Musculoskeletal System Introduction: Introduction

The musculoskeletal system consists of the bones, cartilage, muscles, ligaments, and tendons. Primary functions of the musculoskeletal system include support of the body, provision of motion, and protection of vital organs. The skeletal system serves as the main storage system for calcium and phosphorus and contains critical components of the hematopoietic system. Because many other body systems, including the nervous, vascular, and integumentary systems, are interrelated, disorders of one of these systems may also affect the musculoskeletal system and complicate diagnosis.

Diseases of the musculoskeletal system most often involve motion deficits or functional disorders. The degree of impairment depends on the specific problem and its severity. Skeletal and articular disorders are by far the most common; however, primary muscular diseases, neurologic deficits, toxins, endocrine aberrations, metabolic disorders, infectious diseases, blood and vascular disorders, nutritional imbalances or deficits, and occasionally congenital defects are diagnosed as well.

Disorders of muscles that are part of another body system may induce specific aberrations such as impairment of ocular motion and control, respiratory dysfunction, bladder malfunction, lack of penile retraction, and impairment of mastication and deglutition. Complete paralysis, paresis, or ataxia may be caused by primary muscular dysfunctions of infectious, toxic, or congenital origin; however, in most instances the primary disorder can be attributed to the nervous system (eg, tetanus, rhinopneumonitis, canine distemper, protozoal myelitis), with the muscular system merely representing the effector organ.

The structural and functional unit of skeletal muscle is the motor unit. It consists of a ventral motor neuron with its cell body in the central horn of the spinal cord and its peripheral axon, the neuromuscular junction, and the muscle fibers innervated by the neuron. Each of these components must be functionally intact for the muscle to contract properly. The ventral motor neuron is the final common pathway conducting neural impulses from the CNS to the muscle.

The transmission of a nerve impulse at the neuromuscular junction involves massive release of acetylcholine from small synaptic vessels, where it is stored. The acetylcholine fills the synaptic cleft between the nerve terminal and the muscle fiber membrane, where most of it is destroyed by cholinesterase within a fraction of a second. This short period of activity is sufficient to excite the muscle fiber membrane, which results in a significant increase in membrane permeability to sodium ions and allows rapid influx of sodium into the muscle fiber. The sodium ion increases the endplate potential, which elicits electrical currents that spread to the interior of the fibers where they cause a release of calcium ions from the sarcoplasmic reticulum. The calcium ions initiate, in turn, the chemical events of the contractile process. When this occurs in all the muscle fibers innervated by each motor neuron (possibly thousands), muscle contraction results.

Normal muscle, comprising many motor units, is dynamic, and its function and structure can be influenced by many diseases. Disorders that affect the neuromuscular junction (eg, myasthenia gravis, hypocalcemia, hypermagnesemia) can result in muscle fatigue, weakness, and paralysis. The neuromuscular junction can also be affected by muscle-relaxing drugs (eg, curare, succinylcholine, M99), certain antibiotics, and toxins (eg, botulism, tetanus, venoms).

Disorders primarily of the muscle membrane and, to some extent, of the actual muscle fibers are called myopathies. Muscle membrane disorders may be hereditary (eg, myotonia congenita in goats) or acquired (eg, vitamin E and selenium deficiencies, hypothyroidism, and hypokalemia). Myopathies involving the actual muscle fiber components include muscular dystrophy, polymyositis, eosinophilic myositis, white muscle disease, and exertional rhabdomyolysis. Various laboratory tests, eg, histopathologic examination, determination of serum enzyme levels, electromyographic studies, thermography, and determinations of conduction velocity, are very useful in confirmation of a specific diagnosis.

Tendons act as bridging and attachment structures for the muscles; some bridge long gaps between the muscle bellies and target bone and, therefore, are prone to injury themselves, especially because they are often loaded to the extreme and are only minimally capable of elastic elongation. A prime example is the superficial flexor tendon of horses, which is frequently injured by partial tearing that leads to tendinitis. Another acquired injury of tendons involves traumatic disruptions. Due to the relatively poor blood supply of both tendons and ligaments, healing is delayed and frequently poor. Management of injuries to ligaments and tendons requires patience and prudent longterm rehabilitation.

Bone diseases are generally congenital or hereditary, nutritional, or traumatic. Congenital disorders include in utero malformations and atavisms, such as polydactyly or persistent ulnae or fibulae in foals; examples of genetic defects are atlanto-occipital malformations in Arabian horses or certain cases of spinal ataxia, canine hip dysplasia, and abnormal bone formation such as that caused by parathyroid hypoplasia.

Bone defects due to nutrition are caused primarily by imbalances or deficiencies in minerals, particularly the trace minerals such as copper, zinc, and magnesium. Calcium and phosphorus concentrations must also be present in the correct ratio. Osteomalacia represents the classic example of imbalanced or deficient calcium and phosphorus intake. Other nutritional disorders are caused by excessive protein intake of growing animals. Either deficiency or excess intake of certain vitamins, particularly vitamins A and D, may influence growth and development of bone. Aseptic physitis or special osteochondrotic conditions of the physes may be caused by zinc toxicity or copper deficiency.

Traumatic causes of bone disorders represent the vast majority of cases and include fractures, fissures, periosteal reactions as a result of trauma, sequestrum formation, and insertion desmopathies or tendinopathies, respectively. Lack of weight bearing, reduced motion, instability, pain, heat, or swelling usually accompany these disorders. Diagnostic procedures include inspection, manual palpation, diagnostic imaging (such as radiography, ultrasonography, or thermography, and increasingly scintigraphy, computed tomography, or MRI), and diagnostic anesthesia to determine the specific anatomic structure or region involved in the problem.

Articulations are divided into synarthroses, in which the osseous components are united by fibrous tissue or cartilage, and diarthroses, in which the opposing bone ends are covered with hyaline cartilage and are separated by a joint cavity filled with synovial fluid. Synarthroses are practically immovable and are rarely associated with joint disease other than fractures. In most cases, diarthroses are movable joints, with a variable degree of mobility depending on the anatomic location of the joint. Diarthroses are frequently involved in pathologic changes involving any of their anatomic structures: the fibrous joint capsule, synovial membrane, hyaline articular cartilage, subchondral bone, and intra-articular ligaments (and also the menisci in the stifle joint). Joint disorders may be caused by trauma (acute, sharp, or blunt), chronic inflammation, developmental factors, or infections. Acute trauma frequently results in luxation, subluxation, fracture, or distortion of a joint. Direct articular trauma may also lead to septic arthritis or rupture of a collateral ligament or the joint capsule.

Developmental defects include osteochondritis dissecans, equine ataxia, and lumbar disk syndrome in certain breeds of dogs. Extension of physitis into the adjacent joint and damage due to continuous abnormal weight bearing in animals with angular limb deformities are other inciting causes of joint disease. Bacterial and fungal infections involving joints and other synovial structures, such as tendon sheaths, are usually quite clearly recognizable and require immediate and aggressive treatment.

Chronic inflammation of joints and surrounding structures is most common in articulations associated with locomotion, although other joints, such as the temporomandibular, may occasionally be affected. Normal synovial fluid lubricates the synovial tissues in a joint through boundary lubrication, including a glycoprotein expressed from the cartilage during weight bearing. The synovial fluid also nourishes the articular cartilage. Any joint injury alters the volume and composition of the synovial fluid (as a result of an increased permeability of the inflamed synovial membrane relative to blood components) and increases the intraosseous pressure in the involved bones. The increased WBC count leads to an increased concentration of proteolytic enzymes within the synovial fluid, which leads to proteoglycan washout and eventually cartilage destruction.

Diagnostic procedures to determine the nature, extent, and exact location of the joint disorder include inspection, manual palpation and manipulation, diagnostic imaging techniques, local or intra-articular anesthesia, diagnostic arthroscopy, and laboratory examination of synovial fluid or biopsy of synovial membrane.

The diagnostic and therapeutic options for management of musculoskeletal disorders have greatly expanded during the last few years and allow a return to a useful life for most animals if done early in the disease process.