G S's Sun-Kissed Angel

Sonny's Battle With Degenerative Joint Issues

March 25, 2003 - February 23, 2010

Rest in Peace My Sweet, Gentle Sonny

(Sonny's Pedigree)

Angel

Regarding the lawsuit filed by Hildegard Patton against Carol Kay

Carol Kay and Hildegard Patton have agreed to settle the litigation between them involving several posting and emails on Internet sites maintained by each of them concerning two poodle dogs once acquired by Kay from Patton. Carol, for her part, hereby issues a statement apologizing to Ms. Patton, if the medical information posted on her website concerning the health and medical conditions of the dogs has been construed or interpreted by any readers to impugn the integrity of Hildegard Patton, the name “Gold Star Toy Poodles,” or of her poodle breeding practices and the quality of her poodles in any way. Ms. Kay’s only intentions were to provide information to assist others in obtaining further knowledge and understanding of canine health.

Hildegard hereby issues a similar statement apologizing to Ms. Kay for statements she posted regarding Ms. Kay which suggested Ms. Kay’s actions in posting the medical information may be the result of any health issues relating to Ms. Kay or to any acts of Ms. Kay.

Both Carol and Hildegard affirm their mutual respect for each other, acknowledge their respective accomplishments and express appreciation that this unfortunate misunderstanding has been mutually resolved and put behind them.


On February 23, 2010 my Sonny Angel truly became an angel. We will always love and miss you my sweet, gentle Sonny. Rest in peace.

This is the story of Sonny, a toy poodle, whose body became badly deformed and crippled due to degenerative joint issues including ligamentous/tendinous laxity (generalized joint hypermobility) and degenerative osteoarthritis. Degenerative joint issues can affect any breed. I hope that those who visit this site become aware of the symptoms. I discovered that many veterinarians are unaware of some of the very serious issues caused by abnormal collagen production. We spent many long and expensive months trying to find out what was wrong with my poor boy until we finally received the diagnosis from a board certified veterinary orthopedic surgeon who was familiar with Sonny's condition because he had seen it before.. At the bottom of this page are links to articles discussing both ligamentous laxity (generalized joint hypermobility) and degenerative arthritis.

So much has happened since June of 2007 when Sonny was first diagnosed with crippling, painful, deforming degenerative joint problems including the lawsuit filed by his breeder. Unfortunately, two friendships ended (I guess they never really were friends in the first place-friends don't turn their back on you or verbally attack you when you are in need of comfort and understanding), 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 was totally overwhelmed by the unbelievable support and caring offered by so many people, many of whom I had never known before.

I would like to express my most sincere thank you and deep appreciation to Shirley Malcolm of Shir-Lee's Poodles. Shirley is the breeder of my Sonny's sire, Champion Shir-Lee's Corvette. I didn't know Shirley when I first got Sonny since she is the breeder of his sire, but not the breeder of Sonny. We met a couple of years later on a Yahoo group. I could tell right away from her messages that Shirley was the type of person who cared both about people and her dogs. When Sonny first started showing the signs of his orthopedic issues, Shirley was right there for me with phone calls and e-mails. She truly cared about what was happening to Sonny. She even had a link to Sonny's arthritis website on her website! Through all of this, Shirley has been so caring and supportive with everything that Sonny and I have been going through all the way to the end. She is, I truly believe, an ethical, caring breeder who has become one of my dearest friends. She exemplifies the way you would expect and hope an ethical and responsible breeder would behave when faced with a sad situation like Sonny's.

Video Clips-clips are rather large and may take a while to download especially on dial-up
.

Slow Motion of Sonny Walking-December 13, 2009 (5.65 meg)

This clip clearly shows the bending and floppiness of both front & hind legs. He also now does a strange hopping motion of his right hind leg. When compared to the video clip below taken 16 months earlier, you can see how much his motor coordination has deteriorated.

Slow Motion of Sonny Walking -August 2, 2008 (700k)

Click here for the Quicktime version for Mac (675 k)

This clip clearly shows how deformed his legs had 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.

Although Sonny's legs are now deformed and he is on daily pain medication, he still does manage to get around and he does adore Andy. Sonny tires very easily and can only be active for a couple of minutes at a time

Sonny (.WMV) (1 meg)

Filmed in the summer of 2007

Sonny -September 13, 2009 (6 meg)

Sonny's body is continuing to deteriorate. Walking has become more difficult for him. The floppiness of his legs continues to get worse.

 

Sonny was born on March 25, 2003. 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.

On June 12, 2007 , Sonny had a joint tap procedure done to draw out synovial fluid to be sent to a lab for tesing. 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. On 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. After receiving the diagnosis, we tried prednisone, adequan injections, doxicyclene to try for improvement but nothing worked. Sonny continued to become more deformed. Sonny has also received accupuncture and physical therapy.

August 22, 2007 - An appointment with a neurologist ruled out any neurological issues.

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 he was diagnosed with ligamentous/tendinous laxity. I was told that the ligaments and tendons of his legs were losing their elasticity, had stretched out and were no longer supporting his joints and nothing could be done for him. The only option would be to fuse all the bones of all of the joints in his legs and the orthopedic surgeon advised against that. He was switched from prednisone to Rimadyl to help with pain management.

Sonny's vet bills have exceded $7000

Looking back, I realize the effects of degenerative joint issues 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, showing the progression of his deformity.

Below the pictures are links to websites with information about degenerative osteoarthritis, ligamentous laxity, and abnormal collagen issues..

 

October 5, 2009 - The final comparison pictures of Sonny

 

September 13, 2009

This is a front view of Sonny's front legs. Because the ligaments and tendons no longer offer support,although it is hard to see in this picture, the lower part of his legs now will bend to the side in a 90 degree angle and the paw totally rotates 180 dgrees. He now often cannot put any weight on this leg and tries to hold it up when walking.

Sonny's paws continue to become more deformed. They are badly gnarled, like an elderly human with arthritic hands. When he is not standing on them they curl up into tight little clubs.


 

The progression of Sonny's Degenerative Joint Conditions

The Beginning

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.

 

The picture on the left was taken when Sonny was 15 months old. The picture on the right was 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

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 as much pain. He is also moving more now and appears to be able to get up more easily from lying down.

 

July 4, 2007

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.

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.

poodle with degenerative joint issues

This is a rendition of what has happened to Sonny's skeleton by August 0f 2007.

And this one shows the continuing deformation of his skeleton by September of 2009.


Rather than walking the way a dog should on his phalanges (toes and fingers), Sonny is now literally walking on hands and feet.

(sketches above from http://members.fortunecity.com/tailweaver/inuyasha/anatomy/inuanatomy.html)

 

July 20, 2007

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.

 

August 14, 2007

Sonny's deformation continues to progress. These pictures show just how pathetically deformed he has become.

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).

The 2 pictures below were taken on February 15, 2010

Sonny is having a great deal of difficulty putting weight on his right front leg now and will usually hold it up. His right hind paw now angles out from the leg.

act usClick here to visit Sonny's Memorial Pageu at

The links below discuss degenerative osteoarthritis and ligamentous laxity.

After studying 80% of the dog genome, the Institute for Genomic Research in Maryland, has determined that dogs and humans share almost 19,000 genes. Humans have around 30,000 genes. Indeed, the dog could become man's very-best-and-most-valuable-friend because many canine diseases have human equivalents and studying the canine genetic map could therefore lead to better treatment of human diseases. (http://www.petalia.com.au/templates/storytemplate_process.cfm?specie=Dogs&story_no=1990&pafid=2349)

The successful sequencing of the dog genome sheds light on the structure and function of the human genome, and could help researchers better understand diseases that affect both humans and dogs. "Dogs suffer from more than 350 genetic disorders, many of which resemble human conditions," said Ewen Kirkness, a molecular biologist at the Institute for Genomic Research in Rockville, Maryland, who led the research. "The genes responsible for these are probably constant to humans and dogs." (http://news.nationalgeographic.com/news/2003/09/0925_030925_doggenes.html)

http://files.ali-aba.org/thumbs/datastorage/skoob/articles/BK40-CH04_thumb.pdf

Ligaments are fibrous tissues that connect bone to bone. There are dozens of ligaments in the body and almost every joint has at least two of these structures. Ligaments are short, elastic bands of fibers composed of collagen (protein) bundles. Collagen has great tensile strength, and is the main component of fascia, cartilage, ligaments, tendons, bone and skin. Collagen diseases commonly arise from genetic defects that affect the biosynthesis, assembly, postranslational modification, secretion, or other processes in the normal production of collagen. Ligaments have cells for maintaining the bundles, and some blood vessels. Nerve fibers are found in these bundles, which play an important role in proprioception—the ability to know where the limbs are in space, even without looking at them. When the ligaments are no longer taut, this sense can be lost, causing clumsiness and instability.

In humans, some people have laxity of their connective tissues on a genetic basis and may have a seemingly abnormal examination without any type of an acute event.


http://www.caringmedical.com/conditions/Ligament_Laxity.htm

Ligament laxity is an often overlooked but extremely important cause of chronic body pain characterized by loose ligaments. When this condition affects joints in the entire body, it is called generalized joint hypermobility, ... and may be genetic.

Loose or lax ligaments in turn are not capable of supporting joints as effectively as healthy ones, making the affected individual prone to further injury as well as compensation for the weakness using other parts of the body.

In the case of extreme laxity, or hypermobility, affected individuals often have a decreased ability to sense joint position, which can contribute to joint damage. The resulting poor limb positions can lead to the acceleration of degenerative joint conditions. Many hypermobility patients suffer from osteoarthritis.

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***The following is an excerpt from the book Lovell and Winter's pediatric orthopaedics Vol 1 and 2 (p. 253)***

by Wood W. Lovell, Robert B. Winter, Raymond T. Morrissy, Stuart L. Weinstein

"A variety of proteins play important roles in the connective tissues, including the bones, articular cartilage, ligaments, and skin. Mutations in such genes disrupt the structural integrity of the connective tissues in which they are expressed. In most cases, the phenotype is absent or there are only minor manifestations present at birth; the phenotype evolves with time, because the abnormal structural components slowly fail or wear out with time as the individual grows.... In cases where the structural abnormality involves cartilage, there may be growth abnormality caused by the physeal mechanical failure, or early degenerative disease of the joints caused by the articular cartilage failure. When a protein that is important for ligament or tendon strength is affected, joints often subluxate. ...In patients with mild diesease, life expectancy is normal; however, in patients with more severe desease, life expectancy may be shortened because of secondary effects of the structural defects on vital organs. These disorders tend to be inherited..."

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http://en.wikipedia.org/wiki/Ligamentous_laxity

Ligamentous laxity is a term given to describe "loose ligaments."

In a 'normal' body, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary,

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Ehlers-Danlos Syndrome ("Rubber Puppy Syndrome") - refers to a group of inherited disorders that affect collagen structure and function. Genetic abnormalities in the manufacturing of collagen within the body affect connective tissues, causing them to be abnormally weak.

Hypermobility type
Excessively loose joints are the hallmark of this EDS type, formerly known as EDS type III. Both large joints, such as the elbows and knees, and small joints, such as toes and fingers, are affected. Partial and total joint dislocations are common, and particularly involve the jaw, knee, and shoulder. Many individuals experience chronic limb and joint pain, although x rays of these joints appear normal. The skin may also bruise easily. Osteoarthritis is a common occurrence in adults. EDS hypermobility type is inherited in an autosomal dominant manner.
There are two major clinical diagnostic criteria for EDS hypermobility type. These include skin involvement (either hyperextensible skin or smooth and velvety skin) and generalized joint hypermobility. At this time there is no test for this form of EDS.

(http://medical-dictionary.thefreedictionary.com/Ehlers-Danlos+syndrome)

An important characteristic of dominant gene mutations is that they can have variable expression. This means that some individuals have milder or more severe symptoms than others. In addition, which systems of the body the mutation affects can vary as can the age at which the disease starts, even in the same family. Another important characteristic of dominant gene mutations is that in some cases, they can have reduced penetrance. This means that sometimes a n individual can have a dominant mutation but not show any signs of the condition.

(http://www.healthsystem.virginia.edu/uvahealth/hub_cancer/adi.cfm)

Cutaneous Asthenia-Cutaneous asthenia (literally, weak skin) is part of a group of hereditary disorders characterized by skin that is unusually stretchy and droopy. It is caused by a genetic mutation that is passed from parent to offspring. More than one genetic disorder is suspected, but this condition cannot be determined by skin and tissue samples, it is diagnosed through observation.

This condition is also known as Ehlers-Danlos syndrome, a disease characterized by deficient levels of collagen, the protein molecule necessary for providing strength and elasticity to the skin and ligaments, along with much of the rest of the body. Collagen is the “glue” that holds the body together. A lack of collagen will result in abnormal collagen synthesis and fiber formation.

Dogs affected with this disorder suffer from painful dislocation at the joints due to the instability of the ligament fibers that hold the bones to each other. The ligaments stretch with movement, but without the elasticity needed to return to their form they stay stretched out, allowing the bones to pop out of their connective joints. This creates a painful physical environment for the sufferer of cutaneous asthenia.

The primary cause of this medical condition is heredity. It is caused by a genetic mutation that is passed from parent to offspring, and can be either dominant – from both parents, or recessive – from only one parent.

(http://www.petmd.com/dog/conditions/skin/c_multi_cutaneous_asthenia#)

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http://www.jaoa.org/cgi/content/full/106/9/531

Benign joint hypermobility syndrome (BJHS) is the occurrence of musculoskeletal symptoms in hypermobile individuals in the absence of systemic rheumatologic disease. This syndrome is thought to be an inherited connective tissue disorder.1,2 The primary clinical manifestations of BJHS are hypermobility and pain in multiple joints.

Benign joint hypermobility syndrome needs to be distinguished from other disorders that share many common features, such as Marfan syndrome, EDS, and osteogenesis imperfecta. Generalized hypermobility is a common feature in all these hereditary connective tissue disorders and many features overlap, but often distinguishing features are present that enable differentiating these disorders.

Ehlers–Danlos Syndrome
Ehlers–Danlos syndrome comprises a group of connective tissue disorders that have gross joint laxity and may have purple papyraceous scars, skin hyperelasticity, and skin fragility that leads to easy bruising. Similarly to BJHS, EDS is inherited in an autosomal dominant fashion and is due to a defect in collagen. Of the many different types of EDS that exist, the most common are types I, II, and III. Benign joint hypermobility syndrome is thought to be a mild variation of EDS and most closely resembles EDS type III (hypermoblity type), which consists of joint pain, marked hypermobility, mild extra-articular involvement, and mild skin changes without scarring.18,19 Researchers have suggested that BJHS lies on a continuum with EDS and may be its mildest form because of their overlapping features

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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].


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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.
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This one is from the University of California at Davis College of Veterinary medicine
http://www.vetmed.ucdavis.edu/CCAH/documents/newsletter_2006_spring.pdf

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.
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http://www.niams.nih.gov/hi/topics/arthritis/oahandout.htm

Genetics studies
Osteoarthritis in all its various forms appears to have a strong genetic connection. Gene mutations may be a factor in predisposing individuals to develop osteoarthritis. For example, scientists have identified a mutation (a gene defect) affecting collagen, an important part of cartilage, in patients with an inherited kind of osteoarthritis that starts at an early age. The mutation weakens collagen protein, which may break or tear more easily under stress. Scientists are looking for other gene mutations in osteoarthritis. Researchers have also found that the daughters of women who have knee osteoarthritis have a significant increase in cartilage breakdown, thus making them more susceptible to disease. In the future, a test to determine who carries the genetic defect (or defects) could help people reduce their risk for osteoarthritis by making lifestyle adjustments.

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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.

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http://www.clevelandclinic.org/arthritis/treat/facts/osteoarthritis.htm

What causes osteoarthritis?
Osteoarthritis has two main causes as mentioned earlier: a primary generalized form which appears hereditary and a secondary form which happens when a joint that has previously been damaged by trauma or inflammation.
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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."

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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.

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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.

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http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15910695

Loughlin J.
University of Oxford, Institute of Musculoskeletal Science, Botnar Research Centre, Nuffield Orthopaedic Centre, Oxford, OX3 7LD, UK.

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.

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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.

Why does my dog have arthritis?
Like human arthritis, canine arthritis is widespread and diverse in its causes. Dogs develop arthritic conditions as a result of:

Genetics
Previous injuries or accidents
Infection
Immune system problems
Excessive strain through repeated activity and exercise

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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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