The suspensory ligament is a very important piece in the locomotion of the horse. Also known as Interosseous Muscle (or tendon), due to the presence of muscle fibers in its structure, this ligament has more functions than simply connecting bone to bone and supporting the fetlock joint.
It originates at the distal row of carpal/tarsal bones, running down the 3rd metacarpal/metatarsal bone in between the splint bones. Around the nodules of the splint bones, this ligament bifurcates and connects to the abaxial surfaces of the proximal sesamoids. From there, each emerging branch will connect to the main extensor tendon.
The suspensory apparatus is responsible for a springy support of the fetlock joint. This elastic capability allows the horse to cover a reasonable amount of ground with reduced amount of energy – vital survival ability for wild horses.
Degenerative desmitis often occur in older horses or in those animals with bad conformation or subjected to intense fetlock load such as jumpers and reiners. The prognosis of this condition, also known as DSLD – Degenerative Suspensory Ligament Desmitis, is limited, and horses diagnosed with DLSD eventually are removed from their regular work activities. Through the use of shoes that provide caudal support, ex: fishtail bar shoe, it is possible to provide some comfort to these animals, however this condition usually worsens with time.
The distal sesamoid bone is one of the bones that makes up the distal interphalangeal joint (coffin joint). It is totally immersed in the hoof capsule and acts as a fulcrum point for the deep flexor tendon just before making its final attachment in the flexor surface of the third phalanx (semilunar crest). Two ligaments ensure the correct placement of the navicular bone.
Source: Equine Podiatry – Andrea Floid.
Among limb lameness problems commonly seen, a considerable percentage of them is related to the navicular apparatus of the horse’s hoof. Conformation, age and type of work are directly related to the horse’s propensity to develop navicular issues.
Also diagnosed as palmar heel pain or navicular syndrome, the condition is degenerative , however in some instances prognosis can be delayed through the combination of veterinarian work and proper farriery.
Two schools of thinking try to explain the etiology of this condition. The first one proposes that vascular compromise is the reason for navicular changes. This theory proposes that reduction of distal arterial blood supply and thrombosis of the navicular arteries lead to ischemia and degeneration of the navicular bone. However, scientific studies have proven the inconsistency of this theory as it was not possible to replicate the disease by altering blood supply to the hoof in study cases.
Continue reading The Navicular Apparatus
Long bones grow through endochondral ossification where cartilage is converted into bone. Long bones mainly ossify from the center and from the ends (physis or growth plates). Genetic, weight-bearing and pressure forces greatly affect the growth of bones. Cuboidal bones such as the knee/hock bones, in the other hand, do not have physis and their growth occurs from the center of the bone.
Another process of ossification is through a matrix of connective tissue instead of cartilage This process is called intramembranous ossification and it is seen on the development of flat bones (skull bones).
Epiphyseal growth plates have different closure times which provide us with a limited time window to perform any corrective work on foals. In general, the more distal and caudal plates close first. Some growth plates are closed even before the foal is born such as the distal physis in the proximal phalanx. Some bones are very close to their final length by the time the newborn arrives. Usually the length of a foal’s long pastern does not change anymore and its cannon bone only grows about 20% more.
Some factors can affect the closure times of the growth plates:
- Pressure: Overweight or long-standing lameness can force plates to close sooner.
- Hormones: The use of anabolic steroids which by their nature have male hormone effects (testosterone) can also cause premature closure.
- Castration: Gelding horses prematurely can delay the closure times.
Once the growth plates are closed, bones can only change in shape but not in length. This process is called remodeling. Osteoclasts will absorb the old bones cells while osteoblasts will lay new ones. Based on the pressure forces resulting from conformation and work load, bones will remodel and change their density and thickness in different areas.
It is common to see overfed foals develop an inflammatory process in their growth plates. This process is called physitis and it is usually the result of growth spurts mainly caused by improper nutrition. It is very painful and can lead to limb deformities (Developmental Orthopedic Diseases) due to changes in weight-bearing.
Keratolytic processes (keratolysis) are those in which there is loosening and/or separation of the horny layer of the epidermis. Therefore, White Line Disease can be defined as a keratolytic process on the solar surface of the hoof that is characterized by progressive separation of the inner zone of the hoof wall. This separation occurs in the non-pigmented layer of the hoof wall, in between the stratum medium and the stratum internum, and usually, the sensitive structures underneath are not involved. White Line Disease is also known as Seedy-toe, Onychomycosis and Candida.
White Line Disease is an infection in the white line area by fungi (Scopulariopsis, Aspergillus, PseudoAllsheria) and anaerobic bacteria. It is believed that the separation allows for the entrance of the fungi and bacteria in the white line causing the condition. However, recent studies have proposed that these organisms are simply secondary opportunists because in most cases it is possible to eliminate White Line Disease with debridement without the use of anti-microbial or anti-fungal therapies.
Mechanical and Environmental reasons are the main etiological factors of White Line Disease. Mechanical stress on the hoof wall, especially on horses with long toes and/or poor conformation, can induce the separation of the layers of the hoof wall. Excessive dryness conditions can lead to the presence of cracks in the hoof that can allow for the penetration of fungus and bacteria. Also, extreme wet conditions can stimulate flaring of the hoof wall and consequently separation in the white line region.
The Clinical signs are usually seen during routine trimming. Horses with White Line Disease very seldom suffer from lameness. Small powdery areas located at the dorsal aspect of the wall can be seen. In some instances, infected discharges can be seen. The diagnostics are usually made based on clinical findings. In severe cases, radiographs might be recommended in order to determine the severity of the separation. Gas pockets may be present but differently from those found in laminitic horses, they usually do not involve any sensitive structures.
The treatment mostly consists in removing the infected hoof wall. Topical disinfectants/astringents are often applied after hoof wall resection. In severe cases, support systems (frog support, pour-in pads or therapeutic shoes) may be used to increase weight bearing surface area if a considerable amount of hoof wall needs to be removed. The use of acrylic materials must be carefully analyzed as to avoid covering the infected region with composite allowing for the proliferation of the fungi and bacteria again. Horse should be kept in a clean environment, and the area should be periodically checked to verify correct growth of the new hoof wall. The prognosis for horses with this condition is usually very good with local debridement and appropriate shoeing.