McCance 45

• The musculoskeletal system comprises bones, muscles, cartilage, tendons, ligaments, and connective tissues, providing structure, support, stability, and movement.
• Injuries to this system include fractures, dislocations, sprains, and strains, while alterations can stem from metabolic disorders, infections, inflammatory diseases, or tumors, with osteoporosis being the most common bone disease, increasing with age.
• Trauma is a major cause of injury, particularly for those aged 1-44, with fractures often resulting from falls, car accidents, and athletic injuries, leading to significant personal and societal impacts.

Skeletal Trauma: Fractures

• A fracture is a bone break occurring when applied force exceeds the bone's tensile or compressive strength.
• Fracture incidence peaks in young males (15-24) and older adults (65+), with hip and wrist fractures more common in women.
• Classifications include complete (bone broken into two pieces) or incomplete (bone damaged but in one piece), and open (skin broken) or closed (skin intact).
• Fracture lines are described as linear, oblique, spiral, or transverse.
• A comminuted fracture involves the bone breaking into more than two fragments.
• Incomplete fractures include greenstick (one cortex broken, common in children), buckle/torus (cortex buckles), and bowing (bending of bone, common in children).
• Fragility fractures result from low-level trauma, often due to osteoporosis.
• Pathologic fractures occur at sites weakened by abnormalities like tumors.
• Stress fractures are from cumulative repeated forces, with fatigue fractures from abnormal stress on normal bone and insufficiency fractures in bones lacking normal ability.
• Transchondral fractures involve fragmentation of articular cartilage at a joint, common in adolescents.

Pathophysiology of Fractures

• Bone breakage disrupts the periosteum and blood vessels, causing bleeding and hematoma formation.
• Necrotic tissue and debris trigger an inflammatory response, leading to vasodilation and infiltration by leukocytes and mast cells.
• Cytokines promote healing.
• Vascular tissue invades within 48 hours, increasing blood flow.
• Osteoblasts and osteoclasts form procallus on the bone's outer surface.
• Healing occurs in three phases: inflammation, repair (granulation tissue and callus formation), and remodeling (resorption of callus and trabeculae formation).
• Bone uniquely heals with normal tissue, not scar tissue.

Fracture Clinical Manifestations, Evaluation, and Treatment

• Manifestations vary by fracture type and location, including impaired function, deformity, swelling, muscle spasm, tenderness, pain, and impaired sensation.
• Bone segment position relies on muscle pull, gravity, and the force's direction.
• Trauma typically causes immediate, severe pain, with subsequent pain from muscle spasm or soft tissue damage.
• Pathologic fractures can cause angular deformity or painless swelling.
• Stress fracture pain is gradual, relieved by rest, with local tenderness and swelling.
• Transchondral fractures can be asymptomatic or painful, with limited range of motion and crepitation.
• Treatment involves realigning bone fragments (reduction) and immobilization, with options including closed manipulation, traction, or open reduction.
• Traction uses weights to align bone fragments. Skin traction is for brief use with less force, while skeletal traction involves pins or wires through the bone.
• Open reduction is surgery to align fragments with hardware for internal fixation.
• External fixation uses pins and an external frame for significantly displaced open fractures.
• Bone grafts can be autographs, allografts, or bone substitutes.
• Improper treatment can lead to nonunion (failure to unite), delayed union (occurs after 8-9 months), or malunion (healing in a non-anatomic position).
• Modalities such as electric current devices, electromagnetic fields, ultrasound, stem cells, and gene therapy stimulate new bone formation.

Dislocation and Subluxation

• Caused by trauma, ligamentous laxity, nerve injury, rheumatoid disease, or genetics.
• Dislocation is temporary bone displacement from a joint; subluxation is partial loss of joint surface contact.
• Dislocations are simple or complex (with fracture).
• Dislocations and subluxations are common in those under 20.
• The shoulder, elbow, wrist, finger, hip, and knee joints are most often affected; shoulder dislocations are common due to glenohumeral joint instability.
• Anterior shoulder dislocation is most common, from indirect force causing extreme external rotation.

Pathophysiology of Dislocation and Clinical Manifestations

• Dislocations can cause fractures, nerve and blood vessel damage, and soft tissue injury.
• Shoulder dislocation can damage the axillary nerve.
• Elbow dislocations can lead to ischemic paralysis if pressure on arteries is not relieved.
• Hip dislocations can result in avascular necrosis.
• Knee dislocation often tears collateral and cruciate ligaments.
• Symptoms include pain, swelling, limited motion, and joint deformity.
• Pain comes from inflammatory exudate or ligament injury.
• Deformity is due to muscle contractions or fluid in the joint.
• Dislocated elbows are often flexed and resist movement. Shoulder injuries cause pain aggravated by lifting the arm.
• Hip dislocations cause severe pain, gait abnormalities, and potential limb shortening.

Evaluation and Treatment of Dislocation and Subluxation

• Evaluation involves clinical manifestations and roentgenograms.
• Treatment includes reduction and immobilization for 2-6 weeks, followed by exercises to restore range of motion.
• Healing typically takes months to years.

Support Structure Trauma: Sprains and Strains

• Tendon and ligament injuries can occur with fractures and dislocations.
• A tendon attaches muscle to bone; a ligament connects bones in a joint.
• These structures support and limit motion.
• A strain is a tendon tear; a sprain is a ligament tear.
• Complete separation from bone is an avulsion, seen in young athletes.
• Injuries are classified as first, second (moderate), and third-degree (severe).
• Tendons most often injured include those in the hands, feet, knee, upper arm, thigh, ankle, and heel.

Pathophysiology of Tendon and Ligament Injuries

• Tearing initiates an inflammatory cascade with cytokines, nitric oxide, prostaglandins, and lipoxins.
• Inflammatory exudate develops between torn ends.
• Granulation tissue forms with macrophages, fibroblasts, and capillary buds.
• Collagen forms randomly, then organizes along stress lines.
• Vascular fibrous tissue fuses new and surrounding tissues.
• Healing tendon or ligament lacks strength for 4-5 weeks, risking re-separation.
• Scar remodeling takes months to years.

Clinical Manifestations, Evaluation, and Treatment of Sprains and Strains

• Injuries cause pain and functional limitation, with swelling and contour changes.
• Pain is sharp and localized, with tenderness.
• Joint swelling occurs in finger and elbow sprains.
• Flexion deformities occur in finger injuries.
• Elbow pain is worsened by flexion, supination, and extension, or wrist extension.
• Upper arm injuries cause weakness during forearm flexion.
• Knee injuries cause immobility, instability, or patella shifts.
• Evaluation involves clinical signs, stress radiography, arthroscopy, or arthrography.
• Treatment includes protection, early motion, and rehabilitation.
• Complete rupture may need surgical repair or grafting.

Tendinopathy and Bursitis

• Tendinopathy includes tendinitis, tendinosis, and paratendinitis, involving painful degradation or inflammation. Neovascularization in tendinopathy accompanies nerve ingrowth, facilitating pain transmission.
• Epicondylitis is inflammation at a tendon's origin, often due to tissue degeneration rather than inflammation.
• Lateral epicondylopathy (tennis elbow) affects the extensor carpi radialis brevis tendon.
• Medial epicondylopathy (golfer's elbow) affects pronator teres, flexor carpi radialis, and palmaris longus tendons.
• Bursae are sacs lubricating tendons, muscles, and bony prominences.
• Bursitis is inflammation of bursae, often due to trauma or repetitive irritation.
• Septic bursitis is caused by wound infection or bacterial infection.

Pathophysiology and Manifestations of Tendinopathy and Bursitis

• Tendinitis causes inflammatory fluid accumulation and thickening of the tendon sheath.
• Microtears cause bleeding, edema, and pain, potentially leading to calcific tendinitis.
• Bursitis is inflammation reactive to overuse, causing swelling and potential spread to adjacent tissues.
• Tendinopathy causes localized pain worsened by active motion.
• Bursitis causes gradual or sudden pain without compromising joint movement.
• Shoulder bursitis impairs arm abduction; knee bursitis causes pain climbing stairs; hip bursitis causes pain crossing legs.
• Signs of infectious bursitis include puncture sites, prior corticosteroid injection, severe inflammation, or adjacent infection.

Evaluation and Treatment of Tendinopathy and Bursitis

• Evaluation involves clinical manifestations, physical exam, arthroscopy, ultrasound, and MRI.
• Treatment includes analgesics, ice or heat, local anesthetic and corticosteroids, and aspiration for bursitis.
• Physical therapy follows to prevent loss of function.

Muscle Strains

• Muscle strain is local damage from sudden, forced motion.
• Strains often affect tendons, with muscles rupturing more in young people and tendons in older adults.
• Muscle strain can be chronic from repeated overstretching.
• Tissue disruption, regeneration, and connective tissue repair occur, with hemorrhage and inflammation.
• Muscle cells usually regenerate within 6 weeks with protection.
• A late complication is myositis ossificans or heterotopic ossification (HO), with abnormal bone formation in soft tissue.

Rhabdomyolysis

• Rhabdomyolysis is rapid muscle breakdown releasing intracellular contents into the bloodstream. Delta lesions in the sarcolemmal membrane suggest that it is the release route.
• Myoglobinuria is the presence of myoglobin in urine, often from crush injuries.
• Causes include crush injury, compartment syndrome, or crush syndrome.
• Rhabdomyolysis can lead to hyperkalemia, metabolic acidosis, acute renal failure, and DIC.
• Malignant hyperthermia (MH) is a hereditary disorder causing excessive calcium release from the sarcoplasmic reticulum, leading to hypermetabolic state and muscle rigidity.
• Dantrolene reverses MH effects by inhibiting calcium release.
• Compartment syndromes result from compromised blood flow due to increased pressure, leading to ischemia.
• Symptoms are pain out of proportion to injury, paresthesia, pallor, pulselessness, and paralysis. Fasciotomy and debridement may be required.

Clinical Manifestations, Evaluation, and Treatment of Rhabdomyolysis

• Symptoms include muscle pain, weakness, and dark urine from myoglobinuria.
• Muscular pain and weakness may not be present.
• Renal threshold is low so only 200g of muscle needs to be damaged to visibly change the urine
• Serum creatine kinase (CK) level is most important for evaluation; levels exceeding 5000 units/L indicate likely renal failure.
• Maintain adequate urinary flow and prevent kidney failure, with rapid intravenous hydration.
• Hemodialysis may be needed for hyperkalemia. Some treatments like Mannitol have not improved outcomes.

Disorders of Bones: Metabolic Bone Diseases

• Metabolic bone disease involves abnormal bone structure due to altered biochemical reactions.
• Abnormalities affect genetic, mineral, vitamin, hormone, and structural aspects of bone.

Osteoporosis

• Osteoporosis is characterized by low bone mineral density (BMD), impaired bone integrity, decreased bone strength, and fracture risk.
• Primary (idiopathic) osteoporosis is most common.
• Secondary osteoporosis results from conditions like endocrine diseases, medications, and substances, including tobacco & ethanol
• Cortical bone becomes porous and thin.
• The WHO defines osteoporosis based on bone density: normal (>833 mg/cm2), osteopenia (833-648 mg/cm2), and osteoporosis (<648 mg/cm2).
• Progresses silently until fractures occur; old bone is reabsorbed faster than new bone is made.
• Severe or established osteoporosis involves fragility fracture.
• Bone formation exceeds resorption until age 30, then reverses. Bone loss begins before menopause in women, and is most rapid in the first years after menopause
• More common in women than in men at a rate of one in two women.
• Vertebral fractures are most common but may be asymptomatic, leading to deformity or reduced pulmonary function.
• Mexican-Americans have higher osteoporosis risk, while non-Hispanic blacks have lower risk.
• Whites are more susceptible than races to osteoporosis. Blacks have half the fractures as whites.
• Bone quality is determined by microarchitecture, crystal size and shape, brittleness, vitality of bone cells, structure of bone proteins, water volume, vascular supply, and the ability to repair cracks.
• Testing for bone density may or may not identify those with increased fracture risks.
• The FRAX tool predicts 10-year fracture probability.
• Postmenopausal osteoporosis results from estrogen deficiency.
• Hormonal deficiency can increase with stress, excessive exercise, and low body weight.
• Estrogen deficiency can cause imbalanced remodeling.
• IGF declines by age 60, which is significant in premenopausal bone maintenance.
• Steroid levels are significant, but when estrogen levels decrease circulating androgens become significant effectors on bone metabolism
• Deficiencies of vitamins C, D, E, and K can contribute to bone loss.

Pathophysiology

• ROSs produced by arobic metabolism serve as signaling molecules for osteocytes, osteoblasts and osteoclasts
• When excess ROSs accumulate, it can result in loss of bone mass and bone strength
• Bone loss can be prevented by transcription factors that help against the effects of OS
• Osteoclast differentiation pathway is controlled by hormones, cytokines, and paracrine stromal-cell microenvironment interactions. Interleukins (IL-1, IL-4, IL-6, IL-7, IL-11, IL-17), tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β),prostaglandin E2, and hormones interact to control osteoclast
• Normal bone homeostasis is dependent on the balance between the cytokine receptor activator of nuclear factor κβ ligand (RANKL),its receptor RANK, and its decoy receptor osteoprotegerin (OPG)
• Osteoclast biology and pathogenesis of bone loss are know due to tremendously increased knowledge of molecular events
• RANKL promotes osteoclast development, necessary for osteoblast. Suppresses apoptosis that leads to activation.
• OPG blocks effect of RANKL prevents it from binding which reduces signaling involved in osteoclasts
• Postmenopausal osteoporosis is characterized by increased bone resorption relative to the rate of bone formation, leading to sustained bone loss resulting from estrogen deficiency.

Clinical Manifestations, Evaluation, and Treatment of Osteoporosis

• Common symptoms include bone deformity such as Kyphosis (hunchback) and fractures; fractures are likely to occur as bone becomes thin.
• Fractures include the femur and humerus, distal radius, ribs and vertebrae.
• Diagnosed by Increased radiolucency of bone in radiographic tests.
• Bone density is measured as standard deviations, the T-Score.
• Osteopenia is a bone density score between 1.5 and 2.5 standard deviations below normal.
• A T-score of 2.5 is more standard deviations below normal which is considered osteoporosis.
• Treatment is focused on preventing fractures.
• Calcium supplements are often given. Mg++ for normal calcium absorption and bone development.
• Weightbearing exercise and muscle enhancing exercise is advised
• Postmenopausal women are given SERMs due to their positive effects on bone but minimize estrogen's negative effects on breast and endometrial issues. (Raloxifene and tamoxifen)
• Bisphosphonates improves osteoblast survival because bone loss is prevented by the blocking of osteoclast activation with anti-RANKL
• Treatment of OPG / RANKL ratio, (Biologic agents such as cathepsin K inhibitors, antisclerostin and anti-dickkopf antibodies)

Osteomalacia

• Osteomalacia is the delayed mineralization of osteoid in compact and spongy bone, resulting in soft bone instead of rigid bone leading to abnormal bone matrix mineralization
• Rickets is similar but occurs in growing bones in children Tumors can effect chronically low phosphate levels and that can result in osteomalacia
• Osteomalacia is effected by fibroblast growth factor that maintains serum phosphate levels
• Risk factors are a vitamin D deficiency, diets deficient in vitamin D, decreased endogenous production of vitamin D, intestinal malabsorption of vitamin , renal tubular diseases and anticonvulsant therapy
• Phenobarbital and phenytoin, interfere with calcium absorption and increase degradation of vitamin D metabolism in the liver through activation of the cytochrome P-450 pathway.

Pathophysiology and Clinical Manifestations of Osteomalacia

• Crystal of Minerals in osteoid requires adequate concentrations of calcium and phosphate.
• Vitimin D dificiency, Vitimin D normally regulates and enhances the absorption of calcium ions but they no not so the person is at risk because plasma calcium is low.
• Trabeculae in spongy bone become thinner whereas haversian systems become large and iregular.
• Causes diffuse skeletal pain and tenderness, particularly in the hips and Muscular weakness and proximal muscles are common.
• Facial deformities and bowed knees may be present and Bone fractures and vertebral collapse occur with minimal trauma

Evaluation and Treatment of Osteomalacia

• Elevated blood urea nitrogen (BUN) and elevated creatinine levels, serum calcium levels are normal or low, a serum inorganic phosphate level that is usually higher than 5.5 mg. Alkaline phosphatase and PTH levels are elevated.
• Radiographic findings show pseudofractures andradiolucent bands perpendicular to the surface of involved bones. Bone biopsy
• Diagnosed via serum FGF-23 measurement. If levels are elevated it means the patient could have one of the two hypophosphatemic
• Treatment involves: Adjusting serum calcium and phosphorous levels to normal, suppressing secondary hyperthyroidism, chelate bone aluminum, administer vitamin D, dialysis and/or renal transplant

Paget Disease

• Is characterized by increased metabolic activity, causes accelerated remodeling, and it results in enlarged and softens affected bones
• Genetic plays a significant role due to manipulations in the RANK–NF-κβ signaling pathways which caused increased osteoclast activity
• Classic PDB causes disorderly bone resorption and formation.
• affects vertebrae, skull, sacrum, sternum, pelvis, most often found at age of 40
• 10–30% have mutations of sequestosome-1 and has associations even with gene etiologies

Pathophysiology, Clinical Manifestations, and Treatment of Paget Disease

• Paget disease begins with excessive resorption of spongy bone and deposition of disorganized bone.
• The skull (thickening and asymmetrical), facial bones and long bones are affected.
• compression, sensory impairment , motor impairment, hearing loss, atrophy, obstruction of the lacrimal duct, and headache
• Warmth occurs over affected bone.
• Can lead to cord compression. Rare chance of osteogenic sarcoma.
• Diagnosis is confirmed via bone scan which can detect a build up of radionuclides. X-ray can be used in some cases.
• Levels are high if tested for alkaline phosphate
• Treatment is for pain relief and prevention of deformity or fracture with bisphosphenates
• Surgery is advised if neurologic complications or severe bony deformities

Infectious Bone Disease: Osteomyelitis

• Osteomyelitis is a bone infection caused by a wide range of microorganisms.
• The route could be exogenous (outside the body) or through the blood
• Can be found at any age.
• Staphylococcus aureus can be caused by different types of bacteria can happen at any time
• In infants equal male to female.
• Soft Tissue disorders and Gastrointestinal Tract contamination
• Bones can be exposed from animal or human Bites
• Treatment involves multiple drugs. and Long Term Antibiotic Treatment Regimen. Some are ineffective in many cases.