Study Guide for Patho II Exam 2 (MSK) PDF

STUDY GUIDE FOR PATHO II EXAM 2 (MSK) Bone remodeling units -​ bone remodeling units are bone precursor cells that becomes osteoblasts and clasts These BMUs differentiate into both osteoblasts and osteoclasts. Bone-remodeling units (BMU) are made up of precursor cells that differentiate int...

STUDY GUIDE FOR PATHO II EXAM 2 (MSK) Bone remodeling units -​ bone remodeling units are bone precursor cells that becomes osteoblasts and clasts These BMUs differentiate into both osteoblasts and osteoclasts. Bone-remodeling units (BMU) are made up of precursor cells that differentiate into osteoblasts and osteoclasts. -​ Repairs microscopic injuries and maintains bone integrity The integrity of bone is maintained by bone remodeling, a 3-phase process in which existing bone is resorbed and new bone is laid down to replace it. -​ Osteoclasts and osteoblasts work together as a basic multicellular unit (BMU) to remove old bone by osteoclast activity and to deposit new bone by osteoblast activity. -​ BMUs are made up of bone precursor cells that differentiate into osteoclasts and osteoblasts. Precursor cells are located on the free surfaces of bones and along the vascular channels (especially the marrow cavities). Bone Remodeling Phases 1)​ Phase 1 (activation) - a stimulus (e.g., hormone, drug, vitamin, physical stressor, visible injury) stimulates precursor cells to form osteoclasts, which leads to reabsorption. activates programmed osteocyte cell death (apoptosis). The distribution of these apoptotic osteocytes provides the osteoclasts with information about where to begin resorbing damaged bone. 2)​ Phase 2 (resorption) - Osteoclasts (large cells; multinucleated) gradually absorb bone. the osteoclasts form a “cutting cone,” which gradually resorbs bone, leaving behind an elongated cavity termed a resorption cavity. -​ Lysosomal enzymes produced by osteoclasts “digest” bone; the osteoclasts then release the degraded bone products into the vascular system. 3)​ Phase 3 (formation) - - Osteoblasts (small cells) lay down new secondary bone in the reabsorption cavity (secretes matrix) - When osteoblasts become trapped in their own matrix, they become osteocytes and stop dividing. new bone formation begins as osteoblasts lining the walls of the resorption cavity express osteoid and alkaline phosphatase, forming sites for calcium and phosphorus deposition. New bone is formed as the osteoid mineralizes. -​ Successive layers (lamellae) in compact bone are laid down until the resorption cavity is reduced to a narrow haversian canal around a blood vessel. The old haversian systems are destroyed and new haversian systems are formed. -​ The formation phase takes 4 to 6 months in humans. Bone-remodeling units (BMU) are made up of precursor cells that differentiate into osteoblasts and osteoclasts. -​ Repairs microscopic injuries and maintains bone integrity Phases 1) Activation of the remodeling cycle - There is a stimulus (hormone, physical injury/stressor, vitamin, or drug) that stimulates precursor cells to form osteoclasts, which leads to reabsorption 2) Reabsorption - Osteoclasts (large cells; multinucleated) gradually absorb bone 3) Formation of new bone - Osteoblasts (small cells) lay down new secondary bone in the reabsorption cavity (secretes matrix) - When osteoblasts become trapped in their own matrix, they become osteocytes and stop dividing.  - Osteogenic cell (undergo mitosis) → Osteoblasts (non-mitotic) → Osteocyte - All belong to one cell lineage: Mesenchymal stem cells/Stromal cells - capable of producing reticular, fibroblastic, osteogenic, and adipose cell lines - Osteoclasts are formed by the fusion of several stem cells from hematopoietic progenitors in the bone marrow, which could also give rise to monocytes and macrophages. → Unusually large cells up to 115 micrometers & visible to the naked eye Fracture types/descriptions -​ know common, open, pathologic, avulsion, etc Fracture: a fracture is a break in the continuity of a bone -​ Manifestations: Unnatural alignment, swelling, tenderness, pain, impaired sensation, and possible muscle spasms  -​ A broken bone can cause damage to the surrounding tissue, the periosteum, and the blood vessels in the cortex and marrow Fracture Classifications - Complete or incomplete - Closed (simple fracture) or open (compound fracture; bone is protruding out from the skin) - Comminuted - multifragmentary (3+ pieces of bone from the fracture) - Linear - fracture is parallel to the long axis of the bone - These fractures are sometimes easier to see if we put the x-ray in a vertical position. - Oblique - fracture is slanted across the bone - Spiral - twisting of the bone ends - Transverse - fracture is perpendicular to the long axis of the bone Incomplete Fractures Greenstick, torus & bowing fractures are usually seen in kids dt softer bone - Greenstick - the bone bends and the fracture only occurs on one side (like a young green stick). Lateral force to the bone, doesn’t breath through the whole bone, just a part of it - Torus (Buckle) - buckling on the periosteum - Bowing - secondary to longitudinal stress - Pathologic - no trauma; usually in older people - Could be from a tumor that weakens the bones, or just regular stresses of the bone - Stress - the bones are lacking the ability to deform and recover. Ex: someone who doesn’t exercise runs a marathon, beating of the bones can cause a stress fracture - Transchondral - articular cartilage is involved  Typical Complete Fractures Closed fracture Skin overlying the bone is intact Open fracture Communicating wound between bone and skin Comminuted fracture Multiple bone fragments Linear fracture Fracture line parallel to long axis of bone  Oblique fracture Fracture line at an angle to long axis of bone Spiral fracture Fracture line encircling bone (as in a spiral staircase) Transverse fracture Fracture line perpendicular to long axis of bone Impacted Fracture fragments are pushed into each other Pathologic Fracture occurs at a point in the bone weakened by disease (e.g., bones with tumors or osteoporosis) Avulsion A fragment of bone connected to a ligament or tendon breaks off from the main bone Compression Fracture is wedged or squeezed together on one side of bone Displaced Fracture with one, both, or all fragments out of normal alignment Extracapsular Fragment is close to the joint but remains outside the joint capsule Intracapsular Fragment extends into or is within the joint capsule Fragility Fracture caused by low-level trauma Typical Incomplete Fractures Greenstick fracture Break on one cortex of bone with splintering of inner bone surface (commonly occurs in children and older adults) Torus fracture Buckling of cortex Bowing fracture Bending of the bone Stress fracture Microfracture Transchondral fracture Separation of cartilaginous joint surface (articular cartilage) from main shaft of bone Fracture healing stages -​ hematoma→ pro callous→ callus → callous replacement → remodeling -​ has 5 questions on this 1) Hematoma formation → Occurs w/in a few hours of the fracture -​ There will be damage to the periosteum which causes disruption of the conversion systems which causes cell death. Inflammatory response with increased blood flow to the entire bone. 2) Procallus formation → Occurs w/in a few days; fibrovascular tissue will replace the clot and collagen fibers are laid down w/ osteoblasts coming in.  -​ Osteoblasts secrete osteoid which mineralize and from a callous -​ An osteoid is a newly formed organic bone matrix before calcification 3) Callus formation → Develops over next few weeks; Osteoblasts will attract phosphate and calcium to harden and form a callous -​ Forms first at the periosteum 4) Callus replacement & Remodeling → Could take months to years depending on how bad the fracture is -​ There is a continuation of osteoblastic activity and remodeling of the endosteal and periosteal surfaces to pre-injury size and shape. Callous Formation A) Can’t really see a fracture B) You can see a little fracture after 2 weeks (occult/hidden fracture) - If the Pt has an injury with high suspicion of fracture but the fracture is not seen in X-ray, tell the Pt to return in 2 weeks for repeat X-rays. - If nothing is still seen in 2 weeks, it is probably a contusion. C) Some whitening around the periosteum is the callous forming after 2 months D) At 4 months, we see the callous getting rid of the fracture line. Bone remodeling will then remove the callous to look like pre-injury. Manifestations: -​ Unnatural alignment, swelling, tenderness, pain, impaired sensation, and possible muscle spasms Tx: -​ closed manipulation, traction, and open reduction, immobilzation Improper reduction or immobilization: -​ nonunion -​ delayed union -​ malunion Hematoma (w/in hours) → Procallus → Callus → Callus replacement and remodeling The remodeling process can repair microscopic bone injuries, but gross injuries (fractures, surgeries), heal by the same stages as soft tissue injuries, except that new bone (not scarring) is the final result:  1)​ Hematoma formation: Vessels have been damaged, causing hemorrhage. Fibrin and platelets within the hematoma form a meshwork that is the initial framework for healing with the help of hematopoietic growth factors such as platelet-derived growth factor and TGF-β. -​ Occurs w/in hours of fracture of surgery 2)​ Procallus formation: Fibroblasts, capillary buds, and osteoblasts move into the wound to produce granulation tissue called procallus. Cartilage is formed as a precursor of bone, and types I, II, and III collagen are formed. Enzymes and growth factors, such as insulin and insulin-like growth factors, plus bone morphogenic protein and osteogenin, aid in this stage of healing. -​ Occurs w/in days 3)​ Callus formation: Osteoblasts in the procallus form membranous or woven bone (callus). Enzymes increase the phosphate content and permit the phosphate to join with calcium to be deposited as mineral to harden the callus. -​ Occurs w.in weeks 4)​ Replacement: BMUs of the callus are replaced with lamellar bone or trabecular bone 5)​ Remodeling: The periosteal and endosteal surfaces of the bone are remodeled to the size and shape of the bone before injury. -​ Replacement and contour modeling occur w/in years Bone healing speed depends on: -​ Severity of the bone disruption; -​ The type and amount of bone tissue that must be replaced (spongy bone heals faster); -​ The blood supply and oxygen content at the site -​ The presence of growth and thyroid hormones, insulin, vitamins, and other nutrients -​ The presence of systemic disease -​ The effects of aging -​ The effectiveness of treatment (immobilization + prevention of complications). Malunion, nonunion, delayed union -​ malunion- heals in non-anatomic position -​ non- there's a gap -​ delayed- after a few months of no healing Improper reduction or immobilization of a fractured bone may result in nonunion, delayed union, or malunion. -​ Nonunion is failure of the bone ends to grow together. -​ The gap between the broken ends of the bone fills with dense fibrous and fibrocartilaginous tissue instead of new bone. -​ Occasionally, the fibrous tissue contains a fluid-filled space that resembles a joint, termed a false joint, or pseudarthrosis. -​ Delayed union is union that does not occur until approximately 8-9 months after a fracture. -​ Malunion is the healing of a bone in a non anatomic position. Treatment of delayed union and nonunion Various modalities designed to stimulate new bone formation: -​ Physical modalities (electric current devices, electromagnetic field, and low-density ultrasound) -​ Stem cells and gene therapy -​ Large defects in bone can be filled with bone graft or synthetic materials, such as calcium phosphate cement. Fracture nonunion: failure of a fractured bone to heal and mend after an extended period of time - failure of the bone ends to grow together; the gap between the bone ends will be filled w/ fibrous or cartilaginous tissue → pseudoarthrosis -​ Nonunion Fracture (Third Metatarsal Head/Neck) -​ Note that the margins between the two segments are hypertrophied, sclerotic (increased density), and well-defined in their outline and appearance. -​ Delayed union: if no union w/in 8-9 months Fracture Malunion -​ Fracture malunion: fracture that has healed in a deformed position, or w/ shortening or rotation of the limb. - healing occurs in a non-anatomic position - Left → Malunion in the tibial shaft. - will probably affect ankle joint - Right → Malunion in the fourth metatarsal (distal one third diaphysis) and fifth metatarsal (middle one-third diaphysis). - bony prominence will make wearing shoes uncomfortable. Hallmark of and underlying patho in OA -​ loss of proteoglycans from articular cartilage Noninflammatory Joint Disease -​ Differentiated from inflammatory by: -​ Absence of synovial membrane inflammation -​ Lack of systemic signs and symptoms -​ Normal synovial fluid analysis Osteoarthritis: Degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs (osteophytes) -​ Characterized by local areas of damage and loss of articular cartilage, osteophytosis, subchondral bone changes, and variable degrees of mild synovitis and thickening of the joint capsule -​ Osteophytosis: new bone formation of the joint margins -​ Patho: The synovial fluid demonstrates mononuclear leukocytosis. During inflammation, neutrophils come in the synovial fluid. Calcium crystals may be seen on synovial fluid analysis. -​ Subchondral microfractures can occur. -​ Hallmark of OA: Loss of proteoglycans from articular cartilage. -​ ↑ enzymes: responsible for stromelysin and acid metalloproteinase -​ Also referred to as degenerative joint disease (DJD) - Incidence increases with age - Primary disease is idiopathic  - Manifestations: - Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity - No systemic symptoms! Osteoarthritis (OA) is characterized by local areas of loss and damage of articular cartilage, new bone formation of joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis, and thickening of the joint capsule -​ Classified as noninflammatory joint disease. -​ Low-grade inflammation, calcification of articular cartilage, and interaction between transcription factors, cytokines, growth factors, matrix molecules, and enzymes affect development and progression of OA. -​ Primary/Idiopathic OA - occurs without a known precipitating cause (insidious) with agin -​ Secondary OA - occurs w/ predisposing events (injury, long-term mechanical stress or chronic diseases) or medications. -​ Incidence increases w/ age, Women > Men Pathophysiology The primary pathogenesis in OA is degeneration and then eventual loss and disordered repair of articular cartilage. -​ The chondrocytes of the articular cartilage become damaged early in the disease process because of atypical load bearing as well as both genetic/epigenetic and biochemical factors → remodeling of the articular cartilage and a loss of the smooth, frictionless joint. -​ The cartilage becomes thin and may be absent over some areas, leaving the underlying subchondral bone unprotected. -​ Articular cartilage is lost through a cascade of cytokine, biochemical, and growth factor pathways. Enzymatic processes involving collagenase break down the macromolecules of proteoglycans, glycosaminoglycans, and collagen into large, diffusible fragments. The fragments are then taken up by the chondrocytes and digested by the cell's own lysosomal enzymes. The loss of proteoglycans from articular cartilage is a hallmark of the osteoarthritic process. Describe patho of RA -​ systemic inflammatory autoimmune dz, there’s renckel with osteoclast activation Classic Inflammatory Joint Disease -​ Characterized by inflammatory damage or destruction in the synovial membrane or articular cartilage and by systemic signs of inflammation -​ Fever, leukocytosis, malaise, anorexia, and hyperfibrinogenemia -​ Infectious or noninfectious Rheumatoid Arthritis (RA) RA: an inflammatory joint disease w/ systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane) -​ Manifestations: Ulnar deviation of the digits and subcutaneous nodules, arteritis, neuropathy, scleritis -​ Systems affected: musculoskeletal, hematologic, immunologic, pulmonary, cardiovascular, and Neurologic -​ Some similar symptoms to osteoarthritis -​ OA will have pain w/ use, whereas RA will have improved pain after 15-20 minutes of activity. - Presence of rheumatoid factors (RF) - Antibodies (IgG and IgM) against those antibodies - Joint fluid presents with inflammatory exudates - There will be synovial infiltration by lymphocytes, plasma cells/macrophages + hypertrophy and hyperplasia at the synovial lining cells - In RA, there will be synovitis w/ inflamed synovium showing typical arrangements of macrophages and fibroblastic cells. - Advanced RA: proliferation of synovium and complete destruction of overlying articular cartilage - Synovium gets destroyed by lymphocytes, dendritic cells, plasma cells, and macrophages → Forms immune complexes and brings in neutrophils = Pannus (will erode at the articular cartilage and synovium). Pathogenesis 1) Activation of CD4 T helper cells and other cells in synovial fluid become activated and release cytokines 2) Recruitment and retention of inflammatory cells in the joint sub lining region 3) Vicious cycle of altered cytokine and signal transduction pathways 4) Possible immune complex deposition and inflammatory cytokine release 5) RANKL release and osteoclast activation - RANKL = Receptor Activator of Nuclear Factor Kappa-B Ligand - There will be pannus formation in the synovium with inflammatory cells, granulation tissue, and fibroblasts that grow and destroy the articular surface. 6) Angiogenesis in the synovium Rheumatoid arthritis (RA) is a chronic, systemic inflammatory autoimmune disease that may involve many tissues and organs but particularly affects the joints. -​ RA involves synovial inflammation, joint swelling, and ankylosis and destruction of articular cartilage. -​ Multiple immunoregulatory cytokines and inflammatory enzymes, such as interleukins, B cells, and collagenase, contribute to the development of an exaggerated immune response resulting in leukocyte infiltration into the synovium. → synovitis and eventual joint damage. -​ Inflammation may spread to the articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons, causing pain, joint deformity, and loss of function. -​ RA can also cause fever, malaise, rash, lymph node or spleen enlargement, and Raynaud phenomenon (transient lack of circulation to the fingertips and toes) Pathophysiology Chronic autoimmune reaction with activation of CD4+ helper T cells and possibly other lymphocytes and the local release of inflammatory cytokines and mediators eventually destroy the joint. 1)​ T cells stimulate cells in the joint to produce cytokines that are key mediators of synovial damage. 2)​ Activated T cells and synovial fibroblasts also produce receptor activator of nuclear factor κβ ligand (RANKL), which activates the osteoclasts and promotes bone destruction. 3)​ Cartilage destruction is mediated by collagenase, which activates the synoviocytes to invade the synovium and cartilaginous matrix. In addition, RANKL is expressed by various cells in the synovium and induces osteoclast maturation and activation, thus producing increased bone resorption. 4)​ The immune system's B and T lymphocytes also are activated.  -​ With long-term or intensive exposure to the antigen, normal antibodies (immunoglobulins [Igs]) become autoantibodies and attack host tissues (self antigens) → rheumatoid factors (RFs). -​ RFs bind with their target self antigens in blood and synovial membrane, forming immune complexes (antigen-antibody complexes) 5)​ Inflammation causes hemorrhage, coagulation, and fibrin deposition on the synovial membrane, in the intracellular matrix, and in the synovial fluid 6)​ Pannus is a mass of synovium and synovial stroma with inflammatory cells, granulation tissue, and fibroblasts that grows over the articular surface and causes its destruction. What can lead to crystal precipitation in gout -​ joint trauma, low serum Ph Joint trauma and low serum pH. Gout: Metabolic disorder that disrupts the body’s control of uric acid production or excretion Primary gout: underexcretion of uric caid (MC - 90% of Pts) or overproduction of uric acid (Dx w/ needle aspiration and look under microscope for presence of negatively birefringent uric crystals); uric acid crystalizes into monosodium urate -​ Classic Presentation: Males 40-50 y.o. w/ great toe pain and redness -​ Males usually 30-60 y.o. At onset (peak 40-50 y.o.) -​ Females more common after menopause due to decreased estrogen’s ability to excrete uric acid. -​ MC in Pacific Islanders. -​ Many patients w/ gout also have metabolic syndrome, where the insulin resistance results in renal reabsorption of uric acid (not being excreted) = ↑ renal uric acid stones -​ Manifests high levels of uric acid in the blood and other body fluids -​ Gout is related to purine (adenine and guanine) metabolism -​ Affected patients can have accelerated purine synthesis, breakdown, or poor  uric acid secretion in the kidneys -​ Psuedo gout: calcium pyrophosphate dihydrate crystals (CPPD), gout has monosodium urate crystals (know this) Mechanisms for crystal deposition -​ Lower body temperatures, decreased albumin or glycosaminoglycan levels, changes in ion concentration and pH, and trauma -​ Drugs causing gout: (SPEED) salicylates, pyrazinamide (used for TB), ethambuto (TB)l, ethanol & diuretics - Glucosamine & glycans (GAG-chains) may be covalently linked to a protein to form proteoglycans -​ Water sticks to the proteoglycans which creates the resistance to pressure. Clinical stages -​ Asymptomatic hyperuricemia -​ Acute gouty arthritis (often in foot)- occurs when the uric acid crystalizes -​ Tophaceous gout - formation of “tophi” (collection of gel with monosodium urate crystals) from chronic attacks -​ podagra - foot pain characteristic of gout Pathogenesis 1) Occurs when the uric acid concentration increases to high enough levels to crystallize - ou were to 2) Crystals deposit in connective tissues throughout the body → bone erosions 3) When these crystals occur in the synovial fluid, the inflammation is known as “gouty arthritis” - May present w/ erythema & tophi; squeezes out like toothpaste Gout is an inflammatory response to excessive quantities of uric acid in the blood (hyperuricemia) and in other body fluids, including synovial fluid. -​ Underexcretion of uric acid or overproduction of uric acid → Hyperuricemia -​ These elevated levels lead to the formation of monosodium urate (MSU) crystals in and around joints. When the uric acid concentration is >6.8 mg/dL in fluids, it crystallizes and forms insoluble precipitates of MSU that are deposited in connective tissues throughout the body. -​ The result of crystallization in synovial fluid is acute, painful inflammation of the joint. -​ With time, crystal deposition in subcutaneous tissues causes the formation of small, white nodules, or tophi, that are visible through the skin. -​ Risk factors: age (rare before 30 years), genetic predisposition (X-linked alteration of the enzyme hypoxanthine-guanine phosphoribosyltransferase [HGPRT]), excessive alcohol consumption, obesity, certain drugs (especially thiazides), lead toxicity, and dietary intake of purine-rich foods (organ meats, pork, some fish, and beer) -​ Men 3x > Women In classic gouty arthritis, monosodium urate crystals form and cause joint inflammation. Pseudogout mimics gout; however, it is caused by the formation and deposition of calcium pyrophosphate dihydrate (CPPD) crystals. Calcium pyrophosphate dihydrate crystals predominantly deposit in joint cartilage and intervertebral disks. Patho of DDH -​ dysplastic acetabulum in a normal femur  -​ NOT a cup-shape acetabulum, this makes it less likely to have DDH -​ pain is a very late finding There is a dysplastic acetabulum but a normal femur. -​ Not associated w/ a cup shaped acetabulum Hip dysplasia: Abnormality of the proximal femur, acetabulum, or both -​ Hip can present as subluxated, dislocatable, or dislocated -​ W/ repeated subluxation or dislocation, the acetabulum becomes increasingly shallow. If left dislocated, a false acetabulum forms where the head contacts the ileum and the acetabulum then fills with soft tissue. -​ a deeper cup shaped acetabulum will be less likely to develop in DDH- KNOW this Risk factors: Female sex, metatarsus adductus, torticollis, oligohydramnios, first pregnancy, breech presentation, family Hx. -​ Affects left hip in 60% of patients, right hip in 20%, & BL in 20% Manifestations - Asymmetry of gluteal or thigh folds - Limb length discrepancy - Limitation of hip abduction - Positive Ortolani sign - Positive Barlow test - Positive Trendelenburg gait; when they put weight on affected side, pelvis goes down - Pain - very late finding Tests: -​ Barlow maneuver - clunk of dislocation -​ Ortolani maneuver - clunk of reduction, putting hip back together -​ Galeazzi sign - one leg shorter than the other + crease in buttock Developmental dysplasia of the hip (DDH) is an abnormality in the development of the proximal femur, acetabulum, or both. Although most often present at birth, it may occur at any time in the newborn or infant period. -​ Risk Factors: family Hx, female gender (6:1), metatarsus adductus (20%), torticollis (10%), oligohydramnios, first pregnancy, and breech presentation. MC whites and cultures that swaddle infants w/ the hips in extension and adduction. Pathophysiology The hip can be described as subluxated (partial contact only), dislocated (no contact between femoral head and acetabulum), and acetabular dysplasia (the femoral head is located properly but the acetabulum is shallow or underdeveloped; present in almost all cases). -​ Typically, the acetabulum is shallow or sloping rather than cup shaped. -​ If the hip remains subluxed or dislocated, the acetabulum becomes increasingly shallow and the soft tissues shorten around the proximal femur → early osteoarthritis (OA) -​ If the hip is dislocated, the bone acetabulum fills with soft tissue and a false acetabulum forms where the femoral head contacts the iliac crest. → limb length inequality and hip muscle weakness occur, leading to a waddling gait. Clinical Findings 1)​ Asymmetry of gluteal or thigh folds 2)​ Limb length discrepancy (Galeazzi sign) 3)​ Limitation of hip abduction 4)​ Positive Barlow maneuver (hip reduced, but dislocatable) 5)​ Positive Ortolani sign (hip dislocated, but reducible)  6)​ Positive Trendelenburg gait (waddling) 7)​ Pain (very late) Structural vs. nonstructural scoliosis -​ nonstructural: can become structural if not correction Nonstructural can become structural if there is no treatment done. Scoliosis: Rotational curvature of the spine -​ Nonstructural: Curvature is from a cause other than the spine -​ Ex. Muscle spasm -​ Curve disappears w/ forward flexion, lying down, or traction of the head. -​ Nonstructural can become structural if the cause isn’t diagnosed and treated -​ Structural: Spine curvature associated with vertebral rotation -​ 65% idiopathic -​ Other causes: Skeletal abnormalities, neuromuscular disease, trauma extraspinal contractures, bone infections of the vertebrae, metabolic bone disorders, joint disease, and tumors -​ Soft tissues on the concave side shorten, resulting in progressive rib and vertebral deformity -​ 4-5 x more common in females -​ Worsens oven time and MC in females -​ As the curve increases, pulmonary function can be affected. -​ Manifestations: asymmetry of the hip and shoulder height + shoulder scapular and rib prominence Scoliosis is a rotational curvature of the spine most obvious in the anteroposterior plane. It can be classified as nonstructural or structural. -​ Nonstructural scoliosis results from a cause other than the spine itself, such as posture, leg length discrepancy, or pain. -​ Can become structural if the underlying cause is not found and treated. -​ Structural scoliosis is curvature of the spine associated with vertebral rotation. -​ Can result from congenital skeletal abnormalities (15%), neuromuscular diseases (15%), trauma, extraspinal contractures, bone infections that involve the vertebrae, metabolic bone disorders (rickets, osteoporosis, osteogenesis imperfecta), joint disease, and tumors. Most cases have no cause (idiopathic scoliosis). -​ Idiopathic scoliosis is classified as infantile ( Girls) -​ The severity of the lesion varies from mild tendinitis to a complete separation of the anterior extension of the tibial epiphysis, which is the part of the epiphysis that contributes to growth of the tibial tubercle. Osgood-schlatter disease: Tendinitis of anterior patellar tendon with associated osteochondrosis of tibial tubercle. -​ Usually in kids that participate in running sports (basketball, soccer) - Only occurs in immature bone. -​ MC in males: classic presentation: pre-adolescent male participating in running sport -​ Hypertrophic cartilage = osteochondrosis. -​ The epiphysis in front of the tibia is called an apophysis instead of an epiphysis and there is going to be an inflammatory infiltrate of the apophysis. -​ Mild = Avascular necrosis around tubercle with resultant hypertrophic cartilage (osteochondrosis) during repair. - ANV similar to Perthes disease -​ More severe= true epiphyseal separation + AVN Foot deformities/clubfoot -​ read not in lecture -​ know differences Read this section in the book. Congenital Deformity. Congenital foot deformity is found in approximately 4% of all newborns, and metatarsus adductus accounts for 75% of these deformities. -​ Metatarsus adductus is a forefoot adduction deformity associated with a normal, plantigrade hindfoot and is believed to be secondary to intrauterine positioning. -​ Associated w/ developmental dysplasia of the hip (20%). -​ Classified by flexibility (passively correctable vs. rigid) and degree of deformity (based on heel bisection line). -​ Mild - heel bisection line passes medial to the third toe; -​ Moderate - line passes the third or fourth toes -​ Severe - line is lateral to the fourth toe.  -​ Serial casts during the first 6 months of life are suggested for moderate to severe deformities and those deformities that appear less flexible. -​ Usually correct spontaneously. Clubfoot: Equinovarus Deformity. Clubfoot (equinovarus) describes a range of foot deformities in which the foot turns inward and downward. -​ Heel is positioned varus (inwardly deviated) and equinus (plantar flexed). -​ Can be positional (correctable passively), idiopathic, or teratologic equinovarus (result of another syndrome). -​ Positional - infant's foot is in equinovarus position but does have flexibility without deep creases at the posterior ankle or midfoot. The Achilles tendon is still flexible. The foot can be passively brought to a plantigrade position and is amenable to stretching and casting. -​ Rapid correction by stretching and serial casts -​ Idiopathic - Unknown etiology, decreased muscle fibers or abnormal fiber histology -​ Male 2x > Female -​ Tx w/ weekly casting/manipulation followed by Achilles tenotomy and abduction bracing - Ponseti method -​ Teratologic equinovarus - MC neuromuscular (spina bifida) or syndromic (arthrogryposis or osteochondrodysplasia) -​ Tends to fail Ponseti casting. Require surgical correction or muscle-balancing procedures. Pes Planus (Flatfoot) Deformity. Pes planus (flatfoot) results in a flat arch of the foot that becomes more apparent w/ age. -​ Significant ankle valgus, vertical talus, tarsal coalition, and skewfoot must be accurately differentiated from flexible pes planus. Evaluate occult Achilles contracture by holding the hindfoot in varus position and dorsiflexing the ankle (severe variant). -​ Familial, with occasional association of generalized ligamentous laxity. -​ The flexibility of the hindfoot is evaluated by having the child stand on his or her toes facing away from the examiner. -​ In flexible pes planus, the hindfoot swings into a varus position as the planter fascia tightens in toe raise. -​ Tx unnecessary if asymptomatic. If painful, use shoe inserts and consider cal camels lengthening. -​ In rigid pes planus, the hindfoot stays in valgus and the child has more difficulty going up onto tip-toe. -​ CT scan will reveal a coalition, a bony or cartilaginous connection between the bones—if painful, this can be resected. -​ If nonpainful, treatment is not required. -​ Heel cord contractures can be surgically lengthened if stretching alone is inadequate. Bursitis -​ know definition There is a description on the exam and the correct answer is bursitis. Bursitis: inflammation in bursal sacs. -​ Bursae are small sacs lined with synovial membrane and filled with synovial fluid; they are located between tendons, muscles, and bony prominences. -​ Their primary function is to separate, lubricate, and cushion these structures. When irritated or injured, these sacs become inflamed and swell. Because most bursae lie outside joints, joint movement is rarely compromised with bursitis. -​ Acute bursitis occurs primarily in the middle years and is often caused by trauma; repetitive irritation can cause chronic bursitis. -​ Septic bursitis is caused by wound infection or bacterial infection of the skin overlying the bursae. Pain description in Legg-Calve-Perthes DZ -​ ipsilateral knee, inner thigh, groin pain, aggravated by activity, relieved by rest Ipsilateral (same side) knee, inner thigh and groin. Pain is decreased with rest and increased with activity. Legg-Calve-Perthes disease (Avascular necrosis of proximal femur) is a childhood condition that occurs when blood supply to the femoral head of the hip joint is temporarily interrupted and the bone begins to die. This weakened bone gradually breaks apart and can lose its round shape. The body eventually restores blood supply to the ball, and the ball heals. But if the ball is no longer round after it heals, it can cause pain and stiffness. -​ Range is 2-12 years old (textbook says 3-10); 80% between 4-9y.o. -​ 6.8 mg/dL. This triggers the acute inflammatory response. -​ Initiation of the complement system activates cytokines and interleukins, which draw neutrophils/macrophages out of the circulation to begin phagocytizing the crystals. -​ When macrophages phagocytize MSU crystals, they form a protein scaffold known as an inflammasome, which convert IL-1β and IL-18 into their active forms. -​ Tissue damage begins to occur, principally when the neutrophils release the contents of their phagolysosomes. These contents also perpetuate inflammation. -​ As the process continues, numerous microtophi may be present on the synovial membrane. Clinical manifestations of gout -​ risk of renal calculi, hyperuricemia Pain, Tophi, 40-50 y.o. Male with painful inflamed 1st metatarsal phalangeal joint. Gout is MC in men (3:1) and peaks between 40-50 y.o. (occurs later in women b/c estrogen is protective). Gout is manifested by: 1)​ an increase in serum urate concentration (hyperuricemia) 2)​ recurrent attacks of monoarticular arthritis (inflammation of a single joint); 3)​ deposits of monosodium urate monohydrate (tophi) in and around the joints; 4)​ renal disease involving glomerular, tubular, and interstitial tissues and blood vessels;  5)​ the formation of renal stones. 3 clinical stages: 1)​ Asymptomatic hyperuricemia: The serum urate level is elevated but arthritic symptoms, tophi, and renal stones are not present; may persist throughout life. 2)​ Acute gouty arthritis: Attacks develop with increased serum urate concentrations; tends to occur with sudden or sustained increases of hyperuricemia but also can be triggered by trauma, drugs, and alcohol. -​ Attacks usually occur in the peripheral joint w/ severe pain (50% in the metatarsophalangeal joint of the great toe). -​ Pain is noticed at night w/ joints becoming hot, red, tender, and swollen. 3)​ Tophaceous gout: The third and chronic stage of disease; can begin as early as 3 years or as late as 40 years after the initial attack of gouty arthritis. Progressive inability to excrete uric acid expands the urate pool until urate crystal deposits (tophi) appear in cartilage, synovial membranes, tendons, and soft tissue. -​ Each tophus consists of a deposit of urate crystals, surrounded by a granuloma made up of mononuclear phagocytes (macrophages) that have developed into epithelial and giant cells. Characteristics of Legg-Calve-Perthes DZ -​ self-limited dz caused by recurrent femoral head ischemia Know that it is self-limited and there is recurrent femoral head ischemia. Legg-Calvé-Perthes (LCP) disease is a self-limited disease of the hip that is presumably produced by recurrent interruption of the blood supply to the femoral head (recurrent femoral head ischemia) -​ The ossification center first becomes necrotic and collapses and then is gradually remodeled by live bone. MC in boys 3-10 y.o. -​ Lasts 2-5 years. Pathophysiology -​ In the initial stage the soft tissues of the hip (synovial membrane and joint capsule) are swollen, edematous, and hyperemic, often with fluid present in the joint. The joint space widens, and the joint capsule bulges. -​ Lasts only a few weeks. -​ In the second stage fragmentation) the entire epiphysis or the anterior half of the epiphysis of the femoral head loses blood supply and the metaphyseal bone at the junction of the femoral neck and capital epiphyseal plate is softened because of decalcification. Soon granulation tissue (procallus) and blood vessels invade the dead bone. -​ This stage lasts several months to 1 year. -​ In the third (or regenerative healing) stage, the dead femoral head is replaced by procallus, and new bone is laid down. Collapse and flattening of the femoral head occur, and the femoral neck becomes short and wide -​ This stage ordinarily lasts 2 to 3 years. -​ In the fourth (or healed) stage, remodeling takes place and the newly formed bone is organized into a live spongy bone. Clinical manifestations of AS -​ loss of lumbar lordosis, increased thoracic kyphosis Decreased lumbar lordosis and increased thoracic kyphosis. -​ Pain is increased with rest and decreased with activity. Ankylosing Spondylitis: Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints -​ Systemic, immune inflammatory disease -​ Primary proposed site is the enthesis → Site where ligaments, tendons, and the joint capsule are inserted into bone -​ Cause unknown, but there is a strong association with HLA-B27 antigen (know this) -​ Early symptoms: Low back pain, stiffness, pain, and restricted motion -​ Symptoms increased w/ rest and decreased w/ activity. -​ Loss of lumbar lordosis (curving inward of the lower back → spine straightens in AK) & ↑ thoracic kyphosis (head to wall sign) -​ Can get pleuritic chest pain and decreased chest lumen secondary to inflammation of the costochondral and costovertebral ligaments, tendons, and muscles. -​ Head and neck are held forward, hips are flexed -​ Patient demonstrates loss of normal lumbar curvature -​ X-ray will show bamboo spine - instead of open space between vertebral discs, the discs are fused and ossified which decreases lumbar lordosis. Pathogenesis 1) Begins with the inflammation of fibrocartilage, particularly in the vertebrae and sacroiliac joint 2) Inflammatory cells infiltrate and erode fibrocartilage -​ Erosive changes complete with bony formation at the tendon-ligament insertion resulting in ossification of periarticular soft tissue. 3) As repair begins, the scar tissue ossifies and calcifies; the joint eventually fuses Ankylosing spondylitis (AS) is a chronic inflammatory joint disease characterized by stiffening and fusion (ankylosis) of the spine and sacroiliac joints. Clinical Manifestations -​ Low back pain and stiffness. -​ Worse after prolonged rest and is alleviated by physical activity.  -​ As the disease progresses, the normal convex curve of the lower spine (lumbar lordosis) diminishes and concavity of the upper spine (kyphosis) increases. The individual becomes increasingly stooped. -​ The thoracic spine becomes rounded, the head and neck are held forward on the shoulders, and the hips are flexed -​ Inflammation in the tendon insertions of the many costosternal and costovertebral muscles can cause pleuritic chest pain and restricted chest movement. -​ Pain in the SI joint. -​ May have peripheral joint involvement, uveitis, fibrotic changes in the lungs, cardiomegaly, aortic incompetence, amyloidosis, and Achilles tendinitis Consequence of improper fracture reduction -​ after cast is removed the bone is not straight After the cast is removed, the bone is not straight. Improper reduction or immobilization of a fractured bone may result in nonunion, delayed union, or malunion. The stage of healing in bone that results in procallus formation involves production of granulation tissue by fibroblasts, capillary beds and osteoblasts, the ion that directly controls muscle contraction is calcium S/sxs: of infl joint disease (like RA, ankylosing spondylitis and gout) are fatigue, fever , leukocytosis Last exam Slides not on here 21-25 OTHER SLIDES Bone Formation -​ Continued growth is on the epiphyseal side. It is more able to remodel a deformity but also more sensitive to injury. Bone Growth -​ Bone growth occurs at the epiphyseal plate through endochondral ossification - Occurs until adult stature is achieved -​ Flat bones however develop through intramembranous ossification → Facial bones, cranium, jaw, clavicle Factors affecting bone growth: - Growth hormone - Nutrition - General health - Many growth factors and regulators Normal Bone Structure -​ Diaphysis: shaft or central part of a long bone -​ Epiphysis: distal; the end part of a long bone, initially growing separately from the shaft. -​ Contains growth plate - Epiphyseal plate -​ Metaphysis: neck portion of long bone between the epiphysis & diaphysis ​ KNOW FOR exam: when the bones fuse: the metaphysis and epiphysis merge together -​ Order (Ends to Shaft): Epiphysis → Epiphyseal plate → Metaphysis → Diaphysis