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.