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===Pathology===
===Pathology===
Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at post-mortem.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. ''Equine Vet J'',41(7):638-44.</ref> These included hyperkeratosis, punctate scars, diffuse erosions or ulcerations and ''margo injuria'' in the squamous region and hyperaemia, focal erosions and ulcerations in the glandular region. A novel finding was glandular metaplasia.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. ''Equine Vet J'',41(7):638-44.</ref>
Equine Vet J. 2009 Sep;41(7):646-51.
Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system.
Martineau H, Thompson H, Taylor D.
This is the first example of a complete pathological scoring system developed specifically for recording gastric lesions in the horse. It provides a thorough and repeatable method with which to examine the equine stomach in microscopic detail. It can be used in diagnostic or research situations and the consistency of the information gathered will enable accurate comparison of data between different studies. It aims to give an indication as to the currently undetermined pathological variations seen in the stomach of healthy and diseased horses, as well as increasing the understanding of the pathogenesis of gastritis and gastric ulceration. Using this information, interpretation of biopsy samples is improved.
Lesions in the squamous region are most usefully compared to those of the pig: animals with similar gastric anatomy and a high incidence of gastric disease. Similarities include not only the most frequent lesion location (squamous glandular junction) but also the histological appearance such as parakeratosis, acanthosis, lengthening of rete pegs, balloon keratinocytes, inflammatory cell infiltration, vessel congestion and oedema (Muggenburg et al. 1964; Bivin et al. 1974; Embaye et al.
1990; Doster 2002).(Martinaeu 2009)
A proposed pathogenesis for lesion formation in the squamous region is now possible. The stratified squamous epithelium reacts to excessive acidic exposure by thickening and becoming para/hyperkeratotic (Fig 2). Sloughing of superficial layers then predisposes to secondary infection with opportunistic bacteria (Fig3) and inflammatory cells migrate to the area. The lesion deepens and progresses from an erosion to ulceration, exposing unprotected tissue to acid contents. Subsequent healing may or may not occur depending on factors influencing acidity and healing capabilities of the individual animal. Existing experiments in vitro act to confirm this theory (Nadeau et al. 2003a,b; Andrews et al. 2006).
The 2 animals that displayed diffuse erosions and ulcerations showed little reactivity in the way of hyperkeratosis, acanthosis and rete peg lengthening. The pathogenesis of these lesions is probably due to scalding from acidic gastric contents and bile acids as both horses were suffering from diseases causing gastric reflux (Berschnieder et al. 1999).
Glandular metaplasia was observed in 2 specific sites. The first showed formation of PAS positive mucous glands within the mid lamina propria, away from the margo plicatus underlying erosions and ulcerations (Fig 5). The vulnerability of the squamous region to damage is partly blamed on lack of mucus production, and it is probable that this tissue metaplasia is occurring as a protective mechanism. The second was not always associated with erosion/ ulceration and occurred at the margo plicatus as an extension of glandular tissue, in islet form, towards and within the nonglandular region (Fig 6). This could be a natural progressive development that occurs throughout the life of the horse due to continual exposure of the squamous epithelium to gastric contents adjacent to the margo plicatus (Husted et al. 2008).
It is more difficult to assign a precise pathogenesis to lesions within the glandular region, particularly as the history of NSAIDs was unknown.
The novel histopathological finding was glandular metaplasia, of which there are no existing reports in the horse, pig or composite stomached animal. In the horse, oesophageal glands are said to be present at the level of the trachea within the submucosa but do not extend towards the thoracic inlet. There is one report that details the presence of surface mucus over the nonglandular region, with a suggestion that it might be nasal, salivary or respiratory mucin or come from the glandular region (Bullimore et al. 2001).
It may be that these glands have gone unnoticed and glandular metaplasia is a potential origin for the mucus in this case. In pigs, there is one report (Curtin et al. 1963) where healing of an erosion at the squamous glandular junction was seen to occur by spread of glandular tissue towards the cardia, without formation of scar tissue. However, histological evidence of this phenomena was not given. A similar feature occurs in man at the glandular squamous junction of the distal oesophagus and glandular cardia region of the stomach. This is named the Z line due to the interdigitation of these 2 types of epithelium. It is said to be a normal occurrence if glandular metaplasia is present in the distal 2 cm of the oesophagus (Dixon et al. 1996). However, intestinal metaplasia of the stratified squamous epithelium is a common sequel (Barretts oesophagus) and it is this condition in man which is preneoplastic (Shaheen and Richter 2009). There is no evidence of an increase incidence of intestinal metaplasia or gastric neoplasia of this region in the horse.
This study illustrated the wide variety of gastric lesions present in a mixed population of horses at post mortem. In the squamous region there were examples of hyperkeratosis, punctate scars, diffuse erosions and glandular metaplasia. Glandular lesions ranged in severity from areas of localised hyperaemia, to large erosions with active haemorrhage.(Martineu 2009)
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