Why does my dog have elbow dysplasia?
Have I walked them too much or given the wrong food?
The term elbow dysplasia refers to a group of different disease entities including:
1) Ununited anconeal process (UAP),
2) Fragmented medial coronoid process (FCP),
3) Osteochondrosis (OC) or osteochondritis dissecans (OCD),
4) Incongruity of the elbow joint.
These four entities can all occur in the elbow joint (although OCD is also observed in other joints), commonly being diagnosed in juvenile, medium to large breed dogs. Often their presence results in clinical lameness (but not in all cases) and it is known that each form of elbow dysplasia will lead to the development of degenerative joint disease (osteoarthritis), the severity of the degeneration varying per individual dog and perhaps even per breed.
Great efforts have been undertaken by different research groups in an attempt to elucidate the aetiology behind elbow dysplasia. Only then can guidelines be developed with the aim of preventing its occurrence. Elbow dysplasia occurs frequently in skeletal immature dogs during the period of high growth velocity. Since developmental skeletal diseases, either due to genetic, nutritional or traumatic influences are frequently seen in juvenile medium to large breed dogs all three factors can to a certain degree be held responsible for the occurrence of elbow dysplasia.
Purebred dog populations represent genetically closed populations, in which high selection intensities and subsequent high levels of consanguinity are common. When only a few of the members of the breed (e.g. mainly the champions) are used for reproduction, then a genetic bottle-neck is created unintentionally but surely, reducing the genetic heterogeneity. It is to be expected that this selection procedure, which is common place in many breeds, may lead to an increased incidence of genetic diseases when the selected breeding stock by chance carry the genetic risk factor for elbow dysplasia or any other genetic disease. When the genetic risk factor has a dominant inheritance pattern leading to clinical signs before breeding age, then the dog and its parent(s) can be discarded from reproduction. However, if the genetic risk factor has a recessive or polygenetic inheritance pattern, has a variable pattern in penetration, or is influenced by environmental aspects then, especially when manifested at an older age, the entity has the opportunity to disseminate in the population before being recognised. This is especially so, when there is a lack of adequate disease registration.
Fragmented coronoid process is seen in many breeds and in large percentages, up to 50% of the screened population (Svenson et al, 1997, Ubbink et al, 1999). When different entities of elbow dysplasia are not differentiated, the disease has been proven to be polygenetic (Kirberger et al, 1998). Given the complex inheritance of elbow dysplasia, an individual dog who fails to show any clinical or radiographic pathology consistent with the presence of elbow dysplasia, may still produce affected progeny. It is however important to note that several studies have demonstrated that breeding with elbow dysplasia-negative dogs (based on radiological screening) will decrease the incidence of dysplasia considerably when compared with breeding of positive x positive, or positive x negative, or negative x unknown (Svenson et al 1997).
The expression of hereditary diseases can be influenced by environmental factors. From the heritability estimates it can be concluded that factors other than genetics may play a significant role in the manifestation of elbow dysplasia. From a variety of studies it has become clear that nutrition has a major impact on skeletal development. Various field and standardized laboratory trials have demonstrated that food with high calcium content (Slater et al,1992; Kallfelz & Dzanis, 1989; Schoenmakers et al, 1999; Schoenmakers et al, 2000) can lead to disturbances in endochondral ossification. This makes the skeleton more vulnerable to mechanical influences in addition to osteochondrosis lesions and possibly chondromalacia. More recently, it has become clear that mild elevations in vitamin D intake will also disturb endochondral ossification by direct influence and not by increasing intestinal calcium absorption (Tryfonidou et al, 2002). High food intake and thereby excessive calcium and vitamin D intake can also lead to osteochondrosis (Hedhammar et al,1974; Lavelle, 1989). High calcium or high vitamin D intake causes cartilage retention in growth plates and thus disturbance of long bone growth, in particular development of the distal ulna and distal radius. Nutritional imbalances (like calcium of vitamin D excess) will not cause skeletal disturbances in dogs which are not genetically predisposed to develop these disturbances (Nap et al, 1993).
These findings are of great value for owners of a single dog, who want to prevent elbow dysplasia from developing in their pet. A high quality commercial dog food prepared particularly for puppies of large breeds should be provided, characterized by a lowered calcium content (~1.0% calcium of dry matter base) and a controlled vitamin D content (~500 IU/ kg food). It has been shown that an increased level of high quality protein does not have a negative influence on skeletal development whereas it is of importance for soft tissue growth and immunological defence systems (Nap et al, 1993).
In summary, elbow dysplasias (including UAP, FCP, OCD and joint incongruence) can spread among certain dog breeds, due to the (over)use of a limited number of breeding dogs carrying a disease allele which is not necessarily expressed in all cases. Based on the published heritability estimates, environmental factors may play a role in the expression of clinical signs in genetically predisposed individuals. Since dietary intake of calcium and vitamin D may cause disturbances in endochondral ossification and thus may play a role in the occurrence of UAP, FCP, OCD and incongruence, unbalanced diets or excessive food (and thereby mineral) intake should be avoided. Although trauma may play a role in the occurrence of FCP the preventive or causative influence of physical activity on elbow joint development in dogs is still largely unknown. When the animal is not genetically at-risk, these environmental factors (e.g. diet and micro-trauma) will not play a significant role in the occurrence of elbow dysplasia. Screening of elbow joints to decrease the incidence of elbow dysplasia in the breeding stock and its offspring is advocated by many researchers and kennel clubs (Swenson et al, 1997, Kirberger et al, 1998). The British Veterinary Association & Kennel Club scheme is designed enable owners to screen for Elbow Dysplasia before breeding and reduce instances of the condition in future generations of dogs Click here to visit the British Veterinary Association page for breed screening.