Laminitis is an inflammation of the lamina of hoofed animals. According to the United States Department of Agriculture (USDA), laminitis impacts approximately 2% of the horse population each year. Because of the severity of the inflammation and chronic pain, it is frequently necessary to euthanize these horses. Surviving horses may be left useless, with resultant economic and social impact on the industry. Current interventions for laminitis are based on supportive care and alteration of biomechanical forces on the digit. The transition from laminitis to laminar failure is believed to be caused by the “weight of the horse and the forces of locomotion driving the bone down into the hoof capsule.” We hypothesize that an important factor is the torsional forces placed on the distal phalanx (coffin bone) by the deep digital flexor muscle and tendon.
Dr Daniel W. Carter of West Florida Veterinary Associates, Gulf Breeze Florida, and Dr J Ben Renfroe of the Child Neurology Center of Northwest Florida developed a new procedure to reduce tension in the DDFT using local Botox injections.
The paralyzing effect of botulinum toxin will result in a decrease of these torsional forces and therefore will aid in the prevention or treatment of the sequelae of laminitis. Seven horses with varying degrees of laminitis were evaluated. Each underwent pretreatment and posttreatment radiographs as well as pretreatment and posttreatment Obel grading. Each horse received botulinum toxin type A injected into the belly of the deep digital flexor muscle. In all cases there was radiographic stabilization of pedal displacement from the dorsal hoof wall. Obel scores showed improvement of 1 to 2 grades during the time monitored.
In humans muscle injuries are frequent in sports and workplace; more than 30% of the injuries seen are related to skeletal muscle. These injuries can occur through a variety of mechanisms, including those arising through direct trauma (e.g., laceration and contusion) and those through indirect trauma (e.g., ischemia, denervation, and strain), but the general process of muscle repair is similar in most cases. After injury, the muscle repair process begins and is divided into interdependent phases: degeneration/ inflammation, regeneration, fibrosis/scar formation, and remodeling. In addition, muscle damage causes an immediate acute ischemic response releasing reactive oxygen species (ROS) including superoxide anion, hydroxyl radical, and hydrogen peroxide. Moreover, ROS may also be released due to the migration, accumulation, and activation of polymorphonuclear cells. These events will finally provoke oxidation of cell membrane lipids, protein oxidation, proteolysis, and DNA fragmentation. Disruption of muscle structural integrity and function will induce changes in transport capacity, energy production, and ionic balance.
Research studies focusing primarily on the effects of photobiomodulation therapy on oxidative stress in experimentally muscle injury have shown that photobiomodulation improves mitochondrial function and reduces the formation of hydroxyl radicals, which contribute to lower muscle cell membrane damage,
The inflammatory phase of the muscle injury is accompanied by an increased ROS and reactive nitrogen species (RNS) production and a reduced activity in antioxidant enzymes.
The muscle traumatic injuries especially in the acute phase benefited from the ROS, which in combination with growth factors and cytokines, are important to the muscle repair due to the redirection of myogenic precursor cells (satellite cells to the injury site).
Satellite cells have the capacity to proliferate and differentiate, with vital properties to repair the injured tissue. In this context, satellite cells and their response to oxidative stress are important to mature skeletal muscle performance. In addition, photobiomodulation causes a protective effect on myoblasts.
However, high levels of ROS for a long period in the injured area can cause oxidative harm (secondary damage) by directly reaching vital cell constituents, such as lipids, proteins, and DNA, in addition to interfering negatively in the differentiation of muscle cells.
Botox when is injected into the muscle a series of events occur blocking the release of acetylcholine which result in flaccid paralysis modifying the horse’s leg torsional forces. Photobiomodulation is a non-invasive procedure well known if its effects reducing inflammation and edema, inducing analgesia, and promoting healing in a range of musculoskeletal pathologies which may help significantly in easing the inflammation and chronic pain of horse’s laminitis avoiding the use of alteration of biomechanical forces on the horse’s digit.
Carmen Care Laser has a specific photobiomodulation protocol for horses with laminitis which may improve their underlying condition, their rehabilitation process while decreasing the pain.