These include:

Enzymatic and inflammatory theories: The enzymatic theory postulates that increased blood flow to the foot brings in inflammatory cytokines or other substances to the hoof, where they increase production of MMPs, which subsequently break down the basement membrane. The inflammatory theory states that inflammatory mediators produce inflammation, but recognizes that MMP production occurs later. Therefore, this is possibly a 2-step process, beginning with inflammation and leading to MMP production and subsequent laminitis. Vascular theory: Postulates that increases in capillary pressure, constriction of veins, and shunting of blood through anastomoses to bypass the capillaries, causes decreased blood and therefore decreased oxygen and nutrient delivery to lamellae. The end-result would be ischemia, leading to cellular death and breakdown between the lamellae. Subsequently, increased vascular permeability leads to edema within the hoof, compression of small vessels, and ischemia. Vasoactive amines may be partially to blame for changes in hoof blood flow. Metabolic theory: Insulin affects multiple processes within the body, including inflammation, blood flow, and tissue remodeling. Change in insulin regulation may lead to laminitis. Hyperinsulinemia has been shown to cause increased length of the secondary lamellae and epidermal cell proliferation. Traumatic theory: Concussion is thought to directly damage lamellae, and increased weight-bearing is thought to decrease blood supply to the foot. Rotation, sinking, and founder
Normally, the front of the third phalanx is parallel to the hoof wall and its lower surface should be roughly parallel to the ground surface.
Fibrofolliculomas are 2 to 4 mm in diameter, dome-shaped, yellowish or skin-colored papules usually located on the head, neck, and upper trunk. They are characteristically seen in Birt–Hogg–Dubé syndrome. : 674

See also
List of cutaneous conditions
List of cutaneous neoplasms associated with systemic syndromes
Trichodiscoma


== References ==