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EQUINE VETERINARY EDUCATION / AE / MARCH 2016
TABLE 1: Candidate genes potentially involved in equine osteochondrosis as identified by quantitative molecular genetic investigations Abbreviation Gene name NCDN
n Phenotypic trait Nerochondrin HECW1
AOAH CLCA4
COL24A1
HECT, C2 and WW domain containing E3 ubiquitin protein ligase 1 Acycloxyacyl hydrolase
Chloride channel, calcium activated, family member 4
Collagen type XXIV, a1
XIRP2 PTH2R
FBXO25
LOC100073151 Protein-coding gene similar to serum/ glucocorticoid-regulated kinase Xin actin-binding repeat containing 2 Parathyroid hormone two receptor F-box protein 25
TBC1D22A
TBC1 domain family, member 22A
2 OC(D) TC; MCP/MTP 4 OC TC; MCP/MTP
4 OCD MCP/MTP 5 OC(D) TC; MCP/MTP
5 OCD TC OC(D) TC; MCP/MTP
10 OC(D) TC; MCP/MTP Breed References
HW Dierks et al. (2010a) HW Dierks et al. (2010b)
SGC Wittwer et al. (2008) Lykkjen et al. (2010)
NT
HW NT
Lampe et al. (2009a) Lykkjen et al. (2010) Lykkjen et al. (2010)
18 OC TC; OC(D) MCP/MTP SGC Wittwer et al. (2009) 18 OC(D) TC; MCP/MTP 27 OC(D) TC; MCP/MTP 28 OC(D) TC; MCP/MTP
Lykkjen et al. (2010) Lykkjen et al. (2010)
HW Lampe et al. (2009b) NT NT
HW, Hanovarian Warmblood; MCP/MTP, metacarpophalangeal/metatarsophalangeal joint; n, number of chromosome; NT, Norwegian Trotter; OC(D), osteochondrosis (dissecans); SGC, South German Coldblood; TC, tarsocrural joint.
horses. It has been shown, however, that in case of a limited number of phenotypic records the same individuals should be phenotyped and genotyped, rather than genotyping parents and phenotyping their progeny, as is often done in commercial livestock breeding. On the condition that the generation interval is substantially shortened (which is possible when using genomic selection), genomic selection can, under those circumstances, be more effective than classic breeding schemes based on either own phenotypically recorded performance or performance of progeny (Van Grevenhof et al. 2012). The Royal Dutch Sport Horse studbook now has changed from progeny testing to genomic selection. However, it should be realised that the genetic component only accounts for a relatively small part of total variation, especially in certain joints such as the stifle, and that environmental factors are more important.
Environmental factors
Two major groups of environmental factors play a role in equine osteochondrosis: biomechanical loading and nutritional factors. Within these main categories, there are several more specific factors.
Biomechanical factors Biomechanical loading of specific sites can explain the well- known existence of consistent predilection sites within joints. It is likely that the great change in loading of the joints
after birth is an important event in the pathogenesis of OC. Tiny areas of chondronecrosis have been found in all animals in a study on 21 fetuses, but these did not feature specific changes in the collagen matrix compatible with early OC and were seen as a feature of normal development (Lecocq et al. 2008) and no real osteochondrotic lesions have thus far been diagnosed in fetuses, which is a strong indication for the influence of post natal joint loading. A triggering role for biomechanical forces acting on vessels during the time window of their greatest vulnerability fits very well with the vascular early pathogenetic mechanism of OC discussed earlier (Ytrehus et al. 2007; McCoy et al. 2013). Also, areas in
the growth cartilage where a dramatic change in collagen fibre organisation has been shown (Lecocq et al. 2008) may
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be prone to biomechanically induced trauma. It is then the character of the insult (magnitude, direction of force, repetition) together with the local ‘tissue quality’ that will determine whether a lesion will result or not. Biomechanical (over)loading of joints is in the horse
strongly related to the exercise regimen the animal is subjected to. Physical exercise in the juvenile period is known to have a crucial role in the conditioning of the entire musculoskeletal system with consequences for injury resistance later in life (Helminen et al. 2000; Brama et al. 2002). It is exactly in this period of rapid growth and development that osteochondrotic lesions develop and OC cannot be seen separately from these developmental processes (Van Weeren and Brama 2003). Hence, exercise of foals is an important factor in the development of OC, as has been shown by several studies. In a large field study, the so- called BOSAC (Breeding, Osteoarticular Status and Athletic Career) study (Robert et al. 2013) it was shown that there were associations of both prevalence and severity of osteochondrotic lesions with irregular access to pasture, and with keeping animals in very large plots (Lepeule et al. 2009, 2013). ‘Mixed housing’ (stabling overnight and pasture access during the daytime, as opposed to continuous housing at the same spot) and rough and slippery grazing grounds were also risk factors (Praud et al. 2013). Another, unrelated, study showed that that foals housed exclusively at pasture until age 1 year are significantly less affected by OC than foals exclusively housed in a box or ‘mixed’ (Vander Heyden et al. 2013). It seems therefore that lack of joint loading, or irregular joint loading in the sense of uneven joint loading over time or with respect to level and/or direction of forces that are exerted on the joints are risk factors for the development of OC.
Nutritional factors Growth rate and energy intake From the onset of research on OC, the impression existed that the disorder was principally a disorder of large-framed, rapidly growing individuals or breeds (Olsson and Reiland 1978; Str€
omberg 1979). There appeared to be no
straightforward relationship with absolute bodyweight, however; but there is now ample evidence that a high
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