Presentation on theme: "Tendons and Muscles PTP 521 Musculoskeletal Diseases and Disorders."— Presentation transcript:
Tendons and Muscles PTP 521 Musculoskeletal Diseases and Disorders
Tendons Transmit force between muscles and bone Store elastic energy when stretched Connect bone to muscle Concentrate the pull of muscle in a small area
Histological Composition of Tendon Dense, parallel fibered, connective tissue Bundles of coarse collagen fibers among scattered rows of fibroblasts with elongated nuclei Endotenon: Collagen Type III Epitenon: Collagen Type I Peritenon (tenosynovium): areolar tissue becomes tendon sheath in some areas
Tendon Cell Composition Behavior of tendon is determined by the amounts, types, and organization of their extracellular components – Collagen (type I): 65-75% dry weight – Elastin: 2 % dry weight – Matrix: composed of proteoglycans – water – Cell types: Tenoblasts Tenocytes
Classification System of Tendon Injury Based on the histology of the tendon at time of elbow surgery
Clinical and Functional Classification -Blazina et al. 1973 4 stages: 1.Pain after sports activity 2.Pain at the beginning of sports activity, disappearing with warm-up and sometimes reappearing with fatigue 3.Pain at rest and during activity 4.Rupture of tendon
Classification according to Chronology of Symptoms Acute: symptoms have been present for 0 – 6 weeks Sub-acute: symptoms present between 6-12 weeks Chronic: symptoms present longer than 3 months
Common Tendon Injury Terminology Paratendinopathy: (Paratenonitis, tenosynovitis, peritendinitis, tenovaginitis) Acute tendinopathy (Tendonitis) Chronic tendinopathy (Tendinosis) Pantendinopathy (Paratnonitis with tendinosis or tendinitis)
Paratendinopathy Definition: Inflammation of the paratenon sheath which becomes thicker and inflammed. Clinical Manifestations: – Swelling, burning, shooting pain, crepitus, dysfunction, tenderness and warmth – Becomes chronic condition, can lead to adhesion of sheath to the tendon underneath Treatment: NSAID’s, corticosteroid injections,
Acute Tendinopathy (Tendonitis) Pathology: minor lesion of the tendon tissue Etiology: caused by tissue fatigue – the tendon is strained such that it can no longer endure tension and stress, structure begins to disrupt microscopically and inflammation, edema and pain result.
Extrinsic Factors: – unaccustomed activity (excessive load on body) – weather (environmental conditions) – training errors – poor equipment
Chronic Tendinopathy (Tendinosis) Pathology: degeneration within the tendon. No inflammatory response, due to atrophy from aging, microtauma and vascular trauma, overuse Clinical Manifestations Signs: palpable tendon, nodule, usually not tender to touch Symptoms: pain with active movement, prolonged stretch
Possible progression of Tendon injury – Inflammation : minimal or absent – Gradual change of tendon tissue – Pain occurs eventually and may be related to the revascularization and neural growth into the tendon – Some tendons rupture without any previous signs or symptoms Zachazewski JE, Magee Dj, Quillen SW. Athletic Injuries and Rehabilitation, p 42. Philadelphia, 1996, WB Saunders.
Pantendinopathy: Tendinosis with Paratenonitis Pathology: both paratendinopathy and acute or chronic tendinopathy occur, separate entities Clinical Manifestations: Signs: inflammatory signs with a palpable tendon nodule, swelling and redness Symptoms: pain
Healing a. Inflammatory stage: within the first 3 days after injury b. Repair stage: seen within one week, initially formed at random, fibroblasts predominate, collagen content increases through the first 4 weeks. Fibers initially are oriented perpendicular to the gap c. Remodeling stage: begins within 2 months after injury. Complete healing occurs when the tensile load strength returns.
Other Types of tendon injuries Tendon Strain: can lead to rupture – Same grades of strain as a ligament sprain Tendon Dislocation: Biceps Brachii Thermal injury: burn or cold Tendon Lacerations
Histology of Muscle Tissue Highly specialized tissue, surrounded by basement membrane or external lamina Contractile, extensibilty, elasticity and excitability properties Three types of muscle tissue – Skeletal Muscle – Cardiac Muscle – Smooth Muscle
Pathological Conditions of Musculotendinous Junction and Muscle Belly Causes of Injury a. Contusion- direct blow b. acute strain: excessive stretching c. chronic strain: repetitive loading d. laceration
Contusion - key points Capillary rupture occurs and bleeding into the muscle followed by an inflammatory reaction Severity of contusion determined by degree to which it limits motion of the joint Most commonly occurs in biceps and quadriceps Injuries graded as mild, moderate or severe Take at least 24 hours to stabilize
Muscle Strains - Key point Some degree of muscle fiber or tendon disruption occurs Acute and chronic strains occur when muscle or tendon lacks flexibility, strength or endurance to accommodate demands placed upon it
Grade I: mild or first degree No disruption of muscle/tendon unit Symptoms – Active contraction and passive stretch are painful, may have mild muscle spasm Signs – Localized swelling and tenderness – no loss of strength in the muscle – No loss of motion in the adjacent joints – No palpable defect – No ecchymosis
Grade II: moderate or 2 nd degree Some degree of disruptions within the muscle/tendon unit. Symptoms: – Tenderness to palpation – Very painful with passive stretching and attempted contraction of the muscle Signs: – Decreased muscle strength – Decrease in ROM in joints – Possible palpable discontinuity – Moderate spasm – echymosis
Grade III: severe or third degree One or more components of the muscle/tendon unit are completely disrupted Symptoms: – No change in pain with passive stretch, may be a little less painful than the grade II strain Signs: – Motion in adjacent joint is severely restricted – Extreme tenderness with swelling – Palpable defect, bunching up of muscle tissue – Possible compartment syndrome with concurrent loss of sensation and pulse distally
Muscle Healing Following a Strain Injury heals with both regeneration and repair Capacity for regeneration is based on type of injury and extent of injury
Phases of Healing Destruction Phase: – Muscle fibers and sheaths are disrupted – Gap between ends of ruptured muscle fibers due to muscle retraction – Necrosis of tissue
Proliferation (repair) Phase Repair – Hematoma formation – Matrix formation Fibronectin and fibrin cross link to form matrix for fibroblasts Fibroblasts synthesize proteins for extracellular matrix – Collagen formation Type I collagen
Regeneration Occurs at same time as proliferation phase – Activation of satelitte cells and myoblastic precursor cells divide, proliferate and differentiate into myotubes then into myofibers – Myofibers fuse with other myofibers on other end of wound. May limit degeneration Mechanism? – Scar tissue between may limit regeneration – Integration of neural structures and formation of a neuromuscular junction last part of regeneration
Maturation Phase Regenerated muscle matures and contracts
Early ischemic damage Fragmentation phase Myotube Muscle fiber
Fibromyalgia Chronic, widespread pain and tenderness to touch Incidence: 5-8% of population – Females 9:1 over males – More common than RA Etiology: theories only – Stress related – Genetically predisposed – Sleep disturbance – Dopamine abnormality – Deposition disease
Clinical Manifestations Symptoms – Widespread pain – Duration: at least three months – Non-radicular pain – Fatigue – Nonrestorative sleep – Defined number of trigger points
Trigger Points in Fibromyalgia Trigger Point: tender point which becomes painful upon pressure 11/18 standardized sites – Sensitivity of 88% and specificity of 81%
Myofascial Pain Syndrome: Trigger Points Definition: – Hyperirritable point within a taut band of skeletal muscle, – Localized in muscle tissue or associated fascia – Painful on compression: jump sign – Evokes a characteristic referred pain pattern and autonomic phenomena
Classification of Trigger Points Active: causes pain at rest Latent: clinical silent for pain, may restrict ROM and may cause weakness of the affected muscle
Associated Trigger Points Develop in response to injury/other trigger points – Satellite Trigger Point: develops in the zone of referred pain from another muscle – Secondary Trigger Point: develops in either a synergist or antagonist of the muscle which first develops a trigger point because it is overloaded.
Trigger Point Signs and Symptoms Pain referred in a specific pattern Dull aching pain, often deep, intensity varies Doesn’t follow known sclerotome, myotome or dermatomal patterns
Activated by acute overload, overwork, fatigue, trauma or chilling Activated by other trigger points, visceral diseases, arthritic joints, emotional stress TP can change from latent to active
Increase pain with active or passive stretching of the muscle ROM is decrease Pain increases with resisted activity Muscle strength is decreased Palpable nodule that has “exquisite” tenderness
Taut, tight, tense muscle, can snap or “twang” Local twitch response, transient, visible, palpable contraction of the muscle Lab tests, imaging tests are negative for other pathology
Myositis Definition: infectious, inflammatory disease of muscle Etiology: viral, bacterial, parasitic agents Incidence: 4% for parasitic agents Most common form: polymyositis (weakness in trunk muscles) and dermatomyositis (weakness plus skin rash)
Clinical Manifestations Medical Diagnosis: Biopsy: – Determines form of myositis EMG Lab Values – Creatine kinase levels in blood indicate muscle breakdown Symptoms: Malaise Pain Tenderness Lethargy Signs: Swelling Fever
Immobilization Effects on Muscle Muscle: length of time/position of immobilization – Changes tend to occur at myotendinous junction – Adjustment in number and length of sarcomeres, occurs within 12-24 hours after immobilization
Muscle belly changes with immobilization – Occurs with muscle atrophy – Contractile elements are lost before noncontractile elements – Result is increase in connective tissue and decrease in tissue extensibility – Endomysium and perimysium may also increase in thickness
Aging Muscle effects: decrease in number of muscle fibers – 39% by age 80 Type II are more affected than Type I fibers (probably denervation) May occur secondary to decrease in demand on the body and can be reversed to some extent with exercise Overall increase in connective tissue and collagen, greater muscle stiffness and less flexibility and strength as age.
Other Connective Tissue Structures Bursa Definition: functions to reduce friction between either muscle and tendon, tendon and tendon, tendon and bone Cause of injury: inflammation from overuse, trauma from a direct injury, infection. Bursitis: inflammation occurs in areas that are close to the surface – Symptoms : localized pain, tenderness over the area – Signs: localized swelling outside the joint, not a joint effusion, warmth, edema, loss of motion, loss of function can occur Fat Pads Closely packed fat cells surrounded by fibrous tissue – Function: act as packing around the joint – Cushions the joint – Assists in Joint lubrication – Symptoms: increase in pain and tenderness – Signs: decrease in ROM around joint, increase in warmth around the fat pad
References Jozsa L, Kannus P. Human Tendons: Anatomy, Physiology, and Pathology. Human Kinetics. Champaign IL 1997. Magee D, Zachazewski J, Quillen W. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. Saunders. St. Louis. 2007.