Changes

===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>  The authors then devised a pathological scoring system - the Equine Gastritis Grading (EGG) system - which used 5 samples of gastric mucosa taken from specific regions of the equine stomach.  For each of these, the inflammatory infiltrate was graded by type, density and location, reactive changes were classified in both squamous and glandular samples and the presence or absence of infectious agents and lymphoid follicles was noted.<ref>Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system.  ''Equine Vet J'',41(7):646-51.</ref>

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>  The authors then devised a pathological scoring system - the '''Equine Gastritis Grading (EGG) system''' - which uses 5 samples of gastric mucosa taken from specific regions of the equine stomach.  For each of these, the inflammatory infiltrate is graded by type, density and location, reactive changes are classified in both squamous and glandular samples and the presence or absence of infectious agents and lymphoid follicles is noted.<ref>Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system.  ''Equine Vet J'',41(7):646-51.</ref> From their findings, a pathogenesis for the development of lesions in the squamous region was proposed:

 

 

 

 

 

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.

 

 

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).

==Treatment==

==Treatment==