I agree with you 100% Laureen. My male has a screwed up knee, and I tried Cosequin and some other dog products with no success. I didn't see any noticeable improvement in him until I started using the supplement with MSM. His limping has improved quite a bit, so this is the supplement I've been using for both of mine.
Originally posted by Wendi: Do you know if that is what causes spondlyosis?
Nobody seems to sure what causes it, some say injury, some say genetic - no definitive cause. My vet suspects my dog's was caused by repeated blows to her back, and she is said to have the worst kind, which they say is ankylosing spondylosis. The degree of her problem they say should mean wagging her tail is painful. http://www.provet.co.uk/health/diseases/Spondylosis.htm
"The genetic transmission of the tendency to develop this disease is obvious to anyone who has watched it appear in offspring of certain dogs, generation after generation. But exactly how (the etiology) is not as sure. Perhaps there is an inherited weakness in how a dog’s vertebrae respond to or withstand repeated microtraumas; perhaps in some lines, the blood vessels that serve the outer layers of the disks regress and disappear faster than the normal or expected three or four years. It seems to be a fairly natural consequence of aging, as 75% of dogs in some breeds are affected to some degree by 9 years, and half by 6 years.459 On the other hand, some work has indicated that spondylosis deformans is more a disease of middle age. Breed and family variables make the incidence figures vary tremendously. It became a very noticeable disorder in the German Shepherd Dog when, for a while, 90% of the "show" German Shepherd Dogs in the USA were allegedly descended from one very popular late-1960s American Grand Victor (estimate based on a pedigree study reported in a GSD magazine several years ago) who had and passed along this disease in a severe form.
A couple of other miscellaneous thoughts about spondylosis: Regarding the effect or influence of environment, small trauma has already been mentioned as a possible factor, but with little evidence. It is suspected that bulls on high-calcium diets may have increased susceptibility.34 Males seem more at risk than females." http://www.caninetimes.com/Articles/fred_lanting_spondylosis_deformans.htm
Thanks for the sites. They were very informative. It makes you wonder if they are actually in pain. My girl doesn't seem like she is in pain but from the looks of her running gait you can tell something is going on. She just turned 4 yrs. Poor girl!
Pamela said (quite some time ago, sorry for the delay)
"Glucosamine will improve 30% of the people, which is about equivalent to the placebo effect. No truly scientific proof to back it up."
My understanding is that there is good evidence that glucosamine helps slow arthritic deterioration of joints. A study was published last year in the prestigious medical journal Lancet that indeed indicated this. The abstract follows:
Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial.
Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C.
Bone and Cartilage Metabolism Research Unit (WHO Collaborating Center for Public Aspects of Osteoarticular Disorders), University of Liege, Belgium. jyreginster@ulg.ac.be<br />
BACKGROUND: Treatment of osteoarthritis is usually limited to short-term symptom control. We assessed the effects of the specific drug glucosamine sulphate on the long-term progression of osteoarthritis joint structure changes and symptoms. METHODS: We did a randomised, double-blind placebo controlled trial, in which 212 patients with knee osteoarthritis were randomly assigned 1500 mg sulphate oral glucosamine or placebo once daily for 3 years. Weightbearing, anteroposterior radiographs of each knee in full extension were taken at enrolment and after 1 and 3 years. Mean joint-space width of the medial compartment of the tibiofemoral joint was assessed by digital image analysis, whereas minimum joint-space width--ie, at the narrowest point--was measured by visual inspection with a magnifying lens. Symptoms were scored by the Western Ontario and McMaster Universities (WOMAC) osteoarthritis index. FINDINGS: The 106 patients on placebo had a progressive joint-space narrowing, with a mean joint-space loss after 3 years of -0.31 mm (95% CI -0.48 to -0.13). There was no significant joint-space loss in the 106 patients on glucosamine sulphate: -0.06 mm (-0.22 to 0.09). Similar results were reported with minimum joint-space narrowing. As assessed by WOMAC scores, symptoms worsened slightly in patients on placebo compared with the improvement observed after treatment with glucosamine sulphate. There were no differences in safety or reasons for early withdrawal between the treatment and placebo groups. INTERPRETATION: The long-term combined structure-modifying and symptom-modifying effects of gluosamine sulphate suggest that it could be a disease modifying agent in osteoarthritis.
I believe that a 0.25 mm difference in joint space narrowing (JSN) of the knee is significant. Certainly values on that order of magnitude are frequently mentioned in the peer-reviewed medical research literature describing studies of OA in knees. The article below mentions that 0.18 mm per year is typical of the JSN in arthritic knees. Others have found that JSN in arthritic knees averages 0.06-0.10 mm per year.
J Rheumatol 1995 May;22(5):937-43
Quantitative microfocal radiography detects changes in OA knee joint space width in patients in placebo controlled trial of NSAID therapy.
Buckland-Wright JC, MacFarlane DG, Lynch JA, Jasani MK.
There have been a LOT of published studies in the medical and veterinary research literature regarding the use of glucosamine for the treatment of osteoarthritis. A review of meta analyses of a number of these studies is available here:
Rheum Dis Clin North Am 1999 May;25(2):379-95
Nutraceuticals as therapeutic agents in osteoarthritis. The role of glucosamine, chondroitin sulfate, and collagen hydrolysate.
Deal CL, Moskowitz RW.
Division of Rheumatology, Case Western Reserve University School of Medicine, University Hospitals, Cleveland, Ohio, USA.
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