Rico Vannini graduated 1981 from the University of Zürich. 1987 he completed his surgical residency at The Ohio State University. For nine years he was faculty surgeon and lecturer at the University of Zürich. 1994 he became Diplomate of the European College of Veterinary Surgeons. Since 1996 he is owner of Bessy's small animal clinic, one of the largest private clinics in Switzerland. He was president of AO and ESVOT. He maintains an active interest in continuing education among others being international speaker and international chairmen of the Education Commission of AOVET. His hobbies are agility, scuba diving and cooking. He is mobile cash machine for two young adults, master of 8 dogs and food provider of a cat.
Failure of the anterior cruciate ligament is a very common orthopedic problem in dogs and one of the most important causes for pain and lameness in the hind limb. There are basically two pathways leading to failure of the anterior cruciate ligament: either the ligament is healthy but traumatized by forces that exceed the normal holding strength of a normal ligament or the ligament is already weakened and therefore unable to withstand normal load bearing. Minor trauma will cause its failure.
In contrast to humans and cats, ligament rupture caused by severe trauma is rare in dogs. Lameness is acute and there is always a history of severe trauma. On radiographs theses stifles look otherwise healthy (i.e., there are usually no signs of osteoarthritis). It is important to recognize the traumatic cases as concurrent injuries of the other stifle ligaments are likely. The medial collateral ligament acts synergistic with the ACL and can also be injured. It is also possible that the ACL has only been sprained or partially torn by trauma. These cases usually do not need any surgery. If there is a full tear, make sure the drawer sign is associated with cranial instability to rule out a caudal cruciate ligament injury. Caudal cruciate ligament ruptures are rare but usually caused by trauma. Again, these dogs usually do not need surgery.
Most common in the dog is the 2nd scenario: the ligament tears, because it is already damaged and weakened. The exact cause leading to the degeneration/deterioration of the ligament is difficult to diagnose in most cases.
There are two possible reasons leading to the degeneration of the ligament:
1. Primary degeneration of the ligament itself.
2. Secondary degeneration of the ligament due to chronic overloading or repetitive injury.
Histological studies have shown that the cruciate ligament of juvenile dogs is well vascularized and interspersed with many blood vessels. After one year, these blood vessels disappear and only a single, central blood vessel is found at most. Often there were no blood vessels found anymore at all. Only ligamentocytes in the margins of the ligament seemed to be adequately nourished by synovial fluid and/or capillaries from the synovial envelope of the ligament.5 It has been suggested, that due to the lack of blood supply, the ligament loses its ability to regenerate. Vasseur and Pool demonstrated in their classical study of torn ligaments, that there were not only signs of degeneration, but also many signs of unsuccessful attempts of healing.6
Recently however evidence is increasing that there are also many mechanical factors that lead to a direct overload or abnormal wear of the ligament. These factors include obesity, muscle weakness (the quadriceps apparatus protects the ACL), as well as congenital or acquired articular or bony malformations such as a steep tibia plateau slope, an intercondylar stenosis or a patella luxation.1 These causes can be referred in a broader sense to stifle dysplasia. It is therefore not surprising, that a third of the dogs having and ACL tear, are also suffering from ACL disease of the opposite leg.
Regardless of the exact cause, weakening of the ACL progresses usually for months until it tears completely. Therefore, most dogs have a history of a chronic lameness. Initially, only a slight lameness for the first few steps after rest is observed. Then they start to avoid maximal flexion of the stifle while sitting. Thus they rotate the affected leg outward while sitting. As the disease progresses the lameness is getting worse. On palpation, the knee feels thickened medially and painful on palpation. Hyperextension usually hurts. In the early stage of the disease (early partial tear) no or only minimal instability, i.e., drawer sign, can be detected. The tibia compression test is negative. Later signs of increased instability can be detected but there is still an end feel on drawer testing (partial tear). Always check the healthy stifle for comparison.
On radiographs signs of osteoarthritis and joint effusion can be detected.
Typically, these dogs respond only temporarily to conservative treatment with non-steroidal antiinflammatory drugs. After giving NSAIDs, the problems show up again.
The goal of treatment in the early stage of cruciate disease should be to stop further tearing of the ligament in order to maintain its functions.
The anterior cruciate ligament has several important functions:
1. It is an important stabilizer of the joint. It counteracts the cranial tibial thrust and prevents the drawer motion of the tibia. It limits hyperextension of the knee and acts synergistically with the medial collateral ligament.
2. It controls the joint kinematics. Together with the other ligaments it induces the classic roll-gliding motion of the femoral condyles during flexion and extension of the knee in relation to the tibia plateau.
3. It converts the forward thrust of the tibia ("cranial tibia thrust") into extension forces.
4. It has proprioceptive, mechanoreceptive and nociceptive nerve fibers and protects the joint from overloading.1
5. It protects the medial meniscus. Meniscal lesions are very rare in dogs with intact ACL.
Preservation of these functions will have an impact on the prognosis for the affected stifle. In order to preserve these functions, the ligament has to be unloaded and protected from further tearing.
The classical surgical techniques such as a lateral suture cannot sufficient unload the ACL as it is still much stronger than any suture. The ACL remains the primary stabilizer and is further loaded until it is fully torn. Thus, it remains a source of irritation, inflammation and pain.
This seems to be different with the high tibia osteotomies such as TPLO, TTA, etc.
Studies have shown that at least TPLO is highly successful to protect the ACL from further tearing.3,6 So far this has not been shown for TTA.
There seems to be at least one situation, in which a TPLO alone may not be sufficient to prevent further tearing: these are dogs suffering from an intercondylar stenosis. In these cases there is not enough room for the ACL and the inner edge of the lateral condyle entraps the ACL and rubs directly against it. Consider an intercondylar stenosis as a cause of ACL disease, if the extension of the knee joint is diminished compared to the healthy side. In these cases a notch sulcoplasty is needed to create room for the ACL, together with a TPLO.
Cruciate ligament rupture in most dogs is the result of a chronic degenerative disease. The exact cause of the ligament degeneration can rarely be determined, thus an etiologic therapy is difficult. However, high tibia osteotomies such as the TPLO are able to unload and protect the ACL sufficiently and to stop a further tearing of the ligament. With this important functions of the ACL can be preserved. It is obvious: the earlier in the course of the disease the surgery is done the better is the prognosis. As every third dog will tear its ACL of the opposite leg to a later time, a proactive approach is highly recommended.
1. Comerford EJ, Tarlton JF, Avery NC, Bailey AJ, Innes JF. Distal femoral intercondylar notch dimensions and their relationship to composition and metabolism of the canine anterior cruciate ligament. Osteoarthritis Cartilage. 2006;14(3):273–278. Epub 2005 Oct 20.
2. Halata Z, Wagner C, Baumann KI. Sensory nerve endings in the anterior cruciate ligament (lig. cruciatum anterius) of sheep. Anat Rec. 1999;254(1):13–21.
3. Hulse D. Second look arthroscopic findings after tibial plateau leveling osteotomy. Vet Surg. 2010;39(3):350–354.
4. Murray MM, Martin SD, Martin TL, Spector M. Histologic changes in the human anterior cruciate ligament after rupture. J Bone Joint Surg Am. 2000;82-A(10):1387–1397.
5. Pool R. Personal communications.
6. Vannini R. Partial ACL tears - can the ligament be saved by TPLO. In: ESVOT meeting. Venice; 2014. Abstract.
7. Vasser PB, Pool RR, Arnosky SP, Lau RE. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res. 1985;46(9):1842–1854.