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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
German Shepherd Dog (Alsatian)
Panosteitis
Related terms: Enostosis; fibrous osteodystrophy; juvenile osteomyelitis; eosinophilic panosteitis
Outline: Panosteitis is said to be a common disease of German shepherd dogs. It is characterized by inflammation of the bone marrow, especially that of the limb bones, with episodes of bone pain, which can be severe, and lameness in young German shepherd dogs. It is thought to have a genetic basis but the genes involved have not been determined.
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Summary of Information
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1. Brief description
Panosteitis is an inflammatory disease primarily of the fatty bone marrow with subsequent effects on the surrounding bone (Shell 2007). It can occur in any bone which contains significant volumes of bone marrow, long bone shafts being the most common sites.
Generally affecting juvenile male German shepherd dogs (GSDs), the disease is usually self-limiting and spontaneously regresses once sexual maturity is reached, although some individuals may be affected up to middle-age (Bohning et al 1970, Berry 2010).
The major clinical sign is pain, which commonly shows as lameness – it is often described as a “shifting lameness” (lameness first affecting one leg and then another) - that may or may not be connected with trauma and can have an acute (rapid) onset (Trostel et al 2003, Shell 2007). Affected dogs may be lethargic, show a loss of appetite and have a raised temperature. These signs generally last a few days to a few weeks, disappear and then reoccur (ie they “wax and wane”). The dog may show a pain response on limb handling. Reoccurrences may coincide with periods of stress (Shell 2007).
2. Intensity of welfare impact
During active bouts of panosteitis, affected GSDs exhibit signs of significant limb pain. Shell (2007) stated that “excruciating pain frequently accompanies the disease”. Affected dogs also often feel ill due to fever.
Medication given to relieve the pain can have significant side effects such as intestinal irritation and the dog’s welfare may also be compromised through restricting activity to help control the condition.
3. Duration of welfare impact
Affected GSDs may suffer recurrent bouts from five months of age, lasting from a few days to weeks, although they may last longer. The disease usually resolves when the dog reaches sexual maturity, at between 5-15 months, but some dogs are affected until middle-age.
4. Number of animals affected
The GSD is the breed most commonly affected with panosteitis. It is considered to be common in this breed but we are unaware of data on the proportion of dogs afflicted (Trostel et al 2003, Shell 2007, Scott & Witte 2011).
5. Diagnosis
The GSD is the breed most commonly affected with panosteitis. It is considered to be common in this breed but we are unaware of data on the proportion of dogs afflicted (Trostel et al 2003, Shell 2007, Scott & Witte 2011).
6. Genetics
The genetics of panosteitis have not been studied and the genes responsible for the condition have not been determined. The GSD breed is considered to be predisposed to the condition (Bohning et al 1970, Shell 2007, Berry 2010, Scott & Witte 2011). There is no genetic test for the disease.
7. How do you know if an animal is a carrier or likely to become affected?
It is not known if unaffected carriers of the gene(s) exist - animals that do not have the disease themselves but are able to pass on the gene(s) that cause the disease to their offspring - and, as far as we know, there is no information about the heritability of panosteitis in GSDs.
8. Methods and prospects for elimination of the problem
As far as we are aware, there are no breeding schemes aimed at reducing the incidence of panosteitis. Generally it seems sensible not to breed from individuals that have been affected by the disease or from their relatives.
For further details about this condition, please click on the following:
(these link to items down this page)
- Clinical and pathological effects
- Intensity of welfare impact
- Duration of welfare impact
- Number of animals affected
- Diagnosis
- Genetics
- How do you know if an animal is a carrier or likely to become affected?
- Methods and prospects for elimination of the problem
- Acknowledgements
- References
1. Clinical and pathological effects
Panosteitis is an inflammatory disease that generally affects the long bones of young, large breed dogs, especially GSDs. Primarily it affects fatty bone marrow and has subsequent effects on the surrounding bone (Shell 2007). It can occur in any bone that contains a significant volume of marrow but, as marrow is largely found in the diaphysis (shafts) of the long bones, these are the most commonly affected sites.
Long bones are the bones of the limbs. They are essentially supporting columns that have to carry the weight of the animal. Each long bone consists of a central, roughly cylinder-shaped, shaft of bone called the diaphysis and two rounded ‘head’ sections at either end, called the epiphyses, which articulate with other bones as joints that allow movement. These epiphyses have an outer layer of compact bone and spongy bone in their centre. Between the epiphyses and the diaphysis in young animals are the growth, or epiphyseal, plates which are the zones in which bone lengthening occurs.
The diaphysis (the shaft of the bone) has, in cross section, an outer thin fibrous layer of tissue called the periosteum and, inside this, a wide layer of compact bone which provides the strength. In the centre of the shaft is the bone marrow cavity that contains the soft, blood cell producing, (haemopoietic) bone marrow and yellow fatty bone marrow.
Bone is a dynamic, living tissue that can slowly respond to the forces exerted on it by remodelling, strengthening and repairing itself. To do this it has cells called osteoblasts which produce bone and osteoclasts which dissolve it.
In animals affected with panosteitis, the fat cells of the yellow marrow degenerate, inflammation occurs and this tissue is replaced with fibrous tissue, which in turn is calcified and turned into spongy bone tissue, as osteoblasts, osteoclasts and fibroblasts (fibrous tissue-producing cells) are activated (Shell 2007, Brooks 2011). Ultimately, as the disease process subsides, this new bone is removed as part of the normal bone remodelling processes and the fatty marrow regenerates.
The causes of panosteitis are unknown (Shell 2007, Brooks 2011). Various possible causes have been proposed as listed below.
- Infection, possibly by a virus, though none has yet been identified (Shell 2007);
- A more recent suggestion is that the disease is related to use of high-protein/ high-calorie commercial diets. The theory is that high protein levels lead to oedema (fluid collection and retention) within the tissues of the medullary cavity. As the bone is rigid this extra volume of fluid causes compression of blood vessels and to inadequate blood supply to the tissues of the bone, leading to inflammation (ischaemia) (Schawalder et al 2002a, b, Shell 2007).
- Because some breeds of dogs (including GSDs and Bassett hounds) are predisposed to the disease, the implication is that there may be a genetic cause to the condition (Brooks 2011). The profile of breeds affected by panosteitis is similar to that of those affected by von Willebrand’s disease and individuals with panosteitis often have an abnormality of blood clotting factor VIII (Dodds 1978), giving additional credence to the proposal that genetic influences play a major part.
- Stress is often thought to play a role (Shell 2007).
Generally affecting juvenile dogs, the disease is usually self-limiting and spontaneously regresses once sexual maturity is reached between 5-15 months of age, but some individuals may be still affected in middle-age (Bohning et al 1970, Berry 2010). Males are affected more frequently than females (Trostel et al 2003, Shell 2007).
The major clinical sign of panosteitis is pain, showing as lameness, often described as “a shifting lameness” (lameness moving from leg to leg), that may or may not be connected with trauma and can have an acute (rapid) onset (Trostel et al 2003, Shell 2007). Affected dogs may be lethargic, show a loss of appetite and have a raised temperature. These signs often last from a few days to a few weeks, disappear and then reoccur (i.e. they “wax and wane”). Handling the limb may elicit a pain response. Reoccurrences of the signs may coincide with periods of stress (Shell 2007).
Until spontaneous regression of the condition occurs, pain-relieving medicating is often needed and reduction of stress and activity levels are also recommended (Shell 2007).
2. Intensity of welfare impact
During bouts of panosteitis, affected GSDs exhibit signs of significant limb pain. They react to having the affected bones touched. Shell (2007) stated that: “excruciating pain frequently accompanies the disease”. Affected dogs also often feel ill due to fever.
Medication given to relieve the pain can have significant side effects, such as intestinal irritation and the dog’s welfare may be compromised through restriction of normal activity.
3. Duration of welfare impact
The disease usually starts at between five and 18 months of age and is often recurrent. It regresses in most individuals once they reach sexual maturity at between 5-15 months, but some GSDs are affected until they are seven years of age (Bohning et al 1970, Berry 2010). Individual bouts may last for weeks to months at a time (Shell 2007).
4. Number of animals affected
The GSD is the breed most commonly affected with panosteitis. It is considered to be common in GSDs but we are unaware of data on the proportion of these dogs that are affected (Trostel et al 2003, Shell 2007, Scott & Witte 2011).
5. Diagnosis
Panosteitis may be suspected in a juvenile GSD showing lameness. However other orthopaedic conditions also commonly occur in young GSDs so confirmation of the diagnosis needs to be made using radiography (x-rays) (Shell 2007, Berry 2010).
The radiographic appearance of the tissues of the bone changes during the course of the condition and such radiographic changes lag behind the clinical signs by about 5-7 days so it is possible for an affected dog to have initial lameness without being able to detect corresponding radiographic changes (Shell 2007). This can make diagnosis difficult. Blood tests may show an eosinophilia (higher than normal concentrations of a particular white blood cell type) (Shell 2007).
It is recommended that dogs suffering from panosteitis are also screened for von Willebrand’s disease as the conditions can occur simultaneously- this can be checked using a blood test.
6. Genetics
The breed is considered to be predisposed to panosteitis but the genetics have not been studied and the genes involved have not been determined (Bohning et al 1970, Shell 2007; Berry 2010, Scott & Witte 2011). There is no genetic test for the disease.
7. How do you know if an animal is a carrier or likely to become affected?
It is not known if unaffected carriers of the gene(s) exist - animals that do not have the disease themselves but are able to pass on the gene(s) that cause the disease to their offspring - and, as far as we know, there is no information about the heritability of panosteitis in GSDs.
8. Methods and prospects for elimination of the problem
As far as we are aware, there are no breeding schemes aimed at reducing the incidence of panosteitis. With the current state of knowledge it is difficult to give good advice. Generally it seems sensible not to breed from individuals that have been affected by the disease or which have more than a very few affected relatives including siblings and siblings of parents (Bell 2010). Prospective dog owners may wish to avoid acquiring dogs of breeds in which there is a high prevalence of the disease (in order to help avoid perpetuating the problem) unless they are able to ascertain that the disease does not occur or is very rare in the particular lineage of the dog they are interested in acquiring.).
9. Acknowledgements
UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.
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10. References
Bell JS (2010) Genetic Testing and Genetic Counseling in Pet and Breeding Dogs 35th World Small Animal Veterinary Association World Congress Proceedings. 2-5th June 2010, Geneva, Switzerland
http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2010&Category=&PID=56159&O=Generic. Accessed 1.10.11.
Berry CR (2010) Developmental Orthopedic Disease in the Dog. Western Veterinary Conference proceeding 14-18th Feb 2010, Las Vegas, USA. http://www.vin.com/Members/Proceedings/Proceedings.plx?CID=wvc2010&PID=pr54707&O=VIN. Accessed 15.8.11
Bohning R, Suter P, Hohn RB and Marshall J (1970) Clinical and radiographic survey of canine panosteitis. Journal of American Veterinary Medicine Association 156: 870–884
Brooks W (2011) Panosteitis: Growing Pains in Dogs. Client information sheet. On-line. http://www.vin.com/Members/SearchDB/vp/vpa03238.htm. Accessed 15.8.11.
Dodds WJ (1978) Inherited bleeding disorders. Canadian Practice 6: 49-58
Schawalder P, Jutzi K, Andres HU and Blum J (2002a) Canine panosteitis--an idiopathic bone disease investigated in the light of a new hypothesis concerning pathogenesis. Part 2: Biochemical aspects and investigations. Schweiz Arch Tierheilkd 144 (4): 163-173
Schawalder P, Andres HU, Jutzi K, Stoupis C and Bösch C (2002b) Canine panosteitis: an idiopathic bone disease investigated in the light of a new hypothesis concerning pathogenesis. Part 1: Clinical and diagnostic aspects. Schweiz Arch Tierheilkd 144 (3): 115-130
Scott H and Witte P (2011) Investigation of lameness in dogs. 1. Forelimb. In Practice 33: 20-27
Shell L (2007) Panosteitis. On-line. VIN Associate. http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1279. Accessed 15.8.11.
Trostel CT, Pool RR and McLaughlin RM (2003) Canine lameness caused by developmental orthopedic diseases: Panosteitis, Legg-Calve-Perthes disease, and hypertrophic osteodystrophy. Compendium of Continuing Education for the Practicing Veterinarian 25 (4): 282-292
© UFAW 2011
