Laurie's Blogs.

This week’s blog comes about after reading a journal abstract on the subject of knee osteoarthritis (OA) after different types of knee injuries in young adults.¹  No surprise, the study found that knee OA increased almost 6x in young adults who had a knee injury (compared to those that didn’t).  Those injuries included, cruciate damage, meniscal tears, and intra-articular fractures.  Yes, it’s a human study, but do we really think it would be different in dogs?

I did a quick PubMed search (because I’m a nerd) and found a 1975 study² whereby the researchers radiographed then dissected 150 cadaver stifles from veterinary practices.  20% of those dogs had stifle arthritis.  When looking at the total number of stifles with osteoarthritis, 37% had some form of mechanical derangement (i.e. cruciate tear, meniscal tear, or patellar dislocation), whereas 61% the cause of OA was unknown.  Well, that’s weird… I would wonder if the remaining 61% has partial cruciate tears that would account for joint inflammation and/or a tear of the contralateral limb… which we know can cause issues in BOTH joints.

Subsequently, I went down the rabbit hole to see what new information could be found since 1975 (ha ha… just a bit!) and found the following.  “Synovitis is an early feature of the CrCLR arthropathy in dogs before development of joint instability clinically. Severity of synovitis is correlated with radiographic arthritis in joints with minimal to no clinically detectable CrCL damage.”³  Great!  That fits with current knowledge and with where I’m going here!



Let’s go back to the concept that joint injuries lead to osteoarthritis.  Joint inflammation leads to cruciate disease and eventually osteoarthritis. KNOWING IS HALF THE BATTLE!!!  What can we do about it?

One Canadian research group did an in-vitro study and compared supplementation with glucoasamine sulfate to the NSAID, carprophen and found that both compounds examined were able to significantly reduce the release of PGE2 and TNFα and were associated with reductions in cyclooxygenase-2 (COX-2) expression and nuclear factor-kappaB (NF-κB) phosphorylation.⁴  Carprophen was better… but the glucosamine still worked.

A research group based in Germany conducted another in-vitro study looking at ‘preloading’ canine chondrocytes by incubating them in polyunsaturated fatty acids (eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA)) and then adding a compound to induce osteoarthritic changes.⁵   “Our results reveal molecular mechanisms by which PUFA affect degenerative joint disease in dogs. Of particular importance is that not only EPA but also AA decreased several inflammatory markers in our model.”

What I want to know is whether or not we can prevent of minimize osteoarthritis in joints following an injury in a LIVE animal (treated humanely of course)!

So, I started to look for randomized controlled trials (RCTs) on osteoarthritis prevention supplements in dogs (or rats, because I figured that’s a rat-study sort of a thing!)  One review paper identified two RCTs and noted that the nutraceuticals alone or in combination did not seem to prevent subchondral bone changes, synovial inflammation, or osteophyte formation, but did note improvements in cartilage status and biomarkers.⁶  Beneficial effects were associated with the pre-emptive administrations, higher doses and, multimodality approaches with some combined therapies.

Another study evaluated the prevalence of hip and elbow dysplasia on growing Labrador retrievers fed a fish-based diet enriched with nutraceutical with chondroprotective properties compared to puppies fed a high quality chicken based food.⁷  All in all at a year of age, there was no difference between groups in the prevalence of the dysplasia, however the fish-nutraceutical fed puppies had less severe grades of OA.

In vitro rat-studies have shown that chondroitin sulfate and probiotics can play a role in reducing inflammation and pain in chemically-induced-OA models.⁸

Another rat-study added Greenshell mussel (or not) to a high-fat/high-sugar diet designed to created metabolic dysregulation and obesity.⁹  While all rats got fat, and developed OA on the diet, the group fed the Greenshell mussel had less serum levels of biomarkers that indicate cartilage degeneration.

Now, my intention is not to do a full review on the topic.  I’ve already reviewed more papers than I anticipated already.  However, with just these papers to look at, I think it would be safe to say that after a joint injury (or known dysplasia), we should be advising that owners look into joint supplements for their dogs!   How much and of what?  Well, that’s another topic for another day… maybe next week!



For now, I think with just these 9 studies, I believe that as rehab professionals, we should be advocating for joint supplementation asap in dogs with joint injuries or dysplasias.  For now, we can say that glucosamine, chondroitin sulfate, polyunsaturated fatty acids, probiotics, and Greenshell mussels show promise!

Stay tuned for part 2!

Cheers!  Laurie

References:

1.  Snoeker B, Turkiewicz A, Magnusson K, Frobell R, Yu D, Peat G, Englund M. Risk of knee osteoarthritis after different types of knee injuries in young adults: a population-based cohort study. Br J Sports Med. 2020 Jun;54(12):725-730.

2.  Tirgari M, Vaughan LC. Arthritis of the canine stifle joint. Vet Rec. 1975 May 3;96(18):394-9. doi: 10.1136/vr.96.18.394. 

3.  Bleedorn JA, Greuel EN, Manley PA, Schaefer SL, Markel MD, Holzman G, Muir P. Synovitis in dogs with stable stifle joints and incipient cranial cruciate ligament rupture: a cross-sectional study. Vet Surg. 2011 Jul;40(5):531-43. 

4.  AlRaddadi EA, Winter T, Aukema HM, Miller DW. Effects of various dietary supplements on inflammatory processes in primary canine chondrocytes as a model of osteoarthritis. Can J Vet Res. 2019 Jul;83(3):206-217.

5.  Adler N, Schoeniger A, Fuhrmann H. Polyunsaturated fatty acids influence inflammatory markers in a cellular model for canine osteoarthritis. J Anim Physiol Anim Nutr (Berl). 2018 Apr;102(2):e623-e632. 

6. Fernández-Martín S, González-Cantalapiedra A, Muñoz F, García-González M, Permuy M, López-Peña M. Glucosamine and Chondroitin Sulfate: Is There Any Scientific Evidence for Their Effectiveness as Disease-Modifying Drugs in Knee Osteoarthritis Preclinical Studies?-A Systematic Review from 2000 to 2021. Animals (Basel). 2021 May 29;11(6):1608. 

7. Manfredi S, Di Ianni F, Di Girolamo N, Canello S, Gnudi G, Guidetti G, Miduri F, Fabbi M, Daga E, Parmigiani E, Centenaro S, Volta A. Effect of a commercially available fish-based dog food enriched with nutraceuticals on hip and elbow dysplasia in growing Labrador retrievers. Can J Vet Res. 2018 Apr;82(2):154-158. 

8. Korotkyi OH, Vovk AA, Dranitsina AS, Falalyeyeva TM, Dvorshchenko KO, Fagoonee S, Ostapchenko LI. The influence of probiotic diet and chondroitin sulfate administration on Ptgs2, Tgfb1 and Col2a1 expression in rat knee cartilage during monoiodoacetate-induced osteoarthritis. Minerva Med. 2019 Oct;110(5):419-424. 

9. Siriarchavatana P, Kruger MC, Miller MR, Tian HS, Wolber FM. The Preventive Effects of Greenshell Mussel (Perna canaliculus) on Early-Stage Metabolic Osteoarthritis in Rats with Diet-Induced Obesity. Nutrients. 2019 Jul 15;11(7):1601.