A Review on Etiopathogenesis and Medicinal Management of Ante Brachial Deformities in Growing Dogs  

Kiranjeet Singh1 , Aswathy Gopinathan2
1. Senior Scientist, Division of Surgery, IVRI, Izatnagar, Bareilly, UP
2. Scientist, Division of Surgery, IVRI, Izatnagar, Bareilly, UP
Author    Correspondence author
International Journal of Molecular Veterinary Research, 2013, Vol. 3, No. 5   doi: 10.5376/ijmvr.2013.03.0005
Received: 28 Jan., 2013    Accepted: 28 Mar., 2013    Published: 16 Apr., 2013
© 2013 BioPublisher Publishing Platform
This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract

The angular limb deformity of the forelimbs in dogs is a well-documented clinical entity and is defined as an axial deviation of limb in the frontal plane. Such ante-brachial deformities are frequently reported in growing dogs (Thorp, 1994). A high incidence of the condition has been reported in fast growing large breed dogs like Great Dane (Ramadan and Vaughan, 1978). Various workers have reported different causes for the ante brachial deformities. The most commonly reported cause being the premature closure of the growth plates (Guthrie and Pead, 1992). Trauma to the limb with or without radiographically visible fracture can induce such closures of the physis (O�Brien, et al., 1971). The distal ulnar physis is the most frequently reported site for such physeal premature closures. This leads to reduced growth of the ulna predisposing to carpus valgus, cranial bowing of radius, carpal laxity, and carpal and elbow subluxation (Johnson et al., 1995).Angular deformities are also seen in association with metabolic bone diseases such as hyperptrophic osteodystrophy, retained cartilage core and nutritional secondary hyperparathyroidism (Riser and Shirer, 1965). Though the exact etiopathology of bone deformities are not clearly understood, in such conditions enlargement of metaphyses of long bones and thinning of cortices are seen, which in turn may lead to bending and bowing of the limbs. Further, retention of cartilage may also cause local disturbance in the bone growth and may produce limb shortening and angular deformities (Burk and Ackerman, 1986). These metabolic disturbances may also lead to variable degree of carpal laxity (Probst and Millis, 1994). Studies on the incidence of angular deformities are limited. Available literature shows only sporadic occurrences of such deformities. Singh et al (2008) reported 23.28 % incidence of angular deformities in the growing dogs of less than one year age.

Keywords
Etiopathogenesis; Medicinal; Ante brachial deformities; Growing dogs

Introduction
The angular limb deformity of the forelimbs in dogs is a well-documented clinical entity and is defined as an axial deviation of limb in the frontal plane. Such ante-brachial deformities are frequently reported in growing dogs (Thorp, 1994). A high incidence of the condition has been reported in fast growing large breed dogs like Great Dane (Ramadan and Vaughan, 1978). Various workers have reported different causes for the ante brachial deformities. The most commonly reported cause being the premature closure of the growth plates (Guthrie and Pead, 1992).

The closure of physis can be induced with a trauma without fracture at the physis (O’Brien et al., 1971). The distal ulnar physis is a common site for such premature physeal closures. This leads to reduced growth of the ulna predisposing to carpus valgus, cranial bowing of radius, carpal laxity, and carpal and elbow subluxation (Johnson et al., 1995). Angular deformities are also seen in association with metabolic bone diseases such as hyperptrophic osteodystrophy, retained cartilage core and nutritional secondary hyperparathyroidism (Riser and Shirer, 1965). Though the exact etiopathology of bone deformities are not clearly understood, in such conditions enlargement of metaphyses of long bones and thinning of cortices are seen.

Further, retention of cartilage may also cause local disturbance in the bone growth and may produce limb shortening and angular deformities (Burk and Ackerman, 1986). These metabolic disturbances may also lead to variable degree of carpal laxity (Probst and Millis, 1994). Studies on the incidence of angular deformities are limited. Available literature shows only sporadic occurrences of such deformities. Singh et al., (2008) reported 23.28 % incidence of angular deformities in the growing dogs of less than one year age.

1 Etiopathogenesis
Bone is a reservoir of minerals in an animal body. About 60%~70% of dry weight of bone is made of minerals, especially calcium-phosphate in the form of hydroxyapatite [Ca10(PO4)6(OH)2]. At birth, long bones of an animal mostly look like poorly mineralized tiny cartilaginous models of woven bone. In dogs, especially in large breeds, longitudinal bone growth is rapid during the first 3 months and exponential during the first 6 months of life (Olsson, 1993), which is largely dependent on the process of physeal growth including multiplication, maturation and orientation of chondroblasts/chondrocytes in columns, their mineralization and replacement of woven bone by a process called endochondral ossification. Simultaneously bone remodeling takes place by bone resorption and formation at the metaphyseal, periosteal and endosteal sites in response to mechanical stress (Ekman and Carlson, 1998). Changes in bone structure and conformation can occur very rapidly in growing dogs, as most of the skeletal growth occurs during the first year of life. Hence, during this period decreased mineralization , thinning of cortices of long bones and defect in endochondral ossification may lead to angular limb deformities (Kushwaha, 2003).

Angular limb deformity disorders occurring during bone growth are either developmental or metabolic in nature and frequently the result of growth plate pathology or abnormalities in bone remodeling (Thorp, 1994).

Bone growth disturbances are mostly originate in the growth plate and are commonly manifested as skeletal abnormalities (Prasad et al., 1972) bone deformity (Poulos, 1978). Etiopathology of angular deformities of the foreleg can occur for various reasons. The two-bone system of the ante-bracheum is predisposed to deformity caused by the continued growth of one bone after premature growth cessation of the other. The bones normally elongate through the process of endochondral ossification, which occurs in growth plate or physis (Fox et al., 2006).

Total or partial premature closure of growth plates can lead to angular limb deformities (Guthrie and Pead, 1992). Ulnar and radial growth plate defects occur most commonly affected (Fox and Bray, 1993). The premature closure of the radius and ulna growth plates resulting in deformity of canine fore limbs has been described (Fox, 1984). Any type of trauma to the limb may lead to such closures, and the premature closure of distal ulnar physis and its resultant deformities is the most frequently (O’ Brien et al., 1971). Angular limb deformities may also be associated with metabolic bone diseases such as hypertrophic osteodystrophy, retained cartilage core and nutritional secondary hyperparathyroidism (Riser and Shirer, 1965).

2 Premature Closure of Physis
Growth plates, peripheral extensions of the primary center of ossification, are responsible for the longitudinal growth of a long bone (Newton, 1985). In dogs, growth plate closure is completed within the first year of life and as in other species, the time of fusion varies between the different ossification centers. Disorders of the growth plate in immature animals will result in shortening and/or angulations of the limb and this can result in secondary joint disorders. The most growth plate disorders involve the radius and ulna, because it receives a disproportionate amount of stress, its growth comes from several physes and it is composed of two parallel long bones, which must grow in unison if the limb is to remain straight (Bennett, 1990).The most common growth plate defect is its premature closure leading to shortening of limb with angular deformity (Fox et al., 2006). The type of defect produced varies according to the plate affected, to the growth potential of the plate, and to the extent of the cellular damage (Vaughan, 1976). It was more common in fore limbs and growth plates involved in decreasing order of prevalence were the distal ulna, distal radius and proximal radius as reported by Fox et al (2006). They also found predominance of unilateral cases. The most common cause of premature growth cessation is trauma to one of the physeal plates (Singh et al., 2012). These injuries to the physes have been classified into five groups by Salter and Harris, based on the fractures and anatomical configurations (Salter and Harris, 1963). A transverse fracture through the weak region of the hypertrophied and degenerating cartilage, which is being invaded by the capillaries and chondroblasts, is called Salter I fracture. A similar fracture that extends into the metaphyseal bone is called as Salter II. A fracture that is partially through the hypertrophied cartilage and extends through the germinal cell layer into the physis is called as Salter III. A Salter IV fracture is being in the metaphysis and extends through the physis and epiphysis and into the joint. A Salter V fracture is causing injury to the chondroblastic cell layer. A Salter IV fracture is not apparent on radiographic examination and often occurs with other injuries and Salter fractures. Consequently, Salter V fractures are not diagnosed at the time of injury. Fracture that damages the germinal cell layer has a higher incidence of premature growth cessation (Salter and Harris, 1963). Consequently, a Salter V crushing injury has a higher incidence of premature closure. The prognosis for the normal growth is also affected by the severity of fracture displacement (Lombardo and Harvey, 1977). This suggests that displacement causes damage to the vascular supply of the germinal cell layer. If sufficient vascular impedance occurs, cartilage production ceases and premature physeal closure ensues. Growth deformities of the canine antebrachium can result from injury to any one of the three physes; distal ulnar, distal radial or of proximal radius. Each of these injuries has a specific set of resultant deformities are which discussed individually.

Radiographicaly there is involvement of entire physis, but the lateral side closes first which appear as a narrowed lateral physis. There is widening of line as approaches the medial aspect of the radius (Newton, 1985). Another radiographic sign may be distal subluxation of the radial head (Passman and Wolff, 1975) because growth of the radius has slowed while the ulna has continued to grow. The ulna continues to grow because the radius holds the humerus by means of the collateral ligaments. In severe cases the condition progresses, the ulna may completely luxated proximally. The continuous closure of the distal radial physis from lateral to medial may lead to valgus deformity of the forepaw, and the radial carpal joint dorsal luxation (Newton, 1985).

Most of the Dogs with distal lateral radial physeal closure are presented with forelimb lameness. Animal show pain on manipulation of the elbow or at the site of angular deformity. Physeal closure, radial derotation, and radial head subluxation will be only confirmed with Radiography (Lucia and Paul, 1989).

Premature closure of distal ulnar physis growth deformities of the antebrachium are well documented in the dog (Fox, 1984). The incidence of premature closure is more in the distal ulnar growth plate of dog and this might be due to its conical shape (Marreta and Schrader, 1983). Among the breed susceptibility, large breeds (eg. Great Dane, Wolfhound, Afghan, Alsatian, Boxer, Old English Sheep dog) are particularly prone, but it was also reported occasionally in small breeds (eg.Shetland collie, Chihuahua, Pug, Fox Terrier). Ramadan and Vaughan (1978) found that male dogs are more prone than females. Trauma, failure of chondrogenesis due to mechanical crush injuries to the plate or its interrupted blood supply were the most common causes of closure of distal ulnar physis (Ramadan and Vaughan, 1978). Ramadan and Vaughan, (1978) studied 58 cases of premature closure of the distal ulnar physes in growing dogs. Fracture of the radius (21 cases) at plate level was common in puppies, heavyweight of large breeds and their vigorous activity was also a cause. Such large breeds were also prone to local injuries in the fore limbs bcasue fore limbs under greatest strain during landing from jumps. The common clinical signs reported by Ramadan and Vaughan (1978) in 58cases of premature closure of distal ulnar physis in dogs were lameness, carrying of leg, curvature of the forearm (latero-medially and antero-posteriorly), carpus valgus (5~35º), plantigrade posture, limb shortening in long-standing cases and muscle atrophy in a few cases. The same authors also reported that there was no pain on palpation in majority of the cases; however, few were showing discomfort on flexion of the carpus and manipulation of the elbow joint. The radiographic findings in premature closure of ulnar physis depend on the duration of the condition (Vaughan, 1976). In early stages the first evidence of plate closure was seen in the trough of the “V” shaped distal ulnar plate. The shaft of the radius and ulna were markedly separated; the diameter of the ulnar diaphysis was greatly increased. Shortening of the bone and greater distance between the distal radial and ulnar plate were also seen (Ramadan and Vaughan, 1978). Fractures were also found in some dogs by the same authors, the commonest site was in the distal third of the radius/ulna.

3 Nutritional/Metabolic Disorders
3.1 Rickets
Rickets is a disease of bone that occurs in young animals because of phosphorus or vitamin D deficiency (Palmer, 1993), where defective minera- lization occurs not only in bone, but also at the cartilaginous portion of the growth plate (Krane and Holick, 1980). Inadequate intake or endogenous production of vitamin-D (Cholecalciferol) in relation to the calcium content of the diet could give rise to rickets (Krane and Holick, 1980). Palmer (1993) reported that phosphorus or vitamin-D deficiency could cause rickets. Sjoberg (1942) claimed that animal on diets with inadequate vitamin-D did not develop rickets when sufficient calcium and phosphorus were given. Hypovitaminosis D was also reported to be an important factor in the etiology of rickets (Mellanby, 1921). Diet deficient in both bio-available calcium and vitamin-D is the most common cause of rickets in the pups (Watson, 1990). Imbalance of vitamin-D, calcium and/or phosphorus might cause rickets, the most common combination being a dietary deficiency of vitamin-D and calcium and/or phosphorus; inadequate sunlight might be another important factor (Bennett, 1976; Kushwaha, 2003). Patients suffering from chronic glomerular renal disease showed rickets as well as osteopenia due to renal secondary hyperparathyroidism (Parson and Potts, 1972). The common clinical findings in such animals include listlessness, profound muscle weakness, lameness, lateral bowing of the antibrachii and focal hard swellings proximal to the tarsi and carpi. Pups’ stance was palmagrade (hyperextended carpus) and plantigrade (hyperextended tarsus). Focal bony swelling that was neither hot norpainful on palpation were presented proximal to the carpi nor tarsi, nor the costochondral junctions were of increased prominence.

3.2 Radiographic finding
Radiographic finding in a litter of racing Greyhound affected with rickets included generalized osteopenia, axial and radial thickening of growth plates andcupping of the adjacent metaphysis; the distal ulnar growth plate were the most severely and consistently affected (Malik et al., 1997). Similar changes were also seen in the distal radius and tibia, although in some instances the changes were not uniform across the full width of the physes, resulting in “peninsular” and “islands” of unmineralized cartilage extending into the metaphyses. Ricketic animals show grossly thickened radiolucent epiphyseal line (growth plate), general undercalci- fication of bones, “mushrooming” or “cupping” of the enlarged metaphyses and the presence of bone deformities. Vitamin-D dependent rickets in a Saint Bernard dog showed physes elongated axially and enlarged radially at the distal ulna, radius and femur. Campbell (1964) described pathognomonic features of rickets, which included poorly mineralized and extremely thin cortices, enlarged, compressed and laterally displaced epiphyses and metaphyses and widening of the epiphyseal growth plate. Haematology and serum biochemistry of vitamin-D dependent rickets in a Saint Bernard dog was recorded by Johnson et al. (1995). Yousif et al. (1986) studied haematological parameters in goats having clinical and sub-clinical rickets. He found significant decrease in hemoglobin in rickets. Leukocytosis was observed only in clinical rickets; hypoproteinaemia, hypocal- caemia, hypophosphataemia, as well as a decrease in serum zinc level were observed in both clinical and subclinical rickets; while serum alkaline phosphatase and transaminase activities were increased. Serum magnesium, copper and iron were decreased significantly in the clinically affected group, while sodium and potassium were normal in both groups. An increased Ca:P ratio (>2) was taken as indicator of both clinical and subclinical rickets. Morris (1968) stated that an adequate dietary intake of vit-D is essential (20 and 7 IU/kg body weight) for growth and maintenance, respectively. Adequate supplies of Ca and P in their correct ratio should also be given.

3.3 Nutritional secondary hyperparathyroidism (NSH)
Nutritional secondary hyperparathyroidism (NSH) is the most commonly encountered bone disease, commonly reported in dogs with the feeding of meat products without bone (Bennett, 1976). The disease also occurs in cats (Rowland et al., 1968) and laboratory animals as well as in many farm animal species (Gilka and Sugden, 1984). Osteogenesis imperfecta, osteodystrophy fibrosa, juvenile osteoporosis, nutritional osteoporosis, osteitis fibrosa and “all meat syndrome” are synonyms to NSH, but have caused confusion (Bennett, 1976).The basic underlying cause is disturbance in mineral homeostasis induced by nutritional imbalances, mainly calcium deficiency (Bennett, 1976) or excessive phosphorus intake, which stimulate the release of parathyroid hormone (PTH) from the parathyroid glands (Bennett, 1976). Hypocalcaemia may arise from inability to absorb dietary calcium, lack of dietary calcium eg. in meat, cereal, grains, fruits etc. (Miller, 1969). Excessive dietary phosphorus (Miller, 1969) and several other factors, which tend to reduce the availability of dietary calcium like deficiency of Vitamin A and D, renal insufficiency, dietary constituents such as magnesium, phytate and fluorine and thyroid disease (Cardielhac, 1971). Hyperparathyroidism also occurs in cases of rickets and osteomalacia, where a calcium deficiency will result in increased PTH secretion (Miller, 1969). NSH has been induced experimentally in 4 cross-bred puppies of 7 week old, by Meier and Wild (1975), by feeding 2/3 beef and 1/3rd cereal flakes, with 50 ml milk and free access to water, giving a Ca:P ratio of 1:5. NSH was commonly seen in dogs reared on meat rich diets containing little calcium and much phosphorus, and clinically it was seen in growing dogs of large breeds, where calcium requirements are greater (Olsson, 1972), although the disease was regularly seen in the small breed dogs and in cats (Krook et al., 1971). NSH, osteoporosis and osteomalacia markedly affect the material properties and composition of bone, resulting in a fracture (Schwarz, 1991). Healing of such fracture is delayed (Bae and Bae, 1999). Bennett (1976) reported pain (bone, joint and associated muscle), lameness, bone deformity and pathological fracture (long bone and vertebral body), abnormal tooth development and deterioration of body attitudes in the diseased dogs. Other signs were swollen metaphyses and costo-chondral junctions, pyrexia, paresis or paralysis from vertebral compression and constipation following pelvic collapse . Blood analysis for calcium and phosphorus levels generally reveal values in the normal range since the metabolic control mechanism endeavour to maintain normal mineral levels (Krook, 1971). Serum concentration of phosphorus and alkaline phosphatase(AP) appear to increase. Meier and Wild (1975) analysed serum Ca, P and AP at weekly intervals in experimental cases of eight cross-bred puppies aged 7 weeks (2 equal groups). They found increased level of alkaline phosphatase in serum of both groups in the first 5 weeks with values for the test dogs clearly lower than for the controls. Serum Ca and P contents in the 2 groups differed only slightly after 10 weeks, although larger differences had been recorded earlier.

The radiographic features of NSH, includes generalized loss of bone density and thinning of cortex. Growth plate appeared normal in most cases and there was an area of increased radio-density in the metaphysis adjacent to the growth plate, which indicated area of preferential bone mineralization and broadening of the metaphyses giving a “saucer” effect rather than the “cupping” seen with rickets (Bennett, 1976). Changes were best appreciated in the distal radius and ulna (Johnson et al., 1995).

3.4 Hypertrophic osterodystrophy (HOD)
Hypertrophic osterodystrophy (HOD) was first described in the veterinary literature by Collett (1935). Hypertrophic osteodystrophy primarily affects the young, rapidly growing large and giant breed dogs (Grondalen, 1976). Woodard (1982) studied HOD in a Weimaraner littermate. Harrus et al. (2002) reported the development of HOD and antibody response in a litter of vaccinated Weimaraner puppies. A deficiency of vitamin C has been implicated as an etiological factor (Watson et al., 1973). Riser and Shirer (1965) suggested mineral overloading as a cause of HOD. Low levels of ascorbic acid have been reported in the blood (Bosch et al., 1971) and urine (Holmes, 1962) of affected dogs but this has not been a constant finding. Hypertropic osteodystrophy may arise by over supplementation of the diet with minerals and vitamins rather than a hypovitaminosis (Bruyer, 1972). Riser and Shirer (1965) suggested that excess of vitamin D could be a cause.Canine Distemper virus RNA was detected recently within the bone cells of dogs with HOD suggesting a role for this virus in etiopathogenesis (Mee, 1993). It has also been seen that dogs inoculated with the blood from the dogs with HOD developed Distemper (Johnson et al., 1995). Schulz et al. (1991) detected E. coli bacteraemia in a 6-month old intact male Great Dane that had hypertrophic osteodystrophy. Most animals the animals develop clinical signs during first 6 months of age (Meier et al., 1957; Watson et al., 1973; Grondalen, 1976), which include slight limp, pain on deep digital palpation of the affected metaphyses, anorexia, weight loss, variable pyrexia, swollen, warm and painful long bone metaphyses; with refusal to bear weight on the affected limbs (Newton, 1985). (Meier et al., 1957; Holmes, 1962; Watson et al., 1973). Clinical signs often subsided after a few days and recurred after number of days. Other clinical sign was haemorrhage in various sites, especially visible in gingivae (Schalm, 1965; Morris, 1968).

3.5 Radiographic changes
Radiographic changes in the early stages of HOD occur in the metaphyses of the long bones and are usually bilaterally symmetric. (Newton, 1985). A radiolucent zone in the metaphysis parallel to the epiphyseal plate was most evident in the distal radius and ulna (Grondalen, 1976). Some times a radiodense line was seen adjacent to the epiphyseal plate (Watson et al., 1973). Surrounding soft tissue might be swollen. Later radiographs might show metaphyseal enlargement with irregular periosteal new bone formation although not all affected dogs developed those changes.

Haematological and biochemical tests contribute little to the diagnosis, although neutrophilia, monocytosis and lymphocytopenia could occur during active disease, reflecting stress and inflammation (Johnson et al., 1995). Haematobiochemical parameters were estimated by Grondalen (1976) in 26 growing dogs.He found microhaematocrit values between 32% and 42% in 14 dogs (normal 37.0~55.0; Schalm, 1965), increased ESR in 13 dogs, hemoglobin (g/dL) between 9.8~14.6 in 13 dogs, total erythrocyte count between 3.2 and 8.0 m/mm3 in 13 dogs and total leukocyte counts were 19000 m/mm3. DLC in fourteen dogs showed no abnormalities. Blood calcium was 7~11.5 mg/dL and phosphorus was 4~14.5 mg/dL in 17 dogs. Serum ascorbic acid (SAA) was found between 0.4~4.6 mg/dL in 18 dogs and serum alkaline phosphatase measured 0.5 and 18.9 Bessey Lowry units in 16 dogs.

4 Developmental Causes
4.1 Retention of endochondral cartilage
Retention of endochondral cartilage occurs in young, large and giant breed dogs (Riser and Shirer, 1965; Johnson, 1981). Any long bone may be involved; however, the distal ulna is most frequently affected (Burk and Ackerman, 1986). Johnson (1981) reported that disturbance in endochondral ossification of the growth plate lead to retained cartilage core, which is responsible for the development of forelimb deformity. In retained cartilage core, physeal hypertrophic chondrocytes fail to mature and mineralize the adjacent matrix and they accumulate in long columns in the primary spongiosa. Clinical signs in dogs with retained cartilage included growth retardation, intermittent lameness and lateral angulation of the foot (carpal valgus) (Burk and Ackerman, 1986). The condition usually affects both limbs in a similar manner. Retarded ulnar growth causes relative shortening of ulna, valgus and rotation of the paw, cranial bowing of the radius and carpal, and elbow subluxation (Johnson et al., 1995).

4.2 Radiographically
Radiographically, cases of RCC showed inverted radiolucent cone extending proximally from the distal ulnar physis into the metaphysis. Irregular metaphyseal radiolucencies and physeal widening might be observed in other bones (Burk and Ackerman, 1986). Irregular patterns of metaphyseal bone density might persist after maturity.

5 Medicinal Management of Angular Limb Deformities
5.1 Vitamins and minerals
Rickets in a litter of racing greyhound pups were treated by feeding diet containing 1.3% calcium, 1.00% phosphorus and 1860 IU vitamin D/kg of food (414 IU/1000 Kcal metabolisable energy), 3~4 times a day and housing outdoors in an open yard for several hours daily. There was an increase in the 25(OH) vitamin- D3 concentration in two pups <8 to 48 and 15 to 40 nmol/L, respectively, after treatment (Malik et al., 1997). Vitamin-D dependent rickets in a Saint Bernard dog was treated with 0.125 mg dihydrotachysterol (AT-10, Winthrop Laboratories) given orally every other day (Johnson et al., 1995). Little (1973) opined that over supplementation with vit D has to be avoided since that would lead to the production of a scanty and defective matrix, which might easily be destroyed by minor trauma. Sharma (2002) treated 100 clinical cases of rickets in canine by administering drugs like anthelmintic, Iron and Vitamin-B complex and high oral dose of Ca and P. He used plaster of Paris cast with well-padded bamboo splints to straighten the already bent forelimbs. Modified Thomas splints were applied in some cases, which were, however, not so effective. The POP casts were changed after every two weeks as the splints were found to injure the bony prominences of the rapidly growing pups. In the pups where the bones were not grossly deformed, olive oil massage of the limb and exposure to early morning sun, feeding of calcium rich diet like cheese, milk etc. were recommended. NSH has been treated by termination of a meat-rich diet and feeding of a commercial, nutritionally balanced diet substituted and supplemented with calcium and phosphorus (Bennett, 1976). Milk and milk products are natural sources of calcium and phosphorus. Dogs could be fed mineral by providing chewing bones (Bennett, 1976). In case of severe muscle pain, the intramuscular injection of a combination of selenium and tocopherols has been suggested (0.1 ml/kg body weight once weekly) (Miller, 1969). It has been confirmed experimentally that the osteopenia in NSH is reversible provided the pathology is not too advanced (Krook et al., 1971). HOD affected dogs might recover in one to two months with complete rest and elimination of excessive vitamins and mineral supplements (Watson et al., 1973). Dogs respond poorly to the vitamin C therapy ( Holmes, 1962). Newton (1985) suggested avoidance of minerals, vitamin C and vitamin D supplements as they might accelerate the rate of dystrophic calcification (Bennett, 1976; Grondalen, 1976).

5.2 Hormones
Transforming Growth Factor Beta (TGF- β) is a dimeric protein of 25 kDa molecular weight originally isolated from platelets (Roberts and Sporn, 1993). There are three distinct mammalian isoforms, TGF β1, TGF β 2 and TGF β3, with TGF β1 being the most abundant isoform. Allmost all cell types express TGF β1 but the highest level of expression is in platelets and bones (Assoian et al., 1983). Mature TGF β1 consists of two identical peptide chains, each containing 112 aminoacids, linked by 9 disulphide bonds (Sharples et al., 1987). TGF β1 is synthesized as part of large, latent protein complex, unable to bind to cellular receptors with mature active TGF β1 produced by cleavage (Miller et al.1990). TGF β1 has a major role in chondroprotective mechanisms and is known to promote matrix synthesis. A recent report indicated that TGF β1 caused synovial hyperplasia and osteophyte formation (Bakker, 2001). TGF beta 1 is a multifunctional cytokine that plays an important role in immunomodulation, inflammation and tissue repair (Sporn and Roberts, 1990). Many studies have suggested that TGF β1 could be a potential therapeutic reagent for the repair of soft tissue and bone following ischemic injury. It may also have applications for the treatment of chronic, inflammatory, fibrotic and autoimmune diseases (Prudhomme and Piccirillo, 2000). In contrast; other studies demonstrated that TGF β1 can cause inflammation and fibrosis (Shuler, 2000). The ability of transforming growth factor- TGF β1 (TGF β1) to stimulate bone healing was evaluated in a rat critical calvarial defect model. Both a low dose and a high dose of TGF β1 were incorporated into two different types of implants: one made from a composite of poly (lactic-co-glycolic acid) (PLPG) (50:50) and demineralized bone matrix (DBM), and the other from calcium sulfate (CaSO4). These preliminary studies show that TGF β1 is capable of inducing new bone formation. Furthermore, the materials used to deliver the growth factor can play a significant role in the bone healing process (Gombotz et al., 1994). TGF β1 has been used to treat osteopaenia in rabbits (Parti et al., 2005) and in dogs (Singh et al., 2011).The hormone calcitonin, which antagonizes the action of parathyroid hormone by inhibiting bone resorption (Foster et al., 1972), has been used experimentally in the treatment of NSH in cats fed on calcium deficient diets.

5.3 Homeopathic drugs
Calcarea Phosphorica is the phosphate of lime, prepared by trituration and solution in the distilled water. This substance is prepared by adding dilute phosphorus acid to lime water. It has an affinity with tissue which is concerned with growth and repair of cells. This is a remedy of special value in the treatment of many conditions of the young growing animals like rickets and milk diarrhea (Liendfield, 1983).Calcarea Phosphorica is essential for proper growth and nutrition of the body. This salt is found in the blood plasma, corpuscles, saliva, gastric juice, bone, connective tissue, teeth, milk etc. It gives solidity to the bones, also supplies new blood cells so that it is the first remedy in anaemia and chlorosis, it is also of importance to soft and growing tissue, promoting cell growth and is necessary to initiate growth. It is a nutritive salt for periosteum and bones (Liendfield, 1983). It is important for blood coagulation. Calcarea Phosphorica is curative for a number of diseases such as in callus formation around the ends of fractured bones, in the unnatural growth and defective nutrition of bone and rickets. The spectrum of action of this remedy includes all diseases of bones, blood deficiencies, dyscrasias and dermoid tissue diseases. When an insufficient amount of phosphate of lime is assimilated, imperfect cell growth and consequent decay and destruction of tissue, specially, osseous and glandular tissue occurs. It shouldn’t be given for long but should be administered intermittently (Madrewar, 2003). It has shown a significant improvement along with Symphytum officinalis to correct osteopaenia in rabbits (Parti et al., 2005) and in dogs (Singh et al., 2011). Symphytum officinalis common name is knit bone. It is prepared from the fresh plant. The root contains a crystalline solid that stimulate the growth of bone cells and epithelium on the ulcerated surface (Liendfield, 1983). Symphytum is a bone remedy; it can be administered internally or externally in many injuries and disesse conditions of bones, ligaments, joints, tendons and the periosteum. It is of great use in wounds, penetrating to perineum, and periosteum and in non union of fractures, Irritable stump after amputation, irritable bone at the site of fracture, psoas absecces, pricking pain and soreness of the periosteum (Madrewar, 2003). It has shown a significant improvement along with Calcarea Phosphorica to correct osteopaenia in rabbits (Parti et al., 2005) and Dogs (Singh et al., 2011).

References
Assoian R.K., Komorriya A., Mayers C.A., and Sporns M.B., 1983, TGF– β1 in human platelets, Identification of major storage site, purification and characterization, J. Biol. Chem., 258: 7155-7160

Bae C.S., and Bae C.S., 1999, Therapeutic effect of 1-a, 25 dihydroxy cholecalciferol on osteoporotic fracture in a rat model, Korean J. Vet. Res., 39: 974-985

Bakker A.C., 2001, Over expression of active TGF– β1 in the murine knee joint: Evidence for synovial layer dependent chondrocyte osteophyte formation, Osteoarthritis Cartilage, 9: 128-136
http://dx.doi.org/10.1053/joca.2000.0368  PMid:11237660   

Burk R.L., and Ackerman N., 1986, Small Animal Radiology: A Diagnostic Altas and Text, Churchill livingstone, New York, Edinburgh, London, Melbourne, pp.277

Bosch F.B., Court A., and Vivaco A.C., 1971, Ein fall von Barlowscher Krankheit beim hund Erste Beschreibung in Chile, Vet. Med. Nachr., pp.363

Bruyer P., 1972, Ann. Med.Vet., 116: 721 [Cited by Bennett, D. (1976). Nutrition and bone disease in the dog and cat. Vet. Rec., 98: 313-320)

Bennett D., 1976, Nutrition and bone disease in the dog and cat, Vet. Rec., 98: 313-320
http://dx.doi.org/10.1136/vr.98.16.313  PMid:775753

Bennett D., 1990, Joints and joint disorders, In: Canine Orthopaedics, Whittick W.G., (Ed.), edn 2, Philadelphia & Febiger, pp.761-853, 154

Baron R.C., 1993, Anatomy and ultrastructure of bone, In: Primer on Metabolic Bone Diseases and the Disorders of Mineral Metabolism, Favus M.J., (Ed.), New York, Raven Press, pp.3-9

Campbell J.R., 1964, Metabolic bone dystrophies, J. Small Anim. Pract., 5: 229-234
http://dx.doi.org/10.1111/j.1748-5827.1964.tb04244.x

Cardielhac P.J., 1971, Textbook of veterinary physiology, J.E. Breazile, Lea and Febiger Ed., Philadelphia

Collett P., 1935, La maladic de Barlow spontanee chez de chien (Scorbut infantile), Revue Vet. Goulorese., 87: 497

Delmas P.D., 1995, Biochemical markers of bone turnover, Acta Orthop. Scand., 66: 178-182

Denny H.R., and Barr A.R.S., 1991, Partial carpal and pancarpal arthrodesis in the dogs: A review of 50 cases, J. Small. Ani. Pract., 32: 329-334
http://dx.doi.org/10.1111/j.1748-5827.1991.tb00943.x

Eakman S., and Carlson C.S., 1998, The pathophysiology of osteochondrosis, Vet. Clin. North. Am. Small Anim. Pract., 28: 17-32

Foster G.V., Byfield P.G.H., and Gudmundsson T.V., 1972, Calcitonin, In: Clinics in Endrocrinology and Metabolism, MacIntyre I., (Ed.), W.B Saunders, Philadelphia, pp.93-124

Fox D.B., Tomlinson J.L., Cook J.L. and Breshears L.M., 2006, Principles of uniapical an biapical radial deformity correction using dome osteotomies and the center of rotation of angulation methodology in dogs, Vet. Surg., 35: 67-77
http://dx.doi.org/10.1111/j.1532-950X.2005.00114.x  PMid:16409412

Fox S.M., 1984, Premature closure of the distal radial and ulnar physis in the dog, Part-I: Pathogenesis and diagnosis, Comp. Cont. Ed., pp.128-138

Fox S.M., and Bray J.P., 1993, Corrective osteotomy for bilateral forelimb varus, Defermeties in a working dog,New Zealand Vet. J., 41: 29-34
http://dx.doi.org/10.1080/00480169.1993.35731  PMid:16031691

Gilka F., and Sugden E.A., 1984, Ectopic mineralization and nutritional hyperparathyroidism in books, Can. J. Comp. Med., 48: 102-107
PMid:6713249 PMCid:1236014

Goddard K.M., Williams G.D., Newberne P.M., and Wilson R.B., 1970, A comparison of all meat, semi-moist and dry-type dog foods as diets for growing Beagles, J. Am. Vet. Med. Assoc., 157: 1233-1236
PMid:4920072

Gombotz W.R., Pankey S.C., Bouchard L.S., Phan D.H., and Puolakkainen P.A., 1994, Stimulation of bone healing by transforming growth factor-beta 1 released from polymeric or ceramic implants, J. Appl. Biomater., 5(2):141-150
http://dx.doi.org/10.1002/jab.770050207  PMid:10172073

Grondalen J., 1976, Metaphyseal osteopathy (hypertrophy osteodystrophy) in growing dogs, A clinical study, J. Small Anim. Pract., 17: 721-735
http://dx.doi.org/10.1111/j.1748-5827.1976.tb06936.x  

Guthrie S., and Pead M., 1992, A complication arising after surgical correction of short radius syndrome, J. Small Anim. Pract., 3: 24-26
http://dx.doi.org/10.1111/j.1748-5827.1992.tb01009.x  

Holmes, J.R., 1962, Suspected skeletal scurvy in the dog. Vet. Rec. 74: 801

Johnson, K.A., 1981, Retardation of endochondral ossification at the distal ulnar growth plate in dogs, Aust. Vet. J., 57: 474-478
http://dx.doi.org/10.1111/j.1751-0813.1981.tb05770.x  PMid:6802120

Johnson K.A., Watson A.D.J., and Page R.L., 1995, Skeletal diseases, In: Textbook of Veterinary Internal Medicine, Ettinger S.J., and Feldman E.C., (eds.), W.B. Saunders, Philadelphia, pp.2077-2103

Krane, S. M. and Holick, M.F., 1980, Metabolic bone disease. In: Harrison'sPrinciples of Internal Medicine, 9th edn. Isselbacher K. J., and Adems R. D., Krook L., Lutwak L., and Henrikson P.A., 1971, Reversibility of nutritionalosteoporosis: Physiochemical data on bones from an experimental study indogs, J. Nutr., 101: 233-246

Kushwaha R.B., 2003, Pathophysiology and management of skeletal abnormalitiesin growing dogs, M.V.Sc. thesis submitted to the Deemed University I.V.R.IIzatnagar Bareilly (U.P), Liendfield G.M.,1983, In: A veterinary materia medica and clinical repertory with M.M of nosodes, 1st edn. W. B. Saunders Co., Philadelphia, pp,42, 43,151

Little K., 1973, Bone behaviour, Academic Press, London

Lombardo S.J., and Harvey J.P., 1977, Fracures of the distal femoral epiphyses, factors influencing prognosis, Review of 34 cases, J. Bone Joint Surg. (A.), 59A: 742

Lucia H.S.H., and Paul C.G., 1989, Premature closure of the ulnar physis in thedog: A retrospective clinical study, J. Am. Anim. Hosp. Assoc., 25: 573-581

Madrewar B.P., 2003, In: Therapeutics of Veterinary Homeopathy and Repertory, B.Jain Publishers PVT (Ltd.), New Delhi. pp.246, 289

Malik R., Laing C., Davis P.E., Allan G.S., and Wigney D.I., 1997, Rickets in alitter of racing Grey Hounds, J. Small Anim. Pract., 38: 109-114
http://dx.doi.org/10.1111/j.1748-5827.1997.tb03330.x  PMid:9097242

Marretta S.A., and Schrader S.E., 1983, Physeal injuries in the dog, Review if 135cases, J. Am. Vet. Med. Assoc., 182: 708
PMid:6841256

Mee A.P., 1993, Canine virus transcripts detected in the bone cells of dogs withmetaphyseal osteopathy, Bone, 14: 59
http://dx.doi.org/10.1016/8756-3282(93)90257-B  

Meier H., Clark S.T., Schnelle G.B., and Will D.H., 1957, Hypertrophicosteodystrophy associated with disturbances of Vit. C synthesis in dogs, J. Am. Vet. Med. Assoc., 130: 483-491
PMid:13438741

Meier S. and Wild P., 1975, Nutritional secondary hyperparathyroidism in youngdog, 2. Experimental cases, Schweizer – Archiv – fur – Tierheilkunde, 117: 569-575
PMid:1209237

Mellanby E., 1921, Sp. Rep. Ser. Med. Res. Coun. No. 61, [Cited by Bennett, D.(1976). Nutrition and bone disease in the dog and cat. Vet. Rec. 98: 313-320.]

Meyer H., and Zentek J., 1992, Uber den einflu beiner unterschiedlichenEnergieversorgung wachsender Doggen auf Korpermasse undskelettentwicklung, J. Vet. Med., 39-A: 130-141

Miller D.A., Pelton R.W., Derynck R., and Mosses H.L., 1990, TGF –beta 1, AFamily of growth regulating peptides, Ann. Ny. Acad. Sci., 596: 208-217
http://dx.doi.org/10.1111/j.1749-6632.1990.tb16113.x  

Miller R.M., 1969, Nutritional secondary hyperparathyroidism, Vet. Med. SmallAnim. Clin., 64: 400
PMid:4976886

Morris M.L., 1968, Canine medicine, Catcott E.J., (Ed.), American VeterinaryPublications Inc., Wheaton, Illinois

Newton C.D., 1985, Radial and ulnar osteotomy, In: C.D. Newton and D.M. Nunamaker (Eds.), Text Book of Small Animal Orthopaedics, J.B. Lippincott,Philadelphia. pp 533-544
PMid:2988645

O'Brien T.R., Morgan J.P., and Suter P.F., 1971, Epihyseal plate injuryin the dog: Radiographic study of growth disturbance in the fore limb, J. SmallAnim. Pract., 12: 19-35
http://dx.doi.org/10.1111/j.1748-5827.1971.tb05631.x  PMid:5103101

Olsson S.E., 1972, Radiology in veterinary pathology, A review with specialreference to hypertrophic osteodystrophy and secondaryhyperparathyroidism in the dog, Acta Radiol. Suppl., 319: 255-270
http://dx.doi.org/10.1080/05678067209174027  PMid:4613126  

Palmer N., 1993, Bones and joints, In: Pathology of Domestic Animals, Jubb K.V.F., Kennedy P.C., and Palmer N,, (eds.), Academic Press, San Diego, pp.1-182

Parson J.A., and Potts Jr., J.T., 1972, Clinics in endocrinology and metabolism, Vol. I, No. 1, Ed. I. Maclntyre, W. B. Saunders and Co. Ltd., London

Parti M.K., Aithal H.P., Amarpal, Kinjavdekar P., Pawde A.M., Singh G.R., Goswami T.K., and Setia H.C., 2005, Evaluation of ertain antiresorptivedrugs in growing dogs affected with osteopenic bone diseases, Paperpresented during XXIX annual congress of Indian society for veterinarysurgery and national symposium (9-11, 2005) at IVRI Izzatnagar BareillyU.P, India

Parti M.K., Aithal, H.P., Kinjavdekar P., Amarpal and Singh G.R., 2005, Effect ofhomeopathic drugs, Symphytum30 and Calcarea phosphorica,on growinglong bones in normal rabbits. Paper presented during XXIX annual congressof Indian society for veterinary surgery and national symposium (9-11,2005) at IVRI Izzatnagar Bareilly U.P, India

Passman D., and Wolff E.F., 1975, Premature closure of the distal radial growthplate in a dog, J. Am. Vet. Med. Assoc., 167: 391
PMid:1158778

Poulos P.W., 1978, Tibial dyschondroplasia (osteochondrosis) in the turkey, Acta Radiol. Scand. Suppl., 358: 197-227

Probst C.W., and Millis D.L., 1994, Carpus and Digits, In Text Book of Small animal Surgery, Slatter D.H., 2nd Edition, W.B Saunders Company, Philadelphia, pp.1757-1769

Prudhomme G.J., and Piccirillo C.A., 2000, The inhibitory effect of TGF – beta 1 in autoimmune disease, J. Autoimmune, 14: 23-42
http://dx.doi.org/10.1006/jaut.1999.0339  PMid:10648114

Ramadan R.O., and Vaughan L.C., 1978, Premature closure of the distal ulnargrowth plate in dogs: A review of 58 cases, J. Small Anim. Pract., 19: 647-667
http://dx.doi.org/10.1111/j.1748-5827.1978.tb05554.x PMid:713493

Riser W.H., and Shirer J.F., 1965, Normal and abnormal growth of the distalforeleg in large and giant dogs, J. Am. Vet. Radiol. Soc., 6: 50
http://dx.doi.org/10.1111/j.1740-8261.1965.tb01315.x  

Rowland G.N., Capen C.C., and Nagode L.A., 1968, Experimentalhyperparathyroidism in young cats, Pathol. Vet., 5: 504-519
PMid:5720304

Salter R.B. and Harris W.R., 1963, Injuries involving the epiphyseal plate, J. Bone Joint Surg. (A.), 45A: 58

Schalm O.W., 1965, Veterinary haematology, 2nd edn., Balliere, Tindall and Cassell, London

Schulz K.S., Payne J.T., and Aronson E., 1991, Escherichia coli bacteremia associated with hypertrophic osteodystrophy in a dog, J. Am. Vet. Med. Assoc., 199: 1170-1173
PMid:1752768

Schwarz P.D., 1991, Biomechanics of fractures and fracture fixation, Sem. Vet. Med. Surg., 6: 4-15

Sharma K.K., 2002, A retrospective study of 100 clinical cases of rickets incanine, Intas Polivet, 3: 305-306

Sharples K., Plowman G.D., Rose T.M., Twardzik D.R., and Purchio A.F., 1987, Cloning and sequence of analysis of simian TGF –beta cDNA, DNA, 6:239-344
http://dx.doi.org/10.1089/dna.1987.6.239 PMid:3474130

Shuler F.D., 2000, Increased matrix synthesis following adenovirus transfer of TGF –beta 1 gene into articular chondrocyte, J. Orthopaedic. Res., 18: 585-595
http://dx.doi.org/10.1002/jor.1100180411 PMid:11052495

Singh K., Kinjavdekar P., Aithal H.P., Gopinathan A., Amarpal Pawde,A.M and Singh, G.R., 2008, Occurrence of antebracheal deformities in growing dogs. Indian Journal of Animal Sciences 78(12): 1373-1375

Singh K., Kinjavdekar P., Aithal H.P., Gopinathan A., Amarpal and Pawde A.M., 2011,. Use of homeopathic drugs in angular limb deformities in growing dogs, IVJ, 88(9): 32-35

Sjoberg K., 1942, Kungl, Lantbruksakad, Tidskr. 81: 137. [Cited by Bennett, D.(1976). Nutrition and bone disease in the dog and cat. Vet. Rec. 98: 313-320.]

Sporn M.B., and Roberts A.B., 1990, TGF –beta: Problems and prospects, Cell Regulation, 1: 875-882
PMid:2100192 PMCid:362858

Thorp B.H., 1994, Skeletal disorders in the fowl: a review, Avian Path., 23: 203-236
http://dx.doi.org/10.1080/03079459408418991 PMid:18671088

Vaughan L.C., 1976, Growth plate defects in dogs, Vet. Rec., 98: 185-189
http://dx.doi.org/10.1136/vr.98.9.165  http://dx.doi.org/10.1136/vr.98.10.185 PMid:1258279

Watson A.D. J., 1990, Diseases of muscle and bone, In: Canine Orthopedics, 2nd edn., Whittick W.G., (Ed.), Lea and Febiger, Philadelphia, pp.664-668

Watson A.D.J., 1981, Nutritional osteodystrophy in dogs, In: The Veterinary Annual, Grunsel C.S.F., and Hill F.W.G., (Eds.), 21st issue, Bristol, Scientechnica, pp.209-218

Watson A.D.J., Blair R.C., Farrow B.R.H., Baird J.D., and Cooper H.C., 1973, Hypertrophic osteodystrophy in the dog, Aust. Vet. J., 49: 433
http://dx.doi.org/10.1111/j.1751-0813.1973.tb06853.x PMid:4777208

Woodard J.C., 1982, Canine hypertropic osteodystrophy, A study of the spontaneous disease in littermates, Vet. Pathol., 19: 337-354
http://dx.doi.org/10.1177/030098588201900401 PMid:6806967

Yousif M.A., El-Attar, H.M., Mahmoud, A.R.M., and El-Magawry S., 1986, Clinical and sub-clinical rickets in goats in relation to some bloodparameters, Assiut. Vet. Med. J., 17: 87, 89-94

International Journal of Molecular Veterinary Research
• Volume 3
View Options
. PDF(162KB)
. FPDF
. HTML
. Online fPDF
Associated material
. Readers' comments
Other articles by authors
pornliz suckporn sex videos bbw mom xxx big fucking arabin porn videos teen gril sex video riding hard cock woman hard vagina . Kiranjeet Singh
. Aswathy Gopinathan
Related articles
. Etiopathogenesis
. Medicinal
. Ante brachial deformities
. Growing dogs
Tools
. Email to a friend
. Post a comment