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Pathogenesis of Laminitis Kent Hoblet, DVM, MS Professor and Chair, Department of Veterinary Preventive Medicine Ohio State University Columbus, Ohio
Introduction Subclinical laminitis has been considered the most important underlying factor predisposing dairy cows to lameness. Subclinical laminitis is a somewhat loose term in that much of the pathology is now thought to involve hoof horn germinative tissues in addition to those of the laminae. Thus, a better umbrella term that has been proposed in claw horn disruption or hoof horn disorder. At the present time, the subclinical laminitis condition is considered to be of multi-factorial etiology. Feeding management, nutrition, parturition, disease, cow management, environment and behavior all may be involved in causation..........
This article is available in its entirety from
1999
Laminitis (Coriosis) And Its Relationship To Claw Disease an excerpt from: Sole Ulcers, White Line Disease, and Infectious Claw disorders: Primary Causes of Lameness in dairy Cattle By Dr. Jan Shearer DVM, MS University of Florida Simply stated, laminitis is an aseptic inflammation of the sensitive lamina (corium) of the foot. Since more than just the laminar portion of the corium is involved, coriosis is considered by some a more accurate term. To most, however, laminitis is founder. The pathogenesis of laminitis is believed to be associated with a disturbance in the micro-circulation of blood in the corium which leads to breakdown of the dermal-epidermal junction between the hoof and pedal bone. Rumen (lactic) acidosis is considered to be a major predisposing cause of laminitis and presumably mediates its destructive effects through various vasoactive substances released in coincidence with development of rumen acidosis. These vasoactive substances initiate a cascade of events in the vasculature of the corium including increased blood flow, thrombosis, ischemia, hypoxia, and arterio-venous shunting (which directs the flow of blood directly from artery to vein). the end result is edema, hemorrhage, and necrosis of corium tissues. By virtue of its anatomical location between the hoof shoe and pedal bone the corium is particularly vulnerable to inflammatory insult. Any increase in size of the corium due to fluid accumulation (blood and lymph) will increase pressure, pain, and tissue damage. Bound on one side by the hoof wall and the other by the pedal bone, inflammation of corium tissues often leads to swelling at the coronary band. Destruction of the dermal-epidermal junction has particular consequences as it permits laminar separation. As the laminae separate the pedal bone begins to :sink "within the hoof horn shoe. The result is compression of the corium between the pedal bone and sole which sets the stage for the development of sole ulcers. In some cases this "pedal bone sinking phenomenon" involves severe rotation of the toe of the pedal bone downward toward the sole. If compression of the corium by the toe is severe enough a toe ulcer may develop. If, on the other hand, sinking of the pedal bone is such that the rear portion sinks furthest, compression and thus sole ulcer development will most likely develop in the area of the heel-sole junction (known by some as the "typical site" or the site most commonly associated with the development of sole ulcers). |
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This article is a reprint from ROCHE ANIMAL NUTRITION AND HEALTH Dairy Nutrition Technical Workshop August 21,1998 DANA POINT, CALIFORNIA, USA |
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