Changing Views On CCL Repair

Cranial cruciate ligament (CCL) injury in dogs is big business. In 2003, the cost of treatment for CCL ruptures in dogs exceeded $1.32 billion.

Cranial cruciate ligament (CCL) injury in dogs is big business. In 2003, the cost of treatment for CCL ruptures in dogs exceeded $1.32 billion.1

However, even in human medicine, “No studies have shown that ACL (anterior cruciate ligament) reconstruction restores dynamic knee stability or enables full return to preinjury activity level in all subjects.”2

Similarly, in a 2005 report in Veterinary Surgery, Aragon and Budsberg noted: “In reviewing the evidence currently available, there is no single surgical procedure that has enough data to suggest a potential for long-term success in terms of return to normal function, prevention of osteoarthritis or any claim of superiority to other surgical techniques. Subjectively, popular opinion on the short-term recovery and function favors the TPLO (tibial plateau leveling osteotomy). However, a recent study evaluated the outcome of surgical techniques on limb function. … The authors concluded at the two- and six-month postoperative evaluations that the lateral suture stabilization technique and TPLO were statistically similar. … Given the overall lack of convincing data available, it is impossible to favor one procedure (TPLO, extracapsular suture stabilization, fibular head transposition, intracapsular ligament replacement) over another at this time.”3

Furthermore, research into the etiopathogenesis of CCL rupture is destabilizing the dogma that wayward biomechanics bear the brunt of the blame. 

Instead of focusing on altering bony relationships by cutting and repositioning them, practitioners may in the future direct their efforts at controlling inflammation and immune dysregulation, the newest suspects in ligament laxity.4-6 Research on its mechanistic origin is pointing toward the intrinsic and gradual degradation of the ligamentous matrix via matrix metalloproteinases and inflammatory mediators over a sudden traumatic episode.7

With this in mind, the prospect of maintaining CCL integrity through diet, exercise, weight loss and other preventive medicine methods gains prominence.

Some food manufacturers are making strides in this regard by eliminating pro-inflammatory substrates such as corn and corn byproducts and by adding antioxidants and anti-inflammatory fatty acids. Inflammation-reducing herbs such as bromelain, boswellia, turmeric and others could be integrated into the diet or provided as a supplement. Even weight loss for obese dogs confers anti-inflammatory benefit.8

Prolotherapy

Without a doubt, the most compelling nonsurgical option about which clients ask most frequently9 is prolotherapy. Prolotherapists typically inject sclerosing or proliferant solutions into or around joints to strengthen lax ligaments.10

Also referred to as regenerative injection therapy, or RIT, the scope of prolotherapy is expanding to include the injection of growth factors or growth factor stimulants that induce regeneration or repair of normal cells or tissues.11 In vivo studies have provided strong evidence that prolotherapy leads to ligament proliferation, thickening and improved tensile strength. 

By reducing mechanical instability and abnormally excessive forces on ligaments, tendons and joint capsules, prolotherapy also reduces nociceptive stimuli emitted from these tissues and ultimately lessens pain. Studies testing prolotherapy for ACL laxity show short and long-term improvement in pain during walking, swelling, flexion and objectively measured ACL laxity.12-13 Further investigation in dogs with high-quality randomized controlled trials seems warranted.

Osteoarthritis

Despite improvements in joint function and stability even with surgery, osteoarthritis often sets in.14 Efforts to limit its progression may involve the administration of chonrdroprotectants. Polysulfated glycosamin-oglycan may inhibit the progression of OA in canine stifles by maintaining chondrocyte viability and protecting against extracellular matrix degradation.15 Orally administered chondroitin sulfate, glucosamine hydrocholoride and manganese ascorbate may modulate the metabolism within the articular cartilage matrix as well.16

Several other integrative pain and rehabilitation methods are similarly taking hold.

Low-level laser therapy for the treatment of soft tissues in and around joints has expanded in recent years.17-18

Pain relief and functional restoration with massage, acupuncture and therapeutic exercise are gaining acceptance. 

Hydrotherapy and underwater treadmill exercise have become wildly popular in recent years, but the risks of overexuberant rehabilitation offset their value in some cases.

Individualized Rehab

While protocol-driven rehabilitation interventions offer the allure of rapid training and implementation, its assembly-line-style implementation sacrifices careful and astute attention to the individual’s biomechanical, cardiovascular and neurologic capabilities in favor of high patient numbers. Instead, a cogently designed, patient-driven format optimized for stabilization and strengthening in light of each patient’s functional demands and unique abilities and limitations will reduce the potential for injury, relapse and pain while maximizing outcomes.19

Certain Chinese herbal prescriptions have been found effective in reducing swelling, pain and joint restriction. A 2005 study on the value of a Chinese herbal preparation designed to improve the strength of previously injured ligamentous tissues demonstrated value even when applied externally, echoing the results of similar reports both from herbal plasters and ingested compounds.20

If change truly comes from within, then modifying the internal milieu by providing reparative biochemical factors through plants, foods, light, regenerative injections and mechanical stimuli may together form a viable alternative to surgical intervention in some cases.21

Deciding which patients qualify as suitable candidates for nonsurgical rehabilitation may be the first step, and randomized, controlled trials comparing outcomes over the long term, the second.

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FOOTNOTES:

1. 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(10):1604-1607.

2. Moksnes H, Snyder-Mackler L, and Risberg MA.  Individuals with an anterior cruciate ligament-deficient knee classified as noncopers may be candidates for nonsurgical rehabilitation.  Journal of Orthopaedic & Sports Physical Therapy.  2008;38(10):586-595.

3. Aragon CL and Budsberg SC.  Applications of evidence-based medicine:  cranial cruciate ligament injury repair in dogs.  Veterinary Surgery.  2005;34:93-98.

4.  Fujita Y, Hara Y, Nezu Y, et al.  Proinflammatory cytokine activities, matrix metalloproteinase-3 activity, and sulfated glycosaminoglycan content in synovial fluid of dogs with naturally acquired cranial cruciate ligament rupture.  Veterinary Surgery.  2006;35:369-376.

5. Muir P, Manley PA, and Hao Z. COL-3 inhibition of collagen fragmentation in ruptured cranial cruciate ligament explants from dogs with stifle arthritis.  The Veterinary Journal.  2007;174:403-406.

6. Barrett JG, Hao Z, Graf BK, et. al. 

7. Krayer M, Rytz U, Oevermann A, et al. Apoptosis of ligamentous cells of the cranial cruciate ligament from stable stifle joints of dogs with partial cranial cruciate ligament rupture.  Am J Vet Res.  2008;69:625-630.

8. Yamka RM, Friesen KG, and Frantz NZ. Identification of canine markers related to obesity and the effects of weight loss on the markers of interest.  Intern J Appl Res Vet Med.  2006;4(4):282-292.

9. Author’s experience.

10-12. Kim SR, Stitik TP, Foye PM, et al.  Critical review of prolotherapy for osteoarthritis, low back pain, and other musculoskeletal conditions:  a physiatric perspective.  Am J Phys Med Rehabil.  2004;83:379-389.

13. Reeves KD and Hassanein KM.  Long term effects of dextrose prolotherapy for anterior cruciate ligament laxity.  Alternative Therapies.  2003;9(3):52-56.

14. Johnson KA, Hulse DA, Hart RC, et al.  Effects of an orally administered mixture of chondroitin sulfate, glucosamine hydrochloride and manganese ascorbate on synovial fluid chondroitin sulfate 3B3 and 7D4 epitope in a canine cruciate ligament transaction model of osteoarthritis.  OsteoArthritis and Cartilage.  2001; 9:14-21.

15. Sevalla K, Todhunter RJ, Vernier-Singer M, and Budsberg SC.  Effect of polysulfated glycosaminoglycan on DNA content and proteoglycan metabolism in normal and osteoarthritic canine articular cartilage explants.  Veterinary Surgery.  2000;29:407-414.

16. Johnson KA, Hulse DA, Hart RC, et al.  Effects of an orally administered mixture of chondroitin sulfate, glucosamine hydrochloride and manganese ascorbate on synovial fluid chondroitin sulfate 3B3 and 7D4 epitope in a canine cruciate ligament transaction model of osteoarthritis.  OsteoArthritis and Cartilage.  2001; 9:14-21.

17. Fung DTC, Ng GYF, Leung MCP, and Tay DKC.  Therapeutic low energy laser improves the mechanical strength of repairing medial collateral ligament.  Lasers Surg Med.  2002;31:91-96.

18. Khan AS, Sherman OH, and DeLay B.  Thermal treatment of anterior cruciate ligament injury and laxity with its imaging characteristics.  Clin Sports Med.  2002;21:701-711.

19. Andersson C, Odensten M, and Gillquist J.  Treatment of acute rupture of the anterior cruciate ligament:  a randomized study with a long-term follow-up period.  Clinical Orthopaedics and Related Research.  1991;264:255-263.

20. Fung DTC and Ng GYF.  Herbal remedies improve the strength of repairing ligament in a rat model.  Phytomedicine.  2005;12(1-2):  93-99.

21. Canapp SO.  The canine stifle.  Clinical Techniques in Small Animal Practice.  2007;22:195-205.

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