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Sonny's Battle With Degenerative Joint Disease |
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This is the story of Sonny, a poodle who has become deformed and crippled. This condition can affect any breed of dog. I hope that those who visit this site become aware of the symptoms.The earlier treatment is started, the better the chances to slow down the progress.
So much has happened since June of 2007 when Sonny was diagnosed with degenerative joint problems. Unfortunately, some friendships ended, but other friendships were strengthened and new friendships were forged. To those friends, old and new, who have offered their support and have been there for Sonny and for me, I would like to say thank you.
I would like to express my most sincere thank you and deep appreciation to Shirley Malcolm of Shir-Lee's Poodles, the breeder of my Sonny's sire, Champion Shir-Lee's Corvette. Through all of this, Shirley has been so caring and supportive with everthing that Sonny and I have been going through.
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Clips-clips are rather large and may take a while to download especially
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Sonny and Andy1 taped August 2, 2008 for the PC This movie is 1.84 meg Click here for Quicktime version for Mac This movie is 2 meg Sonny and Andy 2 taped August 2, 2008 This movie is 2.8 meg Click here for Quitcktime version for Mac This movie is 3 meg Although Sonny's legs are now deformed and he is on daily pain medication, he still does get around and he does adore Andy. Sonny tires very easily and can only be active for a couple of minutes at a time |
This movie is 1.3 meg Sonny does not like the braces at all. I am not sure if we will be successfull with using them.
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Slow Motion of Sonny Walking August 2, 2008 (700 k) Click here for the Quicktime version for Mac (675 k) This clip clearly shows how deformed his legs have become at the pasterns and hocks. His ligaments and tendons are all stretched out and no longer support the joints of his legs making walking much more difficult. |
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Sonny just turned 4 years old on March 25, 2007. Towards the later part of 2006, I noticed his body was changing shape. His back had become very roached (rounded) and his hind paws were pointing outward. His hind legs were also becoming very cowhocked. I was concerned about this and what appeared to be some difficulty with walking. I made an appointment with our vet to have him checked out. January 2, 2007 -Sonny had a complete blood panel done which showed very highly elevated liver enzyme and muscle enzyme levels. We were planning to do x-rays but had to wait to see if we could get the liver enzyme levels to decrease. After one month, they decreased slightly but not enough so I started Sonny on Milk Thistle. May 8, 2007 - Sonny had x-rays taken but they were inconclusive. During this time, the deformation of his body continued. His hind paws were now pointing outward at about a 75 degree angle. His hind legs have become so bent that he is now walking on his hocks. His front legs were beginning to bend and he is now walking on his pasterns. Even though my Sonny was only 3, I began to wonder if he might possibly have arthritis . I asked our veterinarian to test him for arthritis.
On Friday, June 7, 2007, Sonny had blood drawn for a test for arthritis but this came back negative. However, since this blood test often results in false negatives, we decided to do a joint tap. June 12, 2007 - Sonny had the joint tap procedure . The tap was done in the shoulder joint. Our vet was very surprised to find that Sonny has almost no synovial fluid in his joints. Friday, June 15th - The pathology report came in and Sonny was diagnosed with degenerative osteoarthritis. The pathology report found no evidence of infection in the synovial fluid basically ruling that out as a cause. Since the arthritis is affecting Sonny's entire body, that also rules out trauma or injury which generally involves one joint-the joint that had been injured. Looking back, I realize the effects of the arthritis probably began long before I saw the physical changes. When Sonny was only 2, I noticed that he no longer liked to run or even go on walks. He also had developed a very stiff, awkward gate when he walked or ran. ************************************* Below are pictures from before he became deformed and after as well as updates regarding the progression of his deformation and my efforts to try to help him. Below the pictures are links to websites discussing the the causses of degenerative osteoarthritis. |
The picture on the left was taken on April 18, 2006. The one on the right was taken one year later on May 15, 2007. The dramatic deformation of his body is very evident. He is standing in both pictures. |
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The picture at the top was taken when Sonny was 15 months old. The 2 lower pictures were taken on May 15, 2007. This is the way Sonny now stands and walks. His back has become somewhat more rounded since these pictures were taken. If you look closely you can see where his hocks are almost touching the pad on the counter. When he walks, his front paws flop out in front of him as if he were wearing floppy slippers.Sonny is now on a high dose of prednisone hoping to put the arthritis into remission before causing more damage to his young body. |
After Starting The Prednisone
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July 2, 2007 Sonny has been on prednisone for 2 weeks and 2 days. His eyes look brighter and he no longer looks like he is in so much pain. The top picture shows how bowed his front legs are. This is not a grooming error. His legs really are this badly bowed now. He is also moving more now and appears to be able to get up more easily from lying down. |
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July 4, 2007 The pictures below are for comparison to the ones taken on May 15th I don't notice any improvement in shape yet. I have a close-up of the front paws which seem turned inward a little more. |
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Sonny used to be 10" tall at the withers. He now measures a little over 9" because of his badly bent legs. Notice in the picture that his pasterns and hocks almost touch the table when he is standing. |
This is what a normal poodle skeleton looks like. |
July 20, 2007 Sonny has now been on the prednisone for 5 weeks. Below are pictures taken today. I don't see any improvement in the legs or back. I believe is front left paw is more deformed. When I try to stand him in a more "natural" position , he immediately pulls his hind legs underneath him. With his hind legs so much shorter due to the extensive bending that has ocurred at this hocks, his spine and hips can no longer be held in the correct position. |
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| July 30, 2007 - Sonny went in for a liver blood panel and re-evaluation of his condition. The vet was not happy with the continued deterioration she observed in Sonny's front legs and paws. She was concerned that the deformation of his spine and neck might be causing a neurological issue. July 31, 2007 - Sonny's liver enzymes came back normal. This afternoon, we started Sonny on Adequan injection therapy as well as doxycycline, an antibiotic/anti-inflammatory drug hoping that perhaps these 2 might halt the progression of Sonny's degeneration. |
| August 3, 2007 - Sonny was having a great deal of difficulty walking this morning. He looked like he was in pain. I took him back to the vet who agreed that he definitely had taken a turn for the worse and so we put him back on 5 mg of prednisone daily. The prednisone is once again helping to manage the pain. His vet would like him to see a neurologist for an electromyelogram. |
| August 13, 2007 - Sonny has been on the doxycyclene and the Adequan injections for 2 weeks now, but his condition continues to deteriorate. I am beginning to be very much afraid the my darling Sonny is going to have a very short life. I don't know what else to try. I am going to talk to the vet tomorrow about trying accupuncture. |
| August 22, 2007 - Sonny had a very thorough examination done today by a neurologist. The neurologist felt there were no Neurological problems present but that all of the deterioration and deformity was orthopedic. He brought Sonny over to one of the orthopedic specialists at the practice. He also felt that all of the issues were orthopedic. One of the suggestions was to fuse the joints of the hocks and pasterns. There are definite problems and risks associated with the surgery and the outcome cannot be guarenteed. I plan to make an appointment with the orthopedic specialist to discuss the possibility of using either braces or splints. He will have to remain on the high dose of prednisone to attempt to manage the pain and to hopefully slow down the progression of the disease. |
| August 28, 2007 - Sonny did not have a good day today. It is obvious that his condition is continuing to deteriorate. He barely wanted to do any moving today. I had a long talk with Sonny's primary vet today. She does not feel that either braces or splints will help but will cause his muscles to deteriorate. As soon as he finishes the round of doxycyclene, we are going to start him on torbitrol, a pain medication that can be safely used with the prednisone to see if it will help to ease the pain he is in. |
October 2, 2007 - I took Sonny to the vet because he has been vomitting blood. We have taken him off the prednisone for several days to try to give his stomach a rest. He was given a shot of antibiotics as well as something to stop the vomitting. He will be on Flagyl for the next few days. |
August 14, 2007 Sonny's deformation continues to progress. These pictures show just how pathetically deformed he has become. |
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Look at the location of his hocks and pasterns. I can't even begin to imagine how painful it must be to walk like this. |
This picture shows how badly deformed his front paws are now. The outer toes on both paws are so badly bent that his nails now point under his paws and he walks on them. |
This picture was taken in February, 2008. The lower part of Sonny's front legs, especially the left one, now flop around as if his skin is the only thing holding his legs together (see video at top). |
| In April of 2008, Sonny had an appointment with a board certified orthopedic surgeon in the hope that stem cell therapy might help him. He had a very thorough exam as well as 8 x-rays. The xrays confirmed the arthritis but in addition to the arthrititis, I was told that the ligaments and tendons of his legs were completely stretched out and no longer supporting his joints and nothing could be done for him. |
July, 2008-Sonny is now receiving weekly acupuncture treatments and is also working with a physical therapist. Each acupuncture treatment is $45. The first session with the physical therapist was $200 and each succeeding one is $126 so I am limited as to the number of sessions he can have. I am doing my own PT with him which includes some swimming (which he really doesn't like at all!) I ordered neoprene leg braces for Sonny's front legs to give support to the pasterns. I want to see if he can learn to walk with them on. So far, he doesn't like them.
IIf he can learn to use them I can have hock braces custom made for him. |
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The links below on arthritis are from Internet sites.
http://arthritis-research.com/content/2/2/95 Genetic factors are thus recognized as being associated with osteoarthritis, and epidemiological studies [3,4,5,6,7,8,9,10] have illustrated the influence of heredity on common forms of osteoarthritis. Further examples of a genetic predisposition for osteoarthritis are given by rare subtypes of osteoarthritis that appear to have a basis in single gene mutations and are associated with early age onset (for review [11]). Examples of mutated genes that may be responsible for these diseases include those that encode cartilage-specific collagens and cartilage oligomeric matrix proteins [12,13,14,15,16,17,18,19]. Additional reports [20,21,22,23] have presented evidence for and against the association of osteoarthritis with yet other genes that may encode molecules that are related to cartilage function. The availability of DNA collections from large numbers of families and sibling pairs with osteoarthritis, coupled with novel techniques for genome-wide scans, are now identifying evidence for yet other predisposing multiple chromosomal loci for osteoarthritis [24,25,26].
http://arthritis-research.com/content/4/6/337 The role of structural genes in the pathogenesis of osteoarthritic disorders Abstract
Osteoarthritis (OA), one of the most common age-related chronic disorders of articular cartilage, joints, and bone tissue, represents a major public health problem. Genetic studies have identified multiple gene variations associated with an increased risk of OA. These findings suggest that there is a large genetic component to OA and that the disorder belongs in the multigenetic, multifactorial class of genetic diseases. Studies of chondrodysplasias and associated hereditary OA have provided a better understanding of the role of structural genes in the maintenance and repair of articular cartilage, in the regulation of chondrocyte proliferation and gene expression, and in the pathogenesis of OA. OA is a genetically complex disorder.
Mutations in genes encoding structural components of articular
cartilage give rise to rare forms
of highly penetrant inherited diseases that are associated with early-onset
OA, whereas the more common forms of the same disease that occurs with
increased frequency at an older age are associated with genetic risk
factors in the form of common population polymorphisms. As more mutations
in the structural genes of articular cartilage are identified, careful
clinical analyses will be required to understand the genotype–phenotype
spectrum of these forms of hereditary OA. As with other multifactorial
diseases, the initiation, progression, and severity of the OA disorder
may be influenced by multiple environmental, hormonal, and intrinsic
and extrinsic factors, with multiple genes in any given individual.
The identification of the genetic pathways will be difficult and will
represent a great challenge in the near future. Of critical importance
are studies to understand the gene–gene and gene–environment
interactions, using animal models. These efforts should provide a better
understanding of the pathogenesis of OA as well as a basis for developing
earlier preventive strategies and providing targets for the development
of new forms of treatment. This one is from the University of California at Davis College of
Veterinary medicine The severity and progress of degenerative joint disease depend on
genetic predispostion and environmental or traumatic factors. Genetic
predisposition may involve a number of yet undiscovered factors that
accelerate cartilage wear. Genetics studies ------------------------------------------------------------------------------------- http://www.medicinenet.com/script/main/art.asp?articlekey=79164 Spontaneous osteoarthritis is, to a major degree, a result of inherited tendencies. We inherit the tendency to develop osteoarthritis from our parents and their parents, etc. Therefore, prevention is not technically possible. -------------------------------------------------------------------------------------------- http://www.clevelandclinic.org/arthritis/treat/facts/osteoarthritis.htm What causes osteoarthritis? From the University of Maryland Medical Center http://www.umm.edu/news/releases/osteoarthritis.htm .... osteoarthritis, appears to be passed on from one generation to the next. "We know that it is hereditary but we do not know which gene or genes carries the hereditary code. Finding a genetic basis for the disease will open up whole new possibilities for finding effective treatments and even preventive measures for this condition." ---------------------------------------------------------------------------------------------------- http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15823757&dopt=Abstract Recent advances in the genetic investigation of osteoarthritis. Peach CA, Carr AJ, Loughlin J. Nuffield Department of Orthopaedic Surgery, University of Oxford, Nuffield Orthopaedic Centre, Oxford, OX3 7LD, UK. Osteoarthritis (OA) demonstrates considerable clinical heterogeneity, generating heated debate over whether OA is a single disease or a complex mix of disparate diseases and concerning which tissues are principally involved in disease initiation and progression. Epidemiological studies have demonstrated a major genetic component to OA risk. However, these studies have also revealed differences in risk between males and females and for disease at different skeletal sites. This observation has resulted in the concept of genes for specific sites rather than a generalised OA phenotype. Recent breakthroughs have shed considerable light on the nature of OA genetic susceptibility. Many candidate genes have been confirmed, such as the interleukin-1 gene cluster and the oestrogen alpha-receptor gene ESR1. Genome-wide linkage scans have revealed several regions harbouring novel loci, some of which are beginning to yield their genes. ----------------------------------------------------------------------------------------------------- http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=14698640&dopt=Abstract Risk factors for osteoarthritis: genetics. Spector TD, MacGregor AJ. Twin Research & Genetic Epidemiology Unit, St. Thomas' Hospital, London, UK. tim.spector@kcl.ac.uk Although the multifactorial nature of osteoarthritis (OA) is well recognized, genetic factors have been found to be strong determinants of the disease. Evidence of a genetic influence of OA comes from a number of sources, including epidemiological studies of family history and family clustering, twin studies, and exploration of rare genetic disorders. Classic twin studies have shown that the influence of genetic factors is between 39% and 65% in radiographic OA of the hand and knee in women, about 60% in OA of the hip, and about 70% in OA of the spine. Taken together, these estimates suggest a heritability of OA of 50% or more, indicating that half the variation in susceptibility to disease in the population is explained by genetic factors. Studies have implicated linkages to OA on chromosomes 2q, 9q, 11q, and 16p, among others. Genes implicated in association studies include VDR, AGC1, IGF-1, ER alpha, TGF beta, CRTM (cartilage matrix protein), CRTL (cartilage link protein), and collagen II, IX, and XI. Genes may operate differently in the two sexes, at different body sites, and on different disease features within body sites. OA is a complex disease, and understanding its complexity should help us find the genes and new pathways and drug targets. ------------------------------------------------------------------------------------------------------ http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15910695 Loughlin J. Osteoarthritis (OA) is a common disease characterised by the degeneration of the cartilage of synovial joints such as the hip and knee. In the past ten years a large number of twin-pair, sibling-risk and segregation studies have been conducted on the disease, and these have revealed a major genetic component that is transmitted in a nonmendelian manner. OA therefore fits best into the complex, multifactorial class of common diseases. With a genetic component established, genome-wide linkage scans were performed, and these uncovered several genomic intervals likely to harbour OA susceptibility. In the past few years these intervals have started to yield genes containing OA-associated variants. This is therefore a very exciting period in the molecular genetic analysis of this common disease. The genes that have so far been implicated in susceptibility include the interleukin 1 gene (IL1) cluster at chromosome 2q11.2-q13, the matrilin 3 gene (MATN3) at 2p24.1, the IL-4 receptor alpha-chain gene (IL4R) at 16p12.1, the secreted frizzled-related protein 3 gene (FRZB) at 2q32.1, the metalloproteinase gene ADAM12 at 10q26.2 and, most recently, the asporin gene (ASPN) at 9q22.31. ---------------------------------------------------------------------------------------------------- http://www.swiftwaterfarms.com/swiftwater/p22CanineArthritis.htm Osteoarthritis:
is a form of degenerative joint disease. There is often a genetic component
to the disease and symptoms are often progressive with age. It can
involve the deterioration of and changes to the cartilage and bone. Genetics ---------------------------------------------------------------------------------------------------- http://www.fitzpatrickreferrals.co.uk/OSTEOARTHRITIS-THE_STATE_AND_THE_ART.html Osteoarthritis (degenerative joint disease) is a complex disease of joints with multifactorial aetiopathogenesis. In the USA alone, osteoarthritis affects over 21 million people and it is the leading cause of disability in persons greater than 15 years of age. In dogs, 20% of the canine population over one year of age are affected by osteoarthritis. Genetics and heritability can give rise to both primary and secondary arthrosis whilst trauma and inflammatory joint disease give rise to secondary arthrosis only.
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