Bhathal A. et al. 2017
Osteoarthritis is a slowly and debilitating disease affecting 20% of dogs of all breeds over the age of one year. The pain and reduced mobility arising, often have a negative impact on the dog’s quality of life and on dog-owner management. Large dogs can develop more serious clinical signs.
The etiology of the disease can result from a defective cartilage structure, inadequate cartilage biosynthesis, joint trauma and inflammatory mechanisms. The disease has symptoms such as pain, stiffness, lameness and disability. Non-pharmaceutical treatment options can include surgery, weight loss and physiotherapy. Standard therapy involves the use of non-steroidal anti-inflammatory drugs (NSAIDs). Other therapeutic options may include diacerein, corticosteroids and hyaluronic acid or other ingredients like glucosamin and chondrotin sulfate.
Glucosamine regulates collagen synthesis and is a mild anti-inflammatory, while chondroitin inhibits destructive enzymes in joint fluid and cartilage, both also contribute to the synthesis of glycosaminoglycans and proteoglycans.
At the moment there is no evidence that can confirm the inclusion levels for a therapeutic dose of glucosamine (known to have poor bioavailability) in dogs while a dose of chondroitin 15-30 mg/kg body weight has been suggested. A study shows that 10 to 20 times the amount of glucosamine and chondroitin is needed in vivo compared to in vitro studies to be biologically available. Besides appear to be needed from 2 to 6 weeks of somministration to have effect even if clinical supportive evidence is lacking.
Moreau et al. (2003) conducted a prospective, randomized, double-blinded study (some people involved in the study were prevented from knowing information that could have influenced the final result) on 71 owned dogs> 12 months and> 20 kg with lameness and signs radiographs of osteoarthritis, further divided into 4 groups.
In the 1) arm glucosamine HCl, chondroitin and magnesium ascorbate GCSM were given 2) carprofen 3) meloxicam 4) placebo. Primary outcomes included treatment efficacy, tolerability and ease of administration. The effectiveness was demonstrated objectively through tests of ground reaction force (GFR) and subjectively by the owner and orthopedist on day 0, 30 and 60. The GCSM arm and placebo showed no significant improvements. In contrast, both arms taking NSAIDs experienced significant improvements. Eight of 71 subjects were lost to follow-up. Statistical comparisons and treatment rankings were not provided.
McCarty et al. (2007) conducted a prospective, randomized, double-blinded study, which included 42 owned dogs (35 completed the study) who exhibited chronic lameness and pain stiffness. They were divided into 2 arms which received: 1) glucosamine HCl, chondroitin sulfate, N-acetyl_D-glucosamine, ascorbic acid and zinc sulphate 2) carprofen. They were analyzed through a subjective veterinary assessment on day 0, 14, 42, 70 and 98. The clinical parameters included scores for joint mobility, lameness, pain on palpation and scores for clinical conditions. The arm that has been treated with carprofen had shown statistically significant improvements around 70 days. The other arms showed improvements in pain on day 70 but lameness and joint mobility did not improve. The authors concluded that the therapies could be comparable to the 70 day.
The critical point of this study is that the randomization method was determined based on the (alternating) presentation order, plus the therapeutic efficacy scores were based on subjective assessments by the veterinarians. The 16.7% follow-up loss is to be considered high. The placebo arm was missing.
Gupta et al. (2012) conducted a prospective, randomized double-blinded study with approximately 31-37 owned dogs weighing> 20kg with moderate osteoarthritis.
The study was divided into four groups 1) glucosamine HCl and undenatured chondrotin sulfate and type II collagen (UCII) 2) glucosamine HCL and chondrotin sulfate 3) UCII 4) placebo. The results included therapeutic efficacy, tolerability and safety. The effectiveness was assessed objectively through force tests and current impulses with a clamp to evaluate the pain; subjectively through pain assessments on a monthly basis for 150 days. Liver, kidney and cardiac function, weight, temperature were also assessed. The placebo arm showed no change. Arm 2 showed a decrease in pain on day 90 with a peak of 150. The addition of UCII compared to the second did not provide any added value. The weak point of the study was the lack of a detailed history.
D ’Atlio et al. (2007) conducted a study on 20 owned dogs with joint stiffness, lameness, moderate pain, difficulty in movement. The groups were the same as in the study by Gupta et al. (2012). The study lasted 120 days with a 30 day interruption period. The results of D’atilio et al. (2007) differed from those of Gupta et al. (2012) or that the integration of UCII has brought benefits such as the reduction of pain even if this benefit was lost during the interruption of the 30 days. Medical history and follow-up were lacking.
In vitro studies suggest that the use of glucosamine and chondroitin have chondroprotective effects but no significant clinical improvements have been demonstrated.
Pascoe (2002) notes that despite the lack of clinical trials, 62% of the veterinarians interviewed believed they noticed improvements with the use of products containing glucosamine and chondroitin. Henrotin et al. (2005) claim that the use of glucosamine and chondroitin have shown symptomatic action. Neil et al. They claim that the benefits require further study. Johnston et al. (2008) comparing the studies of Arogon et al. (2007), Moreau et al. (2003) and McCarthy et al. (2007) states that, although they have mixed results, they also have strengths that can be taken into consideration. Addleman (2010) identifies the lack of high quality clinical studies that can affirm the efficacy of these nutraceuticals.
McKenzie (2010) says that the evidence from the clinical trial is severely limited and that literature on the use of nutraceuticals in addition to NSAIDs is lacking. KuKanich (2013) concludes that current literature does not support the use of glucosamine and chondroitin although this conclusion is based only on Moreau et al. (2003). Coblain et al. (2016) talks about the negative results of the studies carried out in contrast to the positive ones without however offering conclusions or recommendations on the use of nutraceuticals.
The potential benefits to date cannot be confirmed nor denied as there are conflicting studies. The limitations of the studies are the lack of: therapeutic standardization, source of the ingredients, manufacturers, formulations, treatment doses, regimens and duration, standardized follow-ups, subjectivity and homogeneity of the results. The LOAD (Liverpool Osteoarthritis in Dogs’s Clinical Metrology Instrument) could be an excellent parameter to use since it considers the anamnesis, lifestyle and joint mobility.
Although the clinical benefit remains questionable, the use of glucosamine hydrochloride (HCl) and chondroitin sulfate are commonly used and recommended by veterinarians for canine osteoarthritis as an alternative to NSAIDs, when possible, to avoid adverse effects. Further studies are needed to quantify any existing therapeutic effects.