial plateau in dogs with partial rupture of the cranial cruciate ligament. Am J Vet Res 2006; 67:1855-1860.
10. Reif U, Probst CW. Comparison of tibial plateau angles in normal and cranial cruciate deficient stifles of Labrador retrievers. Vet Surg 2003; 32(4):385-389.
11. Venzin C, Howard J, Rytz U, et al. Tibial plateau angles with and without cranial cruciate ligament rupture. Vet Comp Orthop Trauma 2004; 17:232-236.
12. Buote N, Fusco J, Radasch R. Age, tibial plateau angle, sex, and weight as risk factors for contralateral rupture of the cranial cruciate ligament in Labradors. Vet Surg 2009; 38:481-489.
13. Cabrera SY, Owen TJ, Mueller MG, Kass PH. Comparison of tibial plateau angles in dogs with unilateral versus bilateral cranial cruciate ligament rupture: 150 cases (2000-2006). JAVMA 2008; 232:889-892.
14. Comerford EJ, Innes JF, Tarlton JF, Bailey AJ. Investigation of the composition, turnover, and thermal properties of ruptured cranial cruciate ligaments in dogs. Am J Vet Res 2004; 65:1136-1141.
15. Muir P, Danova NA, Argyle DJ, et al. Collagenolytic protease expression in cranial cruciate ligament and stifle synovial fluid in dogs with cranial cruciate ligament rupture. Vet Surg 2005; 34:482-490.
16. Muir P, Schamberger GM, Manley PA, Hao Z. Localization of cathepsin K and tartrate-resistant acid phosphatase in synovium and cranial cruciate ligament in dogs with cruciate disease. Vet Surg 2005; 34:239-246.
17. Barrett JG, Hao Z, Graf BK, et al. Inflammatory changes in ruptured canine cranial and human anterior cruciate ligaments. Am J Vet Res 2005; 66:2073-2080.
18. Hayashi K, Frank JD, Dubinsky C, et al. Histologic changes in ruptured canine cranial cruciate ligament. Vet Surg 2003; 32:269-277.
19. Comerford EJ, Smith K, Hayashi K. Update on the aetiopathogenesis of cranine cranial cruciate ligament disease. Vet Comp Orthop Trauma 2011; 24:91-98.
20. Cook JL. Cranial cruciate ligament disease in dogs; biology versus biomechanics. Vet Surg 2010; 39:270-277.

James K. Roush, DVM, MS, Diplomate ACVS, is the Doughman Professor of Surgery at the Kansas State University College of Veterinary Medicine. Prior to his current position, he was a clinical instructor at the University of Wisconsin–Madison School of Veterinary Medicine. His research interests include osteoarthritis therapy, gait kinetics, and canine fracture healing. Dr. Roush received his DVM from Purdue University; then worked in private practice before completing a small animal surgical residency and MS degree from University of Wisconsin–Madison.