Non-traumatic Diseases of the Canine Stifle
World Small Animal Veterinary Association Congress Proceedings, 2016
Samantha Woods, BSc, MA, VetMB, CertSAS, DECVS, MRCVS
Royal (Dick) School of Veterinary Studies, Easter Bush Veterinary Centre, University Of Edinburgh, Roslin, Midlothian, UK


The stifle joint is a complex joint that is frequently affected by non-traumatic disease. Cranial cruciate ligament disease or rupture is the most common cause of pelvic limb lameness in the dog; patellar luxation is also commonly seen in practice and causes varied degrees of lameness and disability. Osteochondrosis/osteochondritis dissecans is a less common but nonetheless debilitating condition seen. All these conditions lead to the development of secondary osteoarthritis and early surgical treatment of these conditions is recommended to ameliorate progression of this debilitating condition.

Cranial Cruciate Ligament Disease (CCLD)

CCLD is the most common cause of pelvic limb lameness in the dog. Whilst avulsion injuries of the cranial cruciate ligament (CrCL) and acute traumatic rupture are reported, the most common cause is progressive degeneration of the CrCL. The cause is still unknown and a multifactorial aetiology is implicated.

Large and giant-breed dogs are most commonly affected with no sex predisposition. Neutered dogs have a higher prevalence of CCLD1,2 and smaller dogs are affected later in life than larger dogs.2 In one study of Labrador retrievers 50% of dogs ruptured their contralateral ligament within 5.5 months of the first.3

Physical examination identifies lameness and pain associated with stifle manipulation, especially on extension. Crepitus and a click may be palpable if meniscal pathology is present. A medial buttress of periarticular hypertrophy is often identified. Stifle effusion is palpable and is the most consistent radiographic finding. Arthrocentesis identifies degenerative cytology. Radiographs often identify concurrent stifle osteoarthritic change. Laxity in cranial drawer and cranial tibial thrust are the mainstays of diagnosis. If the tear is only partial the laxity may not be evident.

There are a plethora of treatments available for treatment of CCLD in dogs.

 Extracapsular stabilization

 Lateral fabellotibial suture


 Fibular head transposition

 Intra-articular reconstruction

 Osteotomy procedures

 Cranial tibial closing wedge ostectomy (CCWO)

 Tibial plateau leveling osteotomy (TPLO)

 Combined TPLO/CCWO

 Tibial tuberosity advancement

 Triple tibial osteotomy

 CORA based levelling osteotomy

Breed, age, tibial plateau angle, expertise, patient factors, owner compliance and cost should all be taken into account when making a surgical decision.

Despite the multiple surgical techniques available, the published literature suggests 85–90% of surgically treated dogs have good to excellent function at follow-up, regardless of stabilisation technique. In studies comparing extracapsular suture with intracapsular stabilization and TPLO, at 2 and 6 months postoperatively, there was no significant difference in peak vertical force between the extracapsular and TPLO treated dogs. The intracapsular dogs had lower ground reaction forces suggesting reduced weight-bearing.4 In another study of extracapsular technique versus TPLO, the TPLO patients had improved kinematics and owner satisfaction at one year postoperatively.5 A systematic review of the literature identified TPLO as providing superior functional recovery in patients when compared to the extracapsular tibio-fabellar suture although there was not enough data to compare other techniques.6 In general, large-breed dogs and dogs with bilateral disease or other orthopaedic pathology perform better with osteotomy procedures due to earlier weight-bearing on the operated limb.

Osteochondrosis (OC)

Osteochondrosis is a developmental disorder of articular cartilage caused by a failure of normal endochondral ossification. Cartilage in affected zones is thicker, receives less nutrition from the synovial fluid and is less tolerant of biomechanical loading. The deeper zones of the cartilage can become necrotic, leading to fissure formation and development of a detached flap of cartilage - osteochondritis dissecans (OCD). The aetiopathogenesis of OC is unknown although conditions where rapid growth and excessive weight gain occur seem to be implicated.

Osteochondrosis of the stifle is less common than that of the shoulder, elbow and hock. The lesion is usually identified on the medial aspect of the lateral femoral condyle. It is more prevalent in large and giant-breed dogs between 5–9 months of age7 and a male sex predisposition is reported.

Dogs with OC/OCD normally present with pelvic limb lameness of insidious onset. The lameness is variable and can be aggravated by mild trauma and exercise. Joint effusion is usually present and crepitus, stifle pain, resistance to joint manipulation and muscle atrophy may be noted on examination.

Radiography or computed tomography are required to make the diagnosis with flattening of the articular surface and subchondral sclerosis being the most consistent findings. Joint effusion, joint mice and osteophytosis consistent with osteoarthritis are often seen. Imaging of the contralateral limb is advised since the condition is frequently bilateral.

Whilst lesions identified as incidental findings may be managed conservatively, surgery is usually recommended. The surgical approach is via arthroscopy or lateral or medial parapatellar arthrotomy. The aim of treatment is to excise pathologic cartilage, perform curettage of the subchondral bone to optimise fibrocartilaginous infilling of the defect and to lavage the joint. Joint resurfacing techniques using autogenous osteochondral graft (OATS) or synthetic implants have been reported.8

Following debridement of the defect dogs are rested for at least two weeks and gradually returned to normal exercise levels. The prognosis for dogs undergoing traditional surgical treatment for large lesions on the weight-bearing surface of the joint is guarded to fair. This is due to the loss of articular cartilage and normal joint congruity leading to abnormal joint biomechanics and progression to secondary osteoarthritis. Autogenous osteochondral grafting techniques report more favourable outcomes with significant improvements in lameness and quality of life.8

Patellar Luxation

Non-traumatic patellar luxations are generally linked to conformational abnormalities and can be multifactorial in aetiology. The patella is a sesamoid in the tendon of insertion of the quadriceps femoris muscle. It sits in the trochlear groove of the distal femur to improve efficiency of the quadriceps muscle group and facilitate stifle extension. The extensor mechanism of the stifle joint consists of the quadriceps, patella, femoral trochlea, straight patellar ligament and tibial tuberosity and in normal dogs these should be in alignment all the way from the proximal femur to the hock. Malalignment of this extensor mechanism leads to luxation of the patella and contributes to reluxation in treated cases.

In the majority of patients, patellar luxation is not present at birth but develops because of a congenital anatomic abnormality. In small breed dogs various changes are identified including angular deformities of the femur and tibia leading to "genu varum" or a bow-legged stance and hypoplasia of the trochlear groove occurs due to a lack of patella contact during growth and development. These changes are heritable so affected patients should not be bred.

In small and toy breed dogs >95% luxations are medial and the condition is commonly bilateral.9 The degree of luxation leads to varied clinical signs. Patients with grade 1 luxations usually don't have obvious lameness whilst bilateral grade 4 luxations can lead to significant debilitation.

Diagnosis involves physical evaluation and palpation of the patella during stifle manipulation. The direction of luxation and the height of the patella within the trochlea ridge should be assessed (patella alta or baja). Cranial drawer and stifle stability should be evaluated in case of concurrent CCLD. Radiographs assist in diagnostic planning and identification of the amount of secondary change within the joint. If severe distal femoral abnormalities are present CT scan with 3-D reconstruction may be required for full assessment.

Treatment should be individualised to each patient and all abnormalities identified on evaluation should be addressed. The majority of cases require a combination of treatments with the most common being:

 Trochleoplasty - sulcoplasty, chondroplasty or wedge/ block recession

 Tibial tuberosity transposition - to realign the quadriceps mechanism

 Soft tissue reconstructive techniques - capsular imbrication and retinacular release

In cases of severe deformities of the distal femur or proximal tibia, the combination of surgical techniques listed above may be inadequate to realign the extensor mechanism. In these cases distal femoral osteotomy or corrective osteotomy of the tibia may be required.

Lateral luxations are uncommon but do occur in some small and large breed dogs. The aetiology behind this condition is also unknown but in these cases genu valgum or "knock-knees" are often present. Lateral patellar luxation, especially when severe limb deformities are present is challenging to treat and may require femoral and/or tibial corrective osteotomies.

Most cases of medial patellar luxation do well clinically unless aggressive secondary change is already evident at surgery. The main complication is reluxation of the patella although if this does occur it is usually to a lower grade. Osteoarthritis will develop in all cases. Lateral luxations in large breed dogs carry a more guarded prognosis with complication rates and risk of reluxation being higher for dogs >20 kg.10


1.  Duval JM, Budsberg SC, Flo GL, Sammarco JL. Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet Med Assoc. 1999;215:811–814.

2.  Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc. 1993;203:1016–1019.

3.  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.

4.  Conzemius MG, Evans RB, Besancon MF, Gordon WJ, Horstman CL, Hoefle WD, Nieves MA, Wagner SD. Effect of surgical technique on limb function after surgery for rupture of the cranial cruciate ligament in dogs. J Am Vet Med Assoc. 2005;226:232–236.

5.  Gordon-Evans WJ, Griffon DJ, Bub CJ, Knap KM, Sullivan M, Evans RB. Comparison of lateral fabellar suture and tibial plateau levelling osteotomy techniques for treatment of dogs with cranial cruciate ligament disease. J Am Vet Med Assoc. 2013;243:675–680.

6.  Bergh MS, Sullivan C, Ferrell CL, Troy J, Budsberg SC. Systematic review of surgical treatments for cranial cruciate ligament disease in dogs. J Am Anim Hosp Assoc. 2014;50:315–321.

7.  Montgomery RD, Henderson RA, Milton JL, et al. Osteochondritis dissecans of the canine stifle. Compend Contin Educ Pract Vet. 1989;11:1199.

8.  Cook JL, Hudson CC, Kuroki K. Autogenous osteochondral grafting for treatment of stifle osteochondrosis in dogs. Vet Surg. 2008;37:311.

9.  Hayes AG, Boudrieau RJ, Hungerford LL. Frequency and distribution of medial and lateral patellar luxation in dogs: 124 cases (1982–1992). J Am Vet Med Assoc. 1994; 205:716.

10. Arthurs GI, Langley-Hobbs SJ. Patellar luxation as a complication of surgical intervention for the management of cranial cruciate ligament rupture in dogs. Vet Surg. 2006;35:559.


Speaker Information
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Samantha Woods, BSc, MA, VetMB, CertSAS, DECVS, MRCVS
Royal (Dick) School of Veterinary Studies
Easter Bush Veterinary Centre
University of Edinburgh
Roslin, Midlothian, UK

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