2. ARTICULAR CARTILAGE
• HYALINE CARTILAGE FORMS THE ARTICULAR BEARING SURFACE OF JOINTS IN THE BODY
PROPERTIES:
• SMOOTH, LUBRICATED BEARING SURFACE – DECREASES FRICTION AND DISTRIBUTES LOADS
• COEFFICIENT OF FRICTION LESS THAN ICE ON ICE
• SHOCK ABSORBING CUSHION – RESISTS SHEAR/ COMPRESSION
• VISCOELASTIC PROPERTY
• BIPHASIC – PROPERTY OF SOLID AND LIQUID
• ANISOTROPIC
3. COMPOSITION
• ARTICULAR CARTILAGE CONSISTS MAINLY OF EXTRACELLULAR MATRIX (ECM) (95%) AND A SPARSE
POPULATION OF CHONDROCYTES (5%) THAT MAINTAIN THE ECM THROUGHOUT LIFE.
• IT IS AVASCULAR, ALYMPHATIC, ANEURAL
• THE MAJOR COMPONENTS OF THE ECM ARE -
WATER
COLLAGEN
PROTEOGLYCANS
4. •WATER MAKES UP APPROXIMATELY 75% OF WET WEIGHT
• HIGHEST AT SURFACE LAYERS
• RESPONSIBLE FOR NUTRITION AND LUBRICATION
• DECREASES WITH AGING
• INCREASES IN OSTEOARTHRITIS
INCREASED PERMEABILITY
DECREASED STRENGTH
DECREASED YOUNG’S MODULUS OF ELASTICITY
5. COLLAGEN
• COLLAGEN MAKES UP MORE THAN 50% OF THE DRY WEIGHT OF ARTICULAR CARTILAGE AND
10% TO 20% THE OF WET WEIGHT.
• IT PROVIDES SHEAR AND TENSILE STRENGTH.
• TYPE II COLLAGEN COMPRISES 90% TO 95% OF THE TOTAL COLLAGEN WEIGHT IN HYALINE
CARTILAGE.
• OTHER MINOR TYPES OF COLLAGEN IN ARTICULAR CARTILAGE INCLUDE TYPES V, VI, IX, X, AND
XI
6. • MOST ABUNDANT PROTEIN IN HUMAN BODY
• MAJOR CONSTITUENT OF CONNECTIVE TISSUES
PROPERTIES:
STRONG, INELASTIC, FLEXIBLE
• ABOUT 28 TYPES ARE IDENTIFIED SO FAR
• BUT 80–90% OF THE BODY’S COLLAGEN IS
COMPOSED OF TYPES I, II AND III
COLLAGEN
11. 5 ZONES OF HYALINE CARTILAGE – BASED ON COLLAGEN FIBRE ALIGNMENT
AND BIOMECHANICAL FUNCTION
12. • HYALINE CARTILAGE IS SEPARATED BY SUBCHONDRAL BONY PLATE FROM THE RICHLY
VASCULAR SUBCHONDRAL SPACE
• NUTRITION TO THE CARTILAGE IS DERIVED THROUGH SYNOVIAL FLUID BY DIFFUSION
• MEAN PORE SIZE IS 6nm
• CYTOKINES, VARIOUS GROWTH FACTORS MEDIATE INTERCELLULAR COMMUNICATION
• ALTERATION IN THE CYTOKINE MILIEU IS SEEN IN RHEUMATOID ARTHRITIS, OSTEOARTHRITIS,
OSTEOPOROSIS
13. CYTOKINES AFFECTING CARTILAGE GROWTH
• IGF 1 - STIMULATES CARTILAGE MATRIX SYNTHESIS
• TGF BETA – STIMULATES SYNTHESIS OF PROTEOGLYCANS
• FGF – STIMULATES SYNTHESIS OF DNA IN CHONDROCYTES
• PDGF – IN OA, PDGF PLAYS INCREASED ROLE IN HEALING
• IL -1 BETA, IL- 6, IL- 8 – STIMULATE CHONDROCYTES TO SYNTHESIZE PROTEOGLYCANS
• TNF – DEGARADATION AND SYNTHESIS OF MATRIX
14. • CATHEPSINS - DEGRADATION OF
AGGRECAN
• COLLAGENASE – DEGRADATION
OF HELICAL COLLAGEN FIBRILS
• STROMELYSIN – DEGRADATION OF
PROTEIN CORE
• GELATINASE – SCAVENGES
DENATURED TYPE II AND IV
COLLAGEN
MMPs (MATRIX METALLOPROTEINASES) SUCH AS COLLAGENASES, GELATINASES, STROMELYSIN,
CATHEPSIN B & D ARE INVOLVED IN CARTILAGE TURNOVER
15. • CLINICAL APPLICATION
• INACTIVATION OF MMP, IS AN ONGOING TREND IN THE PREVENTION OF JOINT DEGENERATIVE
DISORDERS
• EX: DOXYCLINE, MINOCYCLINE
• CHLOROQUINE – STRONG INHIBITOR OF CATHEPSIN D
• NON PEPTIDIC ACYLGUANIDE – INHIBITS CATHEPSIN D
16. BIOMECHANICS OF ARTICULAR CARTILAGE
• BIPHASIC THEORY
THE ARTICULAR CARTILAGE INTRINSICALLY MAINTAINS TWO PHASES AS FOLLOWS:
1. FLUID PHASE—HELPS DISSIPATE STRESS AND PROVIDES RESILIENCE AND MAINTAINS
LOW FRICTION.
2. SOLID PHASE—MAINTAINS STRUCTURE AND BEARS THE COMPRESSIVE FORCES.
17. • VISCOELASTIC PROPERTY
• WHEN SUBJECTED TO A MOVING
LOAD THE ARTICULAR CARTILAGE
EXHIBITS A VISCOELASTIC
PROPERTY
• THIS CAN BE I) FLOW DEPENDENT
2) FLOW INDEPENDENT
18. • INTRINSIC MATERIAL PROPERTIES AND
RESISTANCE TO FLOW OF SOLID MATRIX
DEFINE INTERSTITIAL FLUID
PRESSURISATION
• INTERSTITIAL FLUID PRESSURISATION
INFLUENCES
LOAD BEARING CAPACITY
LUBRICATION CAPACITY
33. HEALING
• THE TIDEMARK IS NOT BREACHED IN SUPERFICIAL INJURIES. THEREFORE, HEALING POTENTIAL IS
EXTREMELY LIMITED.
• SUPERFICIAL INJURY TO ARTICULAR CARTILAGE STIMULATES ONLY A SLIGHT REACTION IN
ADJACENT CHONDROCYTES, PRODUCING A TRANSIENT INCREASE IN CELL REPLICATION AND
MATRIX TURNOVER.
• THIS RESPONSE IS LARGELY INEFFECTIVE IN PRODUCING HEALING OF ARTICULAR CARTILAGE
DEFECTS
34. • IN DEEPER INJURIES, PENETRATION OF THE
SUBCHONDRAL BONE LEADS TO A MORE
PRONOUNCED INFLAMMATORY HEALING
RESPONSE.
• A FIBRIN CLOT IS FORMED, AND
UNDIFFERENTIATED MESENCHYMAL STEM
CELLS ARE RECRUITED FROM MARROW
ELEMENTS. THE STEM CELLS PRODUCE A
REPARATIVE TISSUE, FIBROCARTILAGE.
FIBROCARTILAGE PREDOMINANTLY CONSISTS
OF TYPE I COLLAGEN.
• CONSEQUENTLY, IT HAS A REDUCED ABILITY
TO WITHSTAND CYCLICAL LOADING AND IS
PRONE TO EARLY DEGENERATIVE CHANGE.
36. TENDON
• DENSE REGULARLY ARRANGED GROUPS OF COLLAGEN BUNDLES THAT ATTACH MUSCLE TO
BONE
• COMPOSITION - COLLAGEN - 95% - TYPE I COLLAGEN
5% - TYPE III COLLAGEN
ELASTIN
PROTEOGLYCANS – DECORIN (MOST PREDOMINANT)
BIGLYCAN, AGGRECAN
TENOCYTES
38. • TENOCYTES PRODUCE TYPE III COLLAGEN IN RESPONSE TO RUPTURE
• GREATER PROPORTION OF TYPE III COLLAGEN IS FOUND IN ACHILLES TENDON, PREDISPOSES
THE TENDON TO RUPTURE
39. • COLLAGEN IS ARRANGED IN HIERARCHICAL
LEVELS OF INCREASING COMPLEXITY.
• BEGINNING WITH TROPOCOLLAGEN - A
TRIPLE-HELIX POLYPEPTIDE CHAIN THAT
MERGES INTO FIBRILS
--- FIBRES (PRIMARY BUNDLES/ SUB
FASCICLES)
--- FASCICLES (SECONDARY BUNDLES)
--- TERTIARY BUNDLES
--- AND THE TENDON
40. • SUPERFICIALLY, THE EPITENON IS SURROUNDED BY PARATENON
• TENDONS WITH PARATENON- HIGH VASCULARITY
BETTER HEALING
• SYNOVIAL TENDON SHEATHS ARE PRESENT IN AREAS SUBJECTED
TO INCREASED MECHANICAL STRESS
EX: TENDONS OF HAND AND FEET
41. • MYOTENDINOUS JUNCTION (MTJ) - TENDINOUS COLLAGEN FIBRILS ARE INSERTED INTO DEEP
RECESSES FORMED BY MYOCYTE PROCESSES
• THE OSTEOTENDINOUS JUNCTION (OTJ) - COMPOSED OF FOUR ZONES:
ZONE OF DENSE COLLAGEN FIBRES
FIBROCARTILAGE
MINERALIZED FIBROCARTILAGE (SHARPEY FIBRES INTERDIGITATE WITH PERIOSTEUM)
BONE
42. • TENDONS RECEIVE THEIR BLOOD SUPPLY FROM THREE MAIN SOURCES:
THE INTRINSIC SYSTEM AT THE MTJ,
THE INTRINSIC SYSTEM AT THE OTJ, AND
THE EXTRINSIC SYSTEM VIA THE PARATENON OR THE SYNOVIAL SHEATH
• MTJ - PERIMYSEAL VESSELS FROM THE MUSCLE CONTINUE BETWEEN THE FASCICULI
OF THE TENDON, AND SUPPLY APPROXIMATELY THE PROXIMAL THIRD OF THE
TENDON
• OTJ - SPARSE AND LIMITED TO THE INSERTION ZONE OF THE TENDON
EXTRINSIC SYSTEM COMMUNICATES WITH PERIOSTEAL VESSELS AT THE OTJ
43. • IN TENDONS WITH SHEATHS, BRANCHES FROM MAJOR VESSELS PASS THROUGH THE VINCULA
44. • TENDON VASCULARITY IS COMPROMISED AT
JUNCTIONAL ZONES AND SITES OF TORSION,
FRICTION OR COMPRESSION
• IN THE ACHILLES TENDON, CLASSICAL
ANGIOGRAPHIC INJECTION TECHNIQUES HAVE
DEMONSTRATED A ZONE OF HYPOVASCULARITY
2–7 CM PROXIMAL TO THE CALCANEAL
INSERTION
45. • A SIMILAR ZONE OF HYPOVASCULARITY IS PRESENT ON THE DORSAL SURFACE OF THE FLEXOR
DIGITORUM PROFUNDUS TENDON, WITHIN 1 CM OF THE TENDON INSERTION
• IN GENERAL, TENDON BLOOD FLOW DECLINES WITH INCREASING AGE AND MECHANICAL
LOADING.
47. NON-LINEAR ELASTICITY
• THIS UNIQUE MECHANICAL
BEHAVIOUR, REFLECTED BY A
STRESS-STRAIN CURVE
CONSISTING OF THREE DISTINCT
REGIONS
1. TOE REGION
2. LINEAR REGION
3. YIELD AND FAILURE REGION
48. VISCOELASTICITY
• THERE ARE THREE MAJOR
CHARACTERISTICS OF A
VISCOELASTIC MATERIAL OF
TENDONS
1. CREEP
2. STRESS-RELAXATION
3. ENERGY DISSIPATION/
HYSTERESIS
CREEP
STRESS-RELAXATION
ENERGY DISSIPATION/ HYSTERESIS
49. TENDINOPATHIES
• TENDINOSIS – DEGENERATIVE CHANGES IN THE TENDON’S COLLAGEN DUE TO CHRONIC
OVERUSE
• TENDINITIS – INFLAMMATION OF TENDON RESULTING FROM MICROTEARS DUE TO ACUTE
OVERLOAD
• TENOSYNOVITIS – INFLAMMATION OF SYNOVIAL SHEATH THAT ENCLOSES THE TENDON
• CYSTS
• NODULES
• TENDON TUMORS
• TENDON RUPTURES
50. HEALING
• TENDONS AND LIGAMENTS ARE RELATIVELY AVASCULAR STRUCTURES, AND HAVE 7.5 TIMES LOWER
OXYGEN CONSUMPTION THAN SKELETAL MUSCLES
• THEIR LOW METABOLIC RATE AND ANAEROBIC ENERGY GENERATING CAPACITY HELP TO MAINTAIN
TENSION FOR LONG PERIODS, REDUCING THE RISK OF ISCHAEMIA AND SUBSEQUENT NECROSIS
THREE PHASES OF HEALING:
• A. HEMOSTASIS/INFLAMMATION
• B. MATRIX AND CELL PROLIFERATION
• C. REMODELING/MATURATION
52. GENERAL CAUSES OF TENDON RUPTURE
• DIRECT TRAUMA
• ADVANCED AGE, DUE TO DECREASED BLOOD SUPPLY RESULTING IN WEAKENING OF
THE TENDON.
• ECCENTRIC LOADING
• STEROID INJECTION INTO THE TENDON USED FOR SEVERE TENDONITIS
• ANTIBIOTICS SUCH AS FLUOROQUINOLONES INCREASE THE RISK FOR TENDON
RUPTURE, PARTICULARLY THE ACHILLES TENDON.
54. • TA RUPTURE TESTS PICS
THOMPSON TEST MATLES TEST
55. EMPTY CAN TEST –
SUPRASPINATUS/
INFRASPINATUS
BELLY PRESS TEST-
SUBSCAPULARIS
HORN BLOWER TEST –
TERES MINOR
56. TREATMENT
• NONOPERATIVE TREATMENT IS MOST EFFECTIVE IN PARTIAL TENDON RUPTURES
• EVEN IN LARGE TEARS NONOPERATIVE TREATMENT WITH IMMOBILISATION FOLLOWED BY
PHYSIOTHERAPY IS PRACTISED BY MANY SURGEONS
• ARTHROSCOPIC REPAIR
• SURGICAL REPAIR
57. • SURGICAL TENDON REPAIRS ARE WEAKEST AT 7-10 DAYS
• MOST OF THE ORIGINAL STRENGTH IS REGAINED AT 21-28 DAYS
• MAXIMUM STRENGTH IS ACHIEVED AT 6 MONTHS
• PROTECTIVE IMMOBILIZATION IN THE EARLY PERIOD AFTER TENDON REPAIR IS BENEFICIAL
• EXERCISE CAN BE DETRIMENTAL IF STARTED TOO EARLY IN THE REHABILITATION PERIOD, BUT IT IS
BENEFICIAL DURING THE REMODELING PHASE OF HEALING.
• EARLY PASSIVE MOTION IS BENEFICIAL FOR FLEXOR TENDON HEALING. EARLY MOTION SUPPRESSES
ADHESION FORMATION BETWEEN THE TENDON AND THE SHEATH, PREVENTING THE TYPICAL RANGE
OF MOTION LOSSES SEEN WITH IMMOBILIZED TENDONS.
58. • TENDON TRANSFERS (DR. PAUL BRAND) SRINIVASAN TWO TAILED TIBIALIS
POSTERIOR TENDON TRANSFER
59. MUSCLE
• SKELETAL MUSCLE IS A COMPOSITE STRUCTURE THAT CONSISTS OF MYOCYTES, ORGANIZED
NETWORK OF NERVES AND BLOOD VESSELS, AND ECM
• THE BASIC STRUCTURAL UNIT OF SKELETAL MUSCLE IS THE MYOFIBRE, WHICH IS COMPOSED OF
MULTIPLE MYOFIBRILS
• MYOFIBRES ARE SURROUNDED BY A CONNECTIVE TISSUE SHEATH, KNOWN AS ENDOMYSIUM.
• SEVERAL MYOFIBRES GROUP TOGETHER TO FORM A FASCICLE, WHICH IN TURN IS ENCLOSED WITHIN
THE PERIMYSIUM.
• MULTIPLE MUSCLE FASCICLES GROUP TOGETHER TO FORM THE BODY OF THE MUSCLE, WHICH IS
COVERED BY EPIMYSIUM.
60. • MYOFIBRIL, IS A STRING OF
SARCOMERES ARRANGED IN
SERIES.
• ADJACENT MYOFIBRILS ARE
CONNECTED BY A SET OF
SPECIALIZED PROTEINS CALLED
INTERMEDIATE FILAMENTS.
• THESE ALLOW FOR MECHANICAL
COUPLING BETWEEN MYOFIBRILS.
61. • A SPECIALLY DESIGNED MEMBRANE SYSTEM EXISTS WITHIN THE CELL THAT ASSISTS IN
ACTIVATING THE CONTRACTILE PROPERTIES OF THE MUSCLE CELL.
• THE SYSTEM CONSISTS OF TWO MAIN COMPONENTS:
1. THE TRANSVERSE TUBULAR SYSTEM AND
2. THE SARCOPLASMIC RETICULUM
62. • RYANODINE RECEPTORS (RYR1) REGULATE THE RELEASE OF CALCIUM FROM THE
SARCOPLASMIC RETICULUM AND SERVE AS A CONNECTION BETWEEN THE SARCOPLASMIC
RETICULUM AND SARCOLEMMA-DERIVED TRANSVERSE TUBULE.
• AN ABNORMAL RYANODINE RECEPTOR IN SKELETAL MUSCLE IS IMPLICATED IN PERSONS
SUSCEPTIBLE TO MALIGNANT HYPERTHERMIA.
• DANTROLENE DECREASES LOSS OF CALCIUM FROM THE SARCOPLASMIC RETICULUM.
65. TYPE 1 FIBERS/ SLOW TWITCH FIBERS/ SLOW OXIDATIVE
• AEROBIC
• HAVE MORE MITOCHONDRIA, ENZYMES, TRIGLYCERIDES THAN TYPE II FIBRES
• LOW CONCENTRATION OF GLYCOGEN, GLYCOLYTIC ENZYMES
• ‘ARE THE FIRST LOST WITHOUT REHABILITATION ‘
• EX: POSTURAL MUSCLES OF NECK, SPINE
SOLEUS
66. TYPE 2A FIBERS/ FAST TWITCH/ FAST OXIDATIVE FIBERS
• MEDIUM ANAEROBIC CAPACITY
• LESS EFFICIENT THAN TYPE I BUT WITH LARGE AMOUNT OF FORCE PER CROSS-SECTIONAL
AREA, WITH HIGH CONTRACTION SPEEDS AND QUICK RELAXATION TIMES
• WELL SUITED FOR HIGH-INTENSITY, SHORT-DURATION ACTIVITIES (E.G., SPRINTING)
TYPE 2B FIBERS/ FAST TWITCH/ FAST GLYCOLYTIC FIBERS
• HIGH ANAEROBIC CAPACITY
• HIGH STRENGTH AND CONTRACTION SPEEDS
• RAPID FATIGUE
67. • ENDURANCE TRAINING—DECREASED TENSION AND INCREASED REPETITIONS
• INDUCES HYPERTROPHY OF SLOW-TWITCH FIBERS
• INCREASES CAPILLARY DENSITY, MITOCHONDRIA, AND OXIDATIVE CAPACITY
• INCREASES RESISTANCE TO FATIGUE
• STRENGTH TRAINING—INCREASED TENSION AND DECREASED REPETITIONS
• INCREASES MYOFIBRILS AND FIBER SIZE
• INDUCES HYPERTROPHY (INCREASED CROSS-SECTIONAL AREA) OF FAST-TWITCH (TYPE II) FIBERS
68. • A SIGNIFICANT DECLINE IN AEROBIC FITNESS (“DETRAINING”) OCCURS AFTER ONLY 2 WEEKS
OF NO TRAINING.
• MUSCLES THAT CROSS A SINGLE JOINT ATROPHY FASTER
• TYPE 1 FIBERS CONVERTED TO TYPE 2 FIBERS
69. • THE PERCENT OF SLOW-TWITCH, TYPE I FIBERS IN THE QUADRICEPS FEMORIS MUSCLES OF THE
LEGS, CAN VARY FROM UNDER 20% (IN PEOPLE WHO ARE EXCELLENT SPRINTERS) TO AS HIGH AS
95% (IN PEOPLE WHO ARE GOOD MARATHON RUNNERS).
• THESE DIFFERENCES ARE BELIEVED TO BE PRIMARILY THE RESULT OF DIFFERENCES IN GENETICS
• TYPE 1 FIBERS ARE FIRST TO DEGENERATE – OBESITY
DIABETES MELLITUS
COPD AND HEART FAILURE
• TYPE 2 FIBRES ARE FIRST TO DEGENERATE - DUCHENNE MUSCULAR DYSTROPHY
FACIOSCAPULOHUMERAL DYSTROPHY
MYOTONIC DYSTROPHY TYPE 1
AGEING
70. MUSCLE INJURIES
MUSCLE STRAINS
• MOST COMMON AT MYOTENDINOUS JUNCTION
• OCCUR PRIMARILY IN MUSCLES CROSSING TWO JOINTS (HAMSTRING, GASTROCNEMIUS) THAT HAVE
INCREASED TYPE II FIBERS
• INITIALLY THERE IS INFLAMMATION AND LATER FIBROSIS MEDIATED BY TGF-Β.
71. MUSCLE TEARS
• MOST OCCUR AT THE MYOTENDINOUS JUNCTION (E.G., RECTUS FEMORIS TEAR AT ANTERIOR
INFERIOR ILIAC SPINE).
• OFTEN OCCUR DURING A RAPID (HIGH-VELOCITY) ECCENTRIC CONTRACTION
• ECCENTRIC CONTRACTIONS DEVELOP THE HIGHEST FORCES.
• SATELLITE CELLS ACT AS STEM CELLS AND ARE MOST RESPONSIBLE FOR MUSCLE HEALING.
• ALTERNATIVELY, THE DEFECT CAN HEAL WITH BRIDGING SCAR TISSUE. TGF-Β STIMULATES
PROLIFERATION OF MYOFIBROBLASTS AND INCREASES FIBROSIS.
72. • DELAYED-ONSET MUSCLE SORENESS (DOMS)
• THIS PHENOMENON OCCURS 24 TO 72 HOURS AFTER INTENSE EXERCISE.
MAY RESULT FROM ECCENTRIC MUSCLE CONTRACTIONS CAUSED BY EDEMA AND INFLAMMATION
IN THE CONNECTIVE TISSUE, WITH A NEUTROPHILIC RESPONSE PRESENT AFTER ACUTE MUSCLE
INJURY.
• NSAIDS RELIEVE DOMS IN A DOSE-DEPENDENT MANNER.
• MASSAGE HAS VARYING EFFECTS
OTHER MODALITIES (ICE, STRETCHING, ULTRASONOGRAPHY, ELECTRICAL STIMULATION) HAVE NOT
BEEN SHOWN TO AFFECT DOMS.
73. DENERVATION
• CAUSES MUSCLE ATROPHY AND INCREASED SENSITIVITY TO ACETYLCHOLINE
• LEADS TO SPONTANEOUS FIBRILLATIONS AT 2 TO 4 WEEKS AFTER INJURY
IMMOBILIZATION
• ACCELERATES GRANULATION TISSUE RESPONSE
• IMMOBILIZATION IN LENGTHENED POSITIONS DECREASES CONTRACTURES AND MAINTAINS STRENGTH.
• ATROPHY RESULTS FROM DISUSE OR ALTERED RECRUITMENT.
• ATROPHIC CHANGES ARE RELATED TO THE LENGTH AT WHICH MUSCLE IS IMMOBILIZED.
• ELECTRICAL STIMULATION CAN HELP OFFSET THESE EFFECTS.
