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Carbohydrate Alimentary Overload Laminitis - Veterinary Clinics: Equine Practice
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Fig. 1

The leaking hindgut of a horse developing carbohydrate overload laminitis. The hindgut lumen normally has an intact layer (the mucosal barrier) of tightly joined epithelial cells covering its surface (inset). This prevents harmful bacteria and their toxins from being absorbed into the circulation. The hindgut wall is glandular and the cells of the mucosal barrier line the glands (G) and the lumen (L) of the bowel. During carbohydrate-induced colitis the mucosal barrier is damaged providing a possible pathway for laminitis trigger factors to enter the circulation. The submucosa is heavily infiltrated with leukocytes and seems to be a site of intense inflammatory activity. Hematoxylin and eosin (H&E) stain. Bar = 100 μm.

Fig. 2

Grade 1 histologic laminitis (H&E stain). The SELs are longer and thinner than normal and the SELs have pointed instead of the normal rounded tips. The basal cell nuclei are no longer oval in shape and have become round and situated abnormally close to the BM. The tips of the secondary dermal lamellae (arrowed) are still situated close to the primary epidermal lamella (PEL), which is normal. Inset shows normal lamellae. H&E stain. Bar = 10 μm.

Fig. 3

Grade 1 histologic laminitis (PAS stain). Micrograph showing hoof lamellar tissues stained to highlight the BM. The BM (arrowed) is stained dark magenta. At the now tapered tips of the secondary epidermal lamellae (SEL) the BM has lifted away (stars) from the underlying basal cells. Between the SEL bases, the BM is in its normal position, close to the primary epidermal lamella (PEL). Inset shows normal lamellae. PAS stain. Bar = 10 μm.

Fig. 4

Electron micrograph of hoof lamellar tip developing laminitis. The lamina densa (LD) of the BM has separated from the plasmalemma of the lamellar epidermal basal cell (EBC). Some hemidesmosomes (black arrow) appear undamaged but others (white arrow) have faded and have lost their anchoring filament attachment to the EBC plasmalemma. Normally, anchoring filaments (arrowhead) bridge the lamina densa firmly to the EBC but when functional hemidesmosomes are lost (white arrow) the LD separates from the EBC. Bar = 200 nm. D, dermis.

Fig. 5

Grade 2 histologic laminitis (PAS stain). The BM is stained dark magenta. At the tips of the now pointed secondary epidermal lamellae (SEL) the basement membrane (arrowed) has continued to lift from the underlying basal cells to form empty, BM-enclosed, teat-shaped caps (arrowheads). The BM has disappeared at the tips of secondary dermal lamellae (SDL), between SEL bases. The lamellar BM is no longer close to the primary epidermal lamella (PEL). There is a reduced amount of connective tissue between SELs. Bar = 10 μm.

Fig. 6

Transmission electron micrograph of SEL tip affected by grade 2 histologic laminitis. Much of the lamellar basement membrane (arrowheads) is no longer attached to the plasmalemma of SEL basal cells. A polymorphonuclear leukocyte (PMN) is in the dermis of the secondary dermal lamella (SDL). Bar = 2 μm.

Fig. 7

Grade 3 histologic laminitis (type IV collagen immunostain). Only remnants (arrowheads) of the basement membrane remain between the now disorganized SELs. Most of the lamellar epidermal cells have coalesced into an amorphous mass no longer effectively attached to any connective tissue. The remainder of the lamellar BM lies free, in strands (arrowed), among the connective tissue of the primary epidermal lamella (PDL). Inset shows normal lamellae stained the same way. Bar = 10 μm.

Fig. 8

Grade 3 histologic laminitis (type IV collagen immunostain). The basement membrane of the lamellar interface and blood vessels is highlighted by the type IV collagen immunostaining. The tip of the primary epidermal lamella (PEL) has completely detached from its basement membrane and is an unattached amorphous mass. Collapsed tubes of basement membrane, now empty of epidermal cells, are still attached to connective tissue (arrowheads). The PEL has moved 0.61 mm from its normal position in the sublamellar dermis (asterisk), a distance that may be measureable on a radiograph. The inset shows a similar lamellar tip, PAS stained. There are numerous invading leukocytes on both sides of the SEL basement membrane.

Fig. 9

Transmission electron micrograph of an arteriole (Art) in the primary dermal lamella of tissue affected by grade 3 oligofructose-induced laminitis. Numerous polymorphonuclear (PMN) leukocytes, adjacent to the arteriole, have extravasated from the vessel into the dermis.

Fig. 10

Polymorphonuclear leukocytes are rich in MMP-9 and their presence within lamellar epidermal compartments in grade 3 histopathology.

First page of article

In acute laminitis, the suspensory apparatus of the distal phalanx fails at the lamellar dermal/epidermal interface. A grading system for the histopathology of laminitis is based on the consistent pattern of histologic changes to the secondary epidermal lamellae, basal cells, and basement membrane that occur as carbohydrate-induced laminitis develops. The actual trigger factors of carbohydrate-induced laminitis remain unidentified.

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