SKELETAL MUSCLE TISSUE: MUSCLE ,TENDON, LIGAMENT

SKELETAL MUSCLE TISSUE:
MUSCLE ,TENDON,
LIGAMENT
PREPARED BY DR. DAWIT ALEMAYEHU
1

OUTLINE
 Introduction
 Function of muscles
 Skeletal muscle composition and structural organization
 Properties of skeletal muscle
 Muscle injury
 Ligament and tendon function
 Ligament and tendon structural organization
 Tendon and ligament injury
Prepared by Dr. Dawit Alemayehu
2

Introduction
 One of 4 primary tissue types
 40 – 50% of body weight
 Skeletal muscles receive innervation from the somatic peripheral nerve
 Muscle consists primarily of cells/ myocytes/ muscle fibers
 They affect voluntary control of the axial and appendicular skeleton.
 A skeletal muscle consists of a bundle of long fibers
 Adults have a fixed number of muscle cells;
4

Skeletal muscle function
1. Produce movement
2. Maintain posture
3. Stabilize joint
4. Thermogenesis
5. Store Nutrient reserves
6. Guard body openings (entrance/exit)
5

Skeletal muscle composition and structural
organization
 Muscle tissue (muscle cells or fibers)
 Muscles contain highly differentiated cells called myocytes.
 Formed from fusion of multiple small mesenchymal cells called myoblasts
 Connective tissues
 Nerves
 Blood vessels
6

 Are cylindrical in shape
 Are very long
 Multinucleated – in hundreds
 contain unique form of endoplasmic reticulum ( sacroplasmic reticulum)
 composed of contractile protein filaments
 Actin and Myosin are organized into cylindrical organelles called myofibrils.
 Aggregates of myofibrils cluster into bundles called fascicles.
 Aggregates of fascicles + extracellular matrix form a muscle.
Muscle fiber
7

 The smallest (Basic) functional unit of muscle contraction is the sarcomere.
 Adjacent myofibrils are connected by a set of specialized proteins called intermediate
filaments (for mechanical coupling between myofibrils).
 Muscle fibers arrangement is either parallel or oblique to the muscle’s long axis.
8

 Contains
 Sarcolemma ( cell membrane ) – surrounded by endomysium
 T tubles ( vertical invagination of sarcolemma separating A band and I band)
 sarcoplasm ( cytoplasm of muscle cell )
 Sarcoplasmic reticulum (SR) smooth endoplasmic reticulum
 termina cisterna ( collection of SR at A band and I band – contains calcium
 Triad ( two terminal cisterna +T tubule
 Termina cisterna – release available ca+ into sarcoplasm
 T tubules – carries stimulus from sarcolemma into myofibrils
 mitochondria ( power house) – produce ATP requiring glucose and oxygen
 Also known as sarcosomes
9

Muscle contraction
 Is caused by interactions of thick and thin filaments
 Structures of protein molecules determine interactions
 Neural stimulation of sarcolemma:
 causes excitation–contraction coupling
 Cisternae of SR release Ca2+
:
 which triggers interaction of thick and thin filaments
 consuming ATP and producing tension
10

Muscles layers
1. Epimysium
 Exterior collagen layer
 Connected to deep fascia
 Separates muscle from surrounding tissue
2. perimysium-
 Surrounds muscle fiber bundles (fascicles)
 Contains blood vessel and nerve supply to fascicles
11

3. Endomysium
 Surrounds individual muscle cells (muscle fibers)
 Contains capillaries and nerve fibers contacting muscle cells
 Contains satellite cells (stem cells) that repair damage
12

 Level 1
 level2
13

 Level 3
 Level 4
14

Level 5
15

16

Matrix
 It contains collagens, elastin, proteoglycans, and noncollagenous proteins.
 Although the extracellular matrix makes up only a small fraction of muscle volume, it is critical
for
 normal muscle function,
 maintenance of muscle, nerve and vessel structure,
and (Structural support)
 healing.
17

Blood Vessels
 Muscles have extensive vascular systems that:
supply large amounts of oxygen
supply nutrients
carry away wastes
18

Innervation
 Initiation, coordination, and control of muscle contraction require elaborate innervations.
 A motor unit consists of the motor neuron and the muscle fibers it
innervates.
 One motor neuron innervates each myofiber, but each motor neuron generally innervates
more than one myofiber.
 The number of muscle fibers within a motor unit varies widely.
 This can range from 10 (extra-ocular muscles) to 2000 (gastrocnemius)
 Motor nerves attach to myofibers through neuromuscular junction (NMJ).
19

20

Properties of skeletal muscle
 Excitability
: ability to receive and respond to stimuli
 Contractility
:ability to shorten forcibly when get stimulated
 Extensibility
: ability to be stretched
 Elasticity
: ability to recoil to resting length
21

Types of muscle contraction
1. Isotonic —Muscle shortens against a constant load. Muscle tension remains constant. Joint movement occurs.
2. Isokinetic—Resistance (load) varies, but the of contraction stays the constant.(Muscle contracts at a constant velocity.)
3. Isometric—Muscle length remains static as tension is generated. No joint movement. (pushing against immovable object)
4. Concentric—Contraction that decrease in muscle length.
(Muscle force generated > Resisting load ).
5. Eccentric—Contraction that allows increase in muscle length.
(Resisting load > Muscle force generated).
22

23

Energetics
A. Three main energy systems provide fuel for muscular contractions
1. The phosphagen system
a. The adenosine triphosphate (ATP) molecule is hydrolyzed and converted directly to
adenosine diphosphate (ADP), inorganic phosphate, and energy. ADP may also be further
hydrolyzed to create adenosine monophosphate (AMP), again releasing inorganic phosphate and
energy.
 Total energy from the entire phosphagen system is enough to fuel the body to run
approximately 200 yards.
 No lactate is produced via this pathway; also, no oxygen is used
24

2. Anaerobic metabolism (glycolytic or lactic acid metabolism)
 Glucose is transformed into two molecules of lactic acid, creating enough energy to convert two molecules
of ADP to ATP.
 This system provides metabolic energy for approximately 20 to 120 seconds of intense activity.
 Oxygen is not used in this pathway.
25

3. Aerobic metabolism
 Glucose is broken into two molecules of pyruvic acid, which then enter the Krebs cycle,
resulting in a net gain of 34 ATP per glucose molecule.
 Glucose exists in the cell in a limited quantity of glucose-6-phosphate.
 Additional sources of energy include stored muscle glycogen.
 Fats and proteins also can be converted to energy via aerobic metabolism.
 Oxygen is used in this pathway.
26

Types of muscle fibers
1. Slow fibers ( type 1)
 Have small diameter
 More mitochondria,
 Contain myoglobin (red pigment, binds
oxygen)
 Have high oxygen supply
 Are slow to contract ..slow to fatigue
2. Intermediate fibers( type 2A)
 Are mid-sized
 Have low myoglobin
 Have more capillaries than fast fiber, slower
to fatigue
27

3. Fast fibers( type 2B)
 few mitochondria
 Contract very quickly
 Have large diameter, large glycogen reserves,
 Have strong contractions, fatigue quickly
 “The ratio of ST to FT fibres is genetically
determined but different training regimes
can selectively improve these fibres”
28

Comparing Skeletal Muscle Fibers
29

Training effects on muscle
1. Strength training (Resistance training );-
 usually consists of high-load, low-repetition exercise and
 results in increased muscle cross-sectional area.
 This is more likely due to muscle hypertrophy (increased size of muscle fibers) rather than hyperplasia
(increased number of muscle fibers).
 Increase in the contractile proteins with few metabolic changes
 Initially resistance training will produce a rapid increase in strength in the absence of hypertrophy
through increased recruitment of muscle fibres
 After a period of resistance training there is muscle fibre hypertrophy with an increase in the number of
contractile elements thus increasing the strength
 Strength training results in adaptation of all fiber types.
30

2. Endurance training
 Aerobic training results in changes in both central and peripheral circulation as well as muscle
metabolism.
 Prolonged low intensity activity will cause the following effects in all fibre types ( I and IIA
particularly)
 Increase in the number of mitochondria
 Increase the muscle’s capacity to oxidise fatty acids through aerobic metabolism
 Increase in muscle myoglobin content
 Increase in the number of capillary blood vessels
 Energy efficiency is the primary adaptation seen in contractile muscle
31

Muscle injury
BASED ON THE MECHANISMS :
MECHANICAL
Blunt trauma,
lacerations, and
 tearing injuries etc
32

Muscle strains
 Incomplete muscle fiber tears due to overstretching.
 Typically occur at the myotendinous junction, with hemorrhage and fiber disruption.
 These are the most common sports injury.
 They occur primarily in muscles crossing two joints (hamstring, rectus femoris,
gastrocnemius).
 Prevention is by correct warm-up and stretch procedures
33

Muscle tears/ Pull
 Complete muscle tears typically occur near the myotendinous junction.
 They are characterized by muscle contour abnormality.
 They typically heal with dense scarring.
34

Muscle laceration
 Due to penetrating injury causing complete laceration of muscle.
 Fragments heal by dense connective scar tissue.
 Muscle tissue or reinnervation: only partial recovery is likely.
 minimal regeneration of muscle fibers distally, scar formation at the laceration, and recovery
of about half the muscle strength
35

 Incomplete lacerations will result in the muscle be able to generate only 60% of its tension
but it will regain its full ability to shorten
 In complete lacerations a dense scar will form and the muscle will be only able to generate ~
50% of its original tension and 80% of its ability to shorten
36

Muscle contusion
 Is a non penetrating blunt injury to muscle resulting in hematoma and inflammation
 Characteristics include:
1. Scar formation and variable amount of muscle regeneration.
2. New synthesis of extracellular connective tissue within 2 days of the injury, with
peak at 5 to 21 days.
3. Myositis ossificans (bone formation within muscle).
37

Delayed-onset muscle soreness (DOMS)
 Is muscle ache and pain that typically occurs 24 - 72 hours after intense exercise.
Pathogenesis
 Structural muscle injury occurs and leads to progressive edema formation and resultant
increased intramuscular pressure.
 These changes seem to occur primarily in type IIB fibers.
 It may be associated with changes in the I band of the sarcomere.
 More common following excessive eccentric contractions
38

Denervation
 This causes:
 muscle atrophy and
 increased sensitivity to acetylcholine.
 spontaneous fibrillations at 2 - 4 weeks after injury.
39

Immobilization and disuse
 Decreases number of sarcomeres at the Musculotendinous junction.
 They results in muscle atrophy with:
 associated loss of strength and increased fatigability.
 loss of myofibrils within the muscle cells.
 Immobilization in lengthened positions:
 Decreases contractures and maintains strength.
 It accelerates granulation tissue response.
 Atrophy can also results from disuse
40

Muscle healing/repair
 Muscle healing, like healing of the other vascularized
tissues, proceeds through:
inflammation
repair and
remodelling
41

Inflammation
 Includes migration of inflammatory cells into the injured muscle and, in most
injuries, hemorrhage and formation of a hematoma.
 Phagocytic inflammatory cells enter damaged muscle fibers and phagocytize
bundles of contractile filaments and other cytoplasmic debris.
 Cytokines and growth factors regulate the repair processes after muscle
injury.
 Sources of cytokines include infiltrating
 neutrophils, monocytes, and macrophages, activated fibroblasts, and
endothelial cells.
42

Repair
 Spindle-shaped myogenic cells proliferate  fuse with one another
 form long syncytial myotubes Contractile proteins continue to
accumulate and form myofibrils.
 To become functional, innervation, including formation of a
neuromuscular junction is important.
 Fibroblasts : produce granulation tissue necessary to repair the
matrix of the muscle.
 The optimal results of muscle healing require a balance between
myofiber regeneration and synthesis of new matrix.
43

Remodelling
 Extracellular matrix continues to remodel once
muscle fibers have appeared.
44

Introduction
 Are dense, regularly arranged connective tissues that attach bone to muscle (tendon) and
bone to bone(ligament)
 Injuries to these structures are common due to increased athletic activities ,work related
injuries and use of transportation
46

Structure : Tendons
1. Extra cellular matrix -80%
a.70% of matrix is water
b.30% of matrix is solid
 Collagen type I (75%)- glycine ,proline and hydroxy proline comprises 2/3rd of the amino acids in type 1
collagen
47

 Ground substance –proteoglycans- 1-5% of tendon’s dry weight
 Very hydrophilic
 Decorin -most predominant proteoglycan
 regulate collagen fiber formation
 increase tensile strength of tendons by increasing crosslink between
collagen fibers
 Aggrecan (a proteoglycan abundant in articular cartilage) is found in areas of
tendon that are under compression (eg, regions of hand flexor tendons that
wrap around bone).
 Elastin (2%)- help tissues to resume their shape after stretching and contracting
48

2.cells- 20%
 the predominant cell type- fibroblast
 arranged in spaces between collagen bundles
 spindle shaped, dark under microscope, thin cytoplasmic process
 produce mostly type 1 collagen and small amount of type 3 collagen
49

50

Outer structures
 Endotenons – loose connective tissue,
 bound the fascicles together ,
 permit longitudinal movement of collagen fascicles and
 support blood vessels , lymphatics and nerves
 Epitenon –a synovial like membrane deep to the paratenon, facilitating gliding in areas of high
friction eg. the hand
51

 Types of tendons depending on outermost covering structure
1.Paratenon covered tendons
 e.g. patellar tendon, Achilles tendon
 Has rich vascular supply- heal better
2. Sheathed tendon – in tendons that bend sharply
 acts as a pulley and directs the path of the tendon
 e.g. hand flexor tendons
 Often injured due to laceration
 less vascularized -so heal by adhesion
52

 Microfibril
 Subfibril
 Fibril
 Fascicle
 Tendon
53

Tendon nutrition
 Dual pathway
1.Vascular supply-from
 vessels in the perimysium,
 the periosteal insertion
 the surrounding tissue
2.Avascular region – synovial (diffusion pathway)
54

Nerve supply
 Tendon bulk- has no nerve supply
 Epitenons and paratenons have nerve endings
 Golgi tendon organs-
 present at the junction between tendon and muscles which sense tension
 send sensory information to spinal cord
 relaxes the muscle and prevent the tendon from failure
55

Structure : ligament
 similar in structural composition and mechanical behavior with tendons
 Difference Ligament Tendon
connect between bones connect muscle to bone.
shorter and wider Longer and narrower
lower percentage of
collagen (less organized
collagen fibers)
Higher percentage of
collagen
a higher percentage of
ground substance
Lower percentage of
ground substancePrepared by Dr. Dawit Alemayehu
56

57
UP TO 2X COLLAGEN

Blood supply:
 Relatively hypovascular than the surrounding tissues
 Uniform microvascularity, which originates from the insertion sites
 Provide nutrition for the cellular population and maintains the continued process of matrix
synthesis and repair.
Nerve:
 Contain mechanoreceptors and free nerve endings
 play a role in stabilizing joints
58

Function
Tendons
 Primary Function
 Attach muscle to bone thereby transmitting tensile
loads from muscle to bone to produce movement.
 Secondary Function
 Allows the muscle belly to be at an optimal distance
from the joint upon which it acts.
 “Thickness of bone-until age 30 and growth of
ligament and tendon until age 20.”
Ligament
 Connect bone to bone
 Supporting , strengthening joints & Restrict
range of motion to prevent excessive movement
that could cause dislocation and spraining
 Have mechanoreceptors and free nerve endings
that help with joint proprioception
59

Properties of tendon and ligament
 possesses one of the highest tensile strengths of any soft tissue in the body
Reason
1. its main constituent is collagen, one of the strongest fibrous proteins,
2.these collagen fibers are arranged parallel to the direction of tensile force.
60

 Has viscoelastic property
 Viscous property==the ability to resist deformation by shear or tensile stress
 Elastic property == the ability to return back to its original shape and size when
stress is removed
61

Biomechanics
 Tendons exhibit viscoelastic behavior; the mechanical properties of the tissue are dependent on
loading history and time. Time dependence is best illustrated by the phenomena of creep and
stress relaxation.
I. Stress relaxation :-The decrease in load/stress for a constant elongation/strain(decreased stress
with time under constant deformation)
II. Creep :- The increase in elongation/strain for a constant applied load/stress.
III. Hysteresis (energy dissipation):- when tissue is loaded and unloaded, the unloading curve will
not follow the loading curve.
 the difference between the 2 curves is the energy that is dissipated
IV. Stress-strain (load-elongation) curve
62

63

Factors affecting Properties of ligament & tendon
 Age
Till maturation
- till age 20  # & quality of cross-links   tensile strength and collagen
fiber diameter
After age 20
- collagen content    stiffness, strength & ability to withstand deformation
64

Factors affecting Mechanical Properties
 Pregnancy and postpartum
-tensile strength & stiffness in tendons 
-Increased laxity in the pelvic area at the end of pregnancy and
postpartum period
65

 Physical Training
 tendon tensile strength and ligament- bone interface strength
 ligaments become stronger and stiffer, collagen fibers increase in diameter
66

 Immobilization
  tensile strength of ligaments, more elongation, less stiff
  in cross-links
 After 8 weeks of immobilization  12 months to recover strength &
stiffness
67

Effects of Immobilization
68

Effects of Immobilization
Weeks Months
Time
0
Structural/mechanicalproperties
(Experimental/Controlx100)
0
50
100
Control
Exercise
Immobility
Recovery (ligament
substance)
Recovery
(insertion site)
69

Injury, Healing, and Repair
 MOI-
1. Direct –laceration/contusion
2. Indirect –tensile overload
Depends on
 anatomical location,
 vascularity ,
 amount of force applied and MOI
 the presence of previous pathology
 Failure at the weak link-either
 avulsion # or rupture at the musculotendinious junction
 mid-substance rupture is not common
70

Phases of healing
1. Inflammation - within the 1st 24 hrs
• Damaged capillaries within the ligament /tendon and adjacent tissues produce a hematoma
• Release of the potent vasodilators result in influx of inflammatory cells into the injured area
• Phagocytosis of necrotic materials at the injury site
• Angiogenesis in response to an angiogenic factor secreted by the macrophage
• proliferation of fibroblast
• Type III collagen synthesis initiated
71

2. Repair/proliferative phase (48 hours to 6 weeks)
• type III collagens synthesis peaks and proteoglycans concentration remain high
• The gap between the torn ligament ends is filled with a friable, vascular granulation tissue
3.Remodelling (6th week to 1-2 years)
• Devascularisation and the cellularity is decreased
• Change from type III to I
• Reorientation of collagen – fibrils become aligned in the direction of mechanical stress
• Increased crosslinking of the fibrils - increment in the tensile strength
72

73

Ligament injuries
• COMMON SPORT INJURIES
• KNEE AND ANKLE ARE COMMON BECAUSE
OF
 Inadequate protection (uncovered by
muscle)
 Indirect force has larger leverage
• IF NEGLECTED, IT MAY LEAD TO
 Instability
 Formation of adhesions
74

Classification of ligament injuries
A. Severity
Grade I: Slight over streching
Grade II: Partial tear
Grade III: Complete tear
B. Time
Acute: Less than 2 wks.
Sub acute: Between 2-6 wks.
Chronic: More than 6 wks.
75

Grade 1 Grade 2 Grade 3
mild sprain moderate sprains severe sprains
minimal rupture of some
of its soft-tissue fibers
Partial disruption of the
involved ligament
ligament fibers are
completely disrupted
tender to palpation and
pain - induced when
stress is applied
Swelling &pain when the
injured ligament is
stressed
some pain, swelling, and
tenderness
stressing the joint produce
no tenderness
No laxity of the joint with
stress test
some detectable joint
laxity
Joint laxity
relatively good
prognosis
Most do well most guarded and is
more ligament-specific.
76

Enthesis
 Tendon/Ligament-Bone Junction
 Two types of insertions:
1. Direct insertion (e.g., rotator cuff)— fibrocartilaginous transition zone composed of four
elements: tendon, fibrocartilage, mineralized fibrocartilage, and bone
2. Indirect insertion—tendon fibers (Sharpey fibers) inserting directly onto periosteum
 Inflammation of entheses is seen in HLA-B27– positive processes (e.g., Ankylosing
spondylitis), and subsequent ossification results in joint ankylosis.
 Commonly affected joints include:
1. Sacroiliac joints
2. Spinal apophyseal joints
3. Symphysis pubis
77

 History –
 Cause of the injury
 Site of injury
 Position of the limb during the injury
 Able to continue to play or bear weight
 Previous injury
 P/E - Look ,feel and move
-different maneuvers to elicit pain and instability
Diagnosis
78

• Investigation
• X-ray
• U/S
• MRI- Best modality
• Arthroscopy-
• For intra- articular lesions.
• 1cm opening.
• Common site knee.
79

Management of ligament injuries
 FIRST STAGE – to reduce swelling and pain
• RICE therapy (Rest, Ice, Compress, Elevate) for
the first 24 to 48 hours
1. Rest the injured area (reduce regular exercise or activities as needed)
2. Ice the injured area, 20 minutes at a time, four to eight times a day (cold pack,
ice bag, or plastic bag filled with crushed ice and wrapped in a towel can be used)
80

3. Compress the injured area, using bandages,
casts,
 boots, elastic wraps or splints to help reduce
swelling
4. Elevate the injured area, above the level of the
heart, to help decrease swelling while you are
lying or sitting down
81

 SECOND STAGE – 3R
Operative Mx - can be
 Repair
 Reconstruction
 Rehabilitation
 Controlled early Mobilization
 Promote repair
 Prevent adhesion
 effect on muscle strength
82

 After treatment
 Regained tensile strength is 50-70%
 Time needed for full recovery:
 Mild sprain: three to six weeks
 Moderate sprain: two to three months
 Severe sprain: eight to 12 months
83

Factors that impair ligament healing
 intra-articular
 Extra-articular ligaments (e.g. knee MCL)
have a greater capacity to heal compared
with intra-articular ligaments (e.g. knee
ACL)
 increasing age
 immobilization
 reduces strength of both intact and
repaired ligament
 smoking
 NSAIDS
 including indocin, celcoxib, parecoxib
 diabetes
 alcohol intake
 decreased growth factors
 bFGF, NGF, and IGF-1
 decreased expression of genes involved with
tendon and ligament healing
 examples include:- procollagen I, cartilage
oligomeric matrix protein (COMP), tenascin-C,
tenomodulin, scleraxis
84

 ITS SUPERFICIAL
LOCATION MAKES IT
SUSCEPTIBLE TO INJURY
 TENDON CAN BE
INJURED:
 Musculotendinous junction
 Central portion
 Bony attachment
85
Tendon injury

Direct Indirect
Laceration by sharp
instrument
Hands and fingers
 Spontaneous tendon rupture ,usually preceded by undetected damage.
 Chronic degenerative injuries
 Iatrogenic
 As complication of total knee arthroplasty,
 Arthrotomy
Excessive tensile
loads applied to the
tendon structure
Called strains
86

• COMMON SITES ARE HAND FLEXOR AND
EXTENSOR, ACHILLES, PATELLAR AND
QUADRICEPS TENDON
• ENDS ARE PULLED BY THE MUSCLE
87

 Presentation
 Loss of function
 Presentation is based on the position of the site of injury
 Bleeding and Pain at the site of injury
88

 History – MOI, Feeling of a sudden snap
 Physical examination –
 Position of the limb
 Motion (passive & active)
 gap felt in the injured tendon
 Adequate exposure of the wound
 Identification of associated injuries
 Investigation
 X-ray
 CT
 MRI
 US
Diagnosis
89

Treatment
 Conservative
 If open - proper debridement and covering of the exposed tendon
 Immobilization is for 6 week
 Immobilization followed by rehabilitation processes
 if not treated on time – it remains as it is.
90

 Operative
 Tendon to tendon repair & Tendon to bone repair
 Tendon Graft
 autogenous graft
 Allograft
 Grafting is done when the tendon is pulled by the muscle.
 Arthrodesis is an option
91

Tendon repair
• In < 25% no need of suture or immobilize , 25-50 % immobilize and
> 50 % proper repair
• Suture material is Non absorbable
• Technique – different techniques ( Mattress, Figuer of eight,
Modified bunnel, Modified kessler)
• principle – to decrease suture failure
1.Put suture perpendicular to the tendon before passing it across the
injury( parallel to the tendon)
2.Multi grasp suture
3.Prevent gap formation between the stumps
92

• Post operative care
– Splinting eg. Extensor tendon repair
• Static- non movable
• Dynamic- movable
– Rehabilitation
93

• Dynamic Splinting for post flexor
tendon repair
94

Complications
 Wound infection
 Tendon/ligament adhesion
 Joint stiffness
 Risk of re-injury
95

References
1. Miller`s Review of Orthopaedics,7th edition.
2. AAOS Comprehensive Orthopaedic Review.
3. Orthoteers
4. Orthobullet 2017
5. Internet
96

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