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
• Tendon Bone Interface
• Tendon
Musculotendinous Junction
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 activity2. Pain at the beginning of sports activity,
disappearing with warm-up and sometimes reappearing with fatigue
3. Pain at rest and during activity4. 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
Healinga. 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
Skeletal muscle• Large, elongated, multinucleated fibers– Cellular Unit: myofiber of muscle fiber– Basement membrane: contains collagen, laminin,
fibronectin and muscle-specific proteoglycan
• Striated
• Myofilaments– Thin: Actin– Thick: Myosin
Pathological Conditions of Musculotendinous Junction and Muscle Belly
Causes of Injurya. Contusion- direct blowb. acute strain: excessive
stretchingc. chronic strain: repetitive
loadingd. 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 2nd 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
Examination Findings
• 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
MyositisDefinition:
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• LethargySigns:• 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 StructuresBursa• 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.