The document discusses various types of musculoskeletal injuries and disorders. It describes fractures, dislocations, strains, sprains, tendinitis, bursitis, and other injuries. It also covers osteoporosis, osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, osteomyelitis, and other conditions. For fractures, it discusses classifications and the bone healing process. For osteoarthritis and rheumatoid arthritis, it provides details on pathogenesis, risk factors, manifestations, and treatment options.

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Alterations of Musculoskeletal
Function

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Musculoskeletal Injuries
• Complete or incomplete
 Closed or open
• Comminuted
• Linear
• Oblique
• Spiral
• Transverse
• Greenstick
• Torus
• Bowing
• Pathologic
• Stress
 Fatigue and
insufficiency
 Transchondral
 Fractures
 A fracture is a break in the continuity of a bone
 Classifications:

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Fractures

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Bone Fractures
 A broken bone can cause damage to the
surrounding tissue, the periosteum, and
the blood vessels in the cortex and marrow
 Hematoma formation
 Bone tissue destruction triggers an
inflammatory response
 Procallus formation

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Callus Formation

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Callus Formation (cont’d)

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Bone Fractures
 Manifestations:
 Often numbness up to 20 minutes following
injury
 Unnatural alignment, swelling, muscle spasm,
tenderness, pain, impaired sensation, and
possible muscle spasms
 Treatment:
 Closed manipulation, traction, and open
reduction
 Internal and external fixation

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Bone Fractures (cont’d)
 Improper reduction or immobilization
 Nonunion, delayed union, and malunion
 Dislocation
 Temporary displacement of two bones
 Loss of contact between articular cartilage
 Subluxation
 Contact between articular surfaces is only
partially lost

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Bone Fractures (cont’d)
 Dislocation and subluxation are associated
with fractures, muscle imbalance,
rheumatoid arthritis, or other forms of joint
instability

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Support Structure Injuries
 Strain
 Tear or injury to a tendon
 Sprain
 Tear or injury to a ligament
 Avulsion
 Complete separation of a tendon or ligament
from its bony attachment site

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Tendinopathy and Bursitis
 Tendinitis
 Inflammation of a tendon
 Tendinosis
 Painful degradation of collagen fibers
 Bursitis
 Inflammation of a bursa
• Skin over bone, skin over muscle, and muscle and
tendon over bone
 Caused by repeated trauma
 Septic bursitis is caused by a wound infection

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Tendinopathy and Bursitis (cont’d)
 Epicondylitis
 Inflammation of a tendon where it attaches to a
bone
• Tennis elbow (lateral epicondylitis)
• Golfer’s elbow (medial epicondylitis)

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Tendinopathy and Bursitis (cont’d)

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Tendinitis and Epicondylitis

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Muscle Strain
 Sudden, forced motion causing the muscle
to become stretched beyond its normal
capacity
 Local muscle damage
 Muscle strains can also involve the
tendons

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Myositis Ossificans
 Complication of local muscle injury
 Inflammation of muscular tissue with
subsequent calcification and ossification of
the muscle
 Rider’s bone in equestrians
 Drill bone in infantry soldiers
 Thigh muscles in football players

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Rhabdomyolysis
 Rhabdomyolysis (myoglobinuria) is a life-
threatening complication of severe muscle
trauma with muscle cell loss
 Crush syndrome
 Compartment syndromes
• Volkmann ischemic contracture
 Malignant hyperthermia

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Osteoporosis
 Porous bone
 Poorly mineralized bone
 Bone density:
 Normal bone
• 833 mg/cm2
 Osteopenic bone
• 833 to 648 mg/cm2
 Osteoporosis
• <648 mg/cm2

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Osteoporosis (cont’d)
 Potential causes:
 Decreased levels of estrogen and testosterone
 Decreased activity level
 Excess intake of caffeine, phosphorus, alcohol,
nicotine
 Inadequate levels of vitamins D and C, or Mg++

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Osteoporosis (cont’d)
 Demonstrated by reduced bone
mass/density and an imbalance of bone
resorption and formation
 Bone histology is usually normal but it
lacks structural integrity

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Osteoporosis (cont’d)

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Osteoporosis (cont’d)

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Osteoporosis (cont’d)
 Iatrogenic osteoporosis
 Regional osteoporosis
 Postmenopausal osteoporosis
 Glucocorticoid-induced osteoporosis
 Age-related bone loss

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Osteoporosis (cont’d)

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Osteoporosis (cont’d)

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Osteoporosis (cont’d)

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Osteomalacia
 Deficiency of vitamin D lowers the
absorption of calcium from the intestines
 Inadequate or delayed mineralization
 Bone formation progresses to osteoid
formation but calcification does not occur;
the result is soft bones
 Pain, bone fractures, vertebral collapse, bone
malformation

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Paget Disease
 Also called osteitis deformans
 Excessive resorption of spongy bone and
accelerated formation of softened bone
 Disorganized, thickened, but soft bones
 Most often affects the axial skeleton

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Paget Disease (cont’d)
 Thickened bones can cause abnormal
bone curvatures, brain compression,
impaired motor function, deafness, atrophy
of the optic nerve, etc.

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Osteomyelitis
 Osteomyelitis is most often caused by a
staphylococcal infection
 Most common cause is open wound
(exogenous); also can be from a blood-
borne (endogenous) infection

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Osteomyelitis (cont’d)
 Manifestations:
 Acute and chronic inflammation
 Fever
 Pain
 Necrotic bone
 Treatment:
 Very difficult to treat
 Antibiotics, debridement, surgery, hyperbaric
oxygen therapy

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Osteomyelitis (cont’d)

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Osteomyelitis (cont’d)

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Inflammatory vs. Noninflammatory
Joint Disease
 Differentiated by:
 Absence of synovial membrane inflammation
 Lack of systemic signs and symptoms
 Normal synovial fluid analysis

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Osteoarthritis
 Degeneration and loss of articular
cartilage, sclerosis of bone underneath
cartilage, and formation of bone spurs
(osteophytes)
 Also referred to as degenerative joint
disease
 Incidence increases with age
 Primary disease is idiopathic

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Osteoarthritis (cont’d)
 Risk factors:
 Increased age
 Joint trauma, long-term mechanical stress
 Endocrine disorders (hyperparathyroidism)
 Drugs
 Obesity

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Osteoarthritis (cont’d)
 Characteristics:
 Local areas of damage and loss of articular
cartilage
 New bone formation of joint margins
 Subchondral bone changes
 Variable degrees of mild synovitis and
thickening of the joint capsule

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Osteoarthritis (cont’d)
 Manifestations:
 Pain (worsens with activity)
 Stiffness (diminishes with activity)
 Enlargement of the joint
 Tenderness
 Limited motion
 Deformity

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Osteoarthritis (cont’d)

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Osteoarthritis (cont’d)

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Osteoarthritis (cont’d)

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Osteoarthritis (cont’d)

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Rheumatoid Arthritis
 Inflammatory autoimmune joint disease
 Systemic autoimmune damage to
connective tissue, primarily in the joints
(synovial membrane)
 Similar symptoms to osteoarthritis
 Cause unknown; multifactorial with strong
genetic predisposition

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Rheumatoid Arthritis (cont’d)
 Presence of rheumatoid factors (RA or RF
test)
 Antibodies (IgG and IgM) against antibodies
 Joint fluid presents with inflammatory
exudate

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Rheumatoid Arthritis (cont’d)
 Pathogenesis
 Three Processes:
• Neutrophils and other cells in the synovial fluid
become activated
• Inflammatory cytokines (tumor necrosis factor-alpha
(TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-
6), interleukin-7 (IL-7), interleukin-21 (IL-21), induce
enzymatic breakdown of cartilage and bone
• T cells also interact with synovial fibroblasts through
TNF-α, converting synovium into a thick, abnormal
layer of granulation tissue (pannus)

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Osteoarthritis
 Manifestations:
 Insidious onset
 Begins with general systemic manifestations of
inflammation, including fever, fatigue,
weakness, anorexia, weight loss, and
generalized aching and stiffness
 Over a period of weeks or months, the joints
become painful, tender, stiff, swollen, warm,
boggy, and lose range of motion
 Joint deformities

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Rheumatoid Arthritis
 Evaluation
 Four or more of the following:
• Morning joint stiffness lasting at least 1 hour
• Arthritis of three or more joint areas
• Arthritis of the hand joints
• Symmetric arthritis
• Rheumatoid nodules
• Abnormal amounts of serum rheumatoid factor
• Radiographic changes

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Rheumatoid Arthritis (cont’d)

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Rheumatoid Arthritis (cont’d)

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Rheumatoid Arthritis (cont’d)

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Ankylosing Spondylitis
 Inflammatory joint disease of the spine or
sacroiliac joints causing stiffening and
fusion of the joints
 Systemic, immune inflammatory disease
 Primary proposed site is the enthesis
 Site where ligaments, tendons, and the joint
capsule are inserted into bone

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Ankylosing Spondylitis (cont’d)
 Cause unknown, but there is a strong
association with HLA-B27 antigen
 Begins with the inflammation of
fibrocartilage, particularly in the vertebrae
and sacroiliac joint
 Inflammatory cells infiltrate and erode
fibrocartilage
 As repair begins, the scar tissue ossifies
and calcifies; the joint eventually fuses

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Ankylosing Spondylitis (cont’d)
 Manifestations:
 Early symptoms:
• Low back pain that begins in early 20s and
progresses over time
• Stiffness
• Pain
• Restricted motion
 Loss of normal lumbar curvature (lordosis)
 Increased concavity of upper spine (kyphosis)

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Ankylosing Spondylitis (cont’d)

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Gout
 Metabolic disorder that disrupts the body’s
control of uric acid production or excretion
 Gout manifests high levels of uric acid in
the blood and other body fluids
 Occurs when the uric acid concentration
increases to high enough levels to
crystallize

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Gout (cont’d)
 Crystals deposit in connective tissues
throughout the body
 Sites:
• 50% of the initial attacks occur in the
metatarsophalangeal joint of the great toe
• Heel, ankle, instep of the foot, knee, wrist, or elbow
 When these crystals occur in the synovial
fluid, the inflammation is known as gouty
arthritis

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Gout (cont’d)
 Gout is related to purine (adenine and
guanine) metabolism
 Affected patients can have accelerated
purine synthesis, breakdown, or poor uric
acid secretion in the kidneys

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Gout (cont’d)
 Mechanisms for crystal deposition:”
 Lower body temperatures
 Decreased albumin or glycosaminoglycan
levels
 Changes in ion concentration and pH
 Trauma
 Risk factors:
 Male sex
 Increasing age
 High intake of alcohol, red meat, and fructose
 Drugs

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Gout (cont’d)
 Clinical stages:
 Asymptomatic hyperuricemia
 Acute gouty arthritis
 Tophaceous gout

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Gout (cont’d)
 Manifestations:
 An increase in serum urate concentration
(hyperuricemia)
 Recurrent attacks of monoarticular arthritis
(inflammation of a single joint)
 Deposits of monosodium urate monohydrate
(tophi) in and around the joints
 Renal disease involving glomerular, tubular,
and interstitial tissues and blood vessels
 Formation of renal stones

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Gout (cont’d)
 Manifestations of acute gouty attack:
 Severe pain especially at night
 Hot, red, tender joint
 Signs of systemic inflammation:
• Increased sedimentation rate
• Fever
• Leukocytosis)

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Gout (cont’d)

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Disorders of Skeletal Muscle
 Contracture
 Muscle fiber shortening without an action
potential
 Caused by failure of the sarcoplasmic
reticulum (calcium pump) even with available
ATP
 Stress-induced muscle tension
 Neck stiffness, back pain, clenching teeth,
hand grip, and headache
 Associated with chronic anxiety

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Disuse Atrophy
 Reduction in the normal size of muscle
cells as a result of prolonged inactivity
 Bed rest
 Trauma
 Casting
 Nerve damage
 Treatment
 Isometric movements
 Passive lengthening exercises

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Fibromyalgia
 Chronic widespread diffuse joint pain,
fatigue, and tender points
 Vague symptoms:
 Increased sensitivity to touch
 Absence of inflammation
 Fatigue
 Sleep disturbances/non-restorative sleep

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Fibromyalgia (cont’d)
 80% to 90% of individuals affected are
women, and the peak age is 30 to 50
years
 New research indicates a genetic
predisposition and environmental factors
play a role in development of symptoms

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Fibromyalgia (cont’d)
 Viewed as the result of central nervous
system dysfunction, where pain
transmission and interpretation are
amplified (central sensitization)
 Autoimmune disorders often coexist
 Studies of genetic factors have implicated
alterations in genes affecting serotonin,
catecholamines, and dopamine

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Fibromyalgia (cont’d)
 Manifestations:
 Prominent symptom of fibromyalgia is diffuse, chronic
(defined as being present more than 3 months) pain that
is burning or gnawing in nature
 Only reliable finding on examination is the presence of
multiple tender points; the pain often begins in one
location, especially the neck and shoulders, but then
becomes more generalized
 Profound fatigue
 Diagnosis
 Tenderness in eleven pairs of tender points along with a
history of diffuse pain

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Fibromyalgia (cont’d)

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Muscle Membrane Abnormalities
 Myotonia
 Periodic paralysis:
 Hypokalemic
 Hyperkalemic

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Diseases of Muscle Metabolism
 Endocrine disorders
 Hyperthyroidism
 Diseases of energy metabolism:
 McArdle disease
• Myophosphorylase deficiency
 Acid maltase deficiency
• Pompe disease
 Myoadenylate deaminase deficiency (MDD)
 Lipid deficiencies

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Polymyositis and Dermatomyositis
 Collectively described by the term myositis
 Viral, bacterial, and parasitic myositis
 Staphylococcus aureus infections
 Trichinosis
• Trichinella infection
 Toxoplasmosis
 Polymyositis and dermatomyositis

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Polymyositis and Dermatomyositis
(cont’d)

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Toxic Myopathies/”Muscle
Damage”
 The most common cause of toxic
myopathy is alcohol abuse
 Acute attack of muscle weakness, pain, and
swelling
 Chronic weakness in a drinker of long duration
 Necrosis of individual muscle fibers
• Disturbance of energy turnover, gene dysregulation, and
initiation of apoptosis
 Other causes include lipid-lowering agents
(fibrates and statins), antimalarial drugs,
steroids, thiol derivatives, and narcotics

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Toxic Myopathies/”Muscle
Damage” (cont’d)
 Manifestations:
 Acute muscle weakness
 Painless or severe pain if necrosis
 Most severe complication is
rhabdomyolysis (acute muscle fiber
necrosis with leakage of muscle protein
into the bloodstream) that leads to
myoglobinuria and acute renal failure

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Bone Tumors
 May originate from bone cells, cartilage,
fibrous tissue, marrow, or vascular tissue
 Osteogenic
 Chondrogenic
 Collagenic
 Myelogenic

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Bone Tumors (cont’d)
 Malignant bone tumors
 Increased nuclear/cytoplasmic ratio
 Irregular borders
 Excess chromatin
 A prominent nucleolus
 An increase in the mitotic rate

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Bone Tumors (cont’d)

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Bone Tumors (cont’d)
 Patterns of bone destruction:
 Geographic pattern
 Moth-eaten pattern
 Permeative pattern

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Bone Tumors (cont’d)
 Osteosarcoma
 38% of bone tumors
 Predominant in adolescents and young adults;
occurs in seniors if they have a history of
radiation therapy
 Contain masses of osteoid
• Streamers: noncalcified bone matrix and callus
 Located in the metaphyses of long bones
• 50% occur around the knees

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Osteosarcoma

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Bone Tumors
 Chondrosarcoma
 Tumor of middle-aged and older adults
 Infiltrates trabeculae in spongy bone; frequent
in the metaphyses or diaphysis of long bones
 The tumor contains lobules of hyaline cartilage
that expand and enlarge the bone
 Causes erosion of the cortex and can expand
into the neighboring soft tissues

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Bone Tumors (cont’d)
 Fibrosarcoma
 Firm, fibrous mass of collagen, malignant
fibroblasts, and osteoclast-like cells
 Usually affects metaphyses of the femur or
tibia
 Metastasis to the lungs is common

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Bone Tumors (cont’d)
 Myelogenic tumors:
 Giant cell tumor
• Causes extensive bone resorption because of the
osteoclastic origin of the giant cells
• Located in the epiphyses of the femur, tibia, radius,
or humerus
• The tumor has a slow, relentless growth rate
 Myeloma

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Muscle Tumors (cont’d)
 Rhabdomyosarcoma
 Malignant tumor of striated muscle
 Usually muscles of the tongue, neck, larynx,
nasal cavity, axilla, vulva, and heart
 Highly malignant with rapid metastasis
 Types:
• Pleomorphic
• Embryonal
• Alveolar

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Muscular Dystrophy
 Group of inherited disorders that cause
degeneration of skeletal muscle fibers
 The muscular dystrophies cause
progressive, symmetric weakness and
wasting of skeletal muscle groups

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Duchenne Muscular Dystrophy
 Most common of the muscular dystrophies
 X-linked recessive inheritance
 Deletion of a segment of DNA or a single gene
defect on the short arm of the X-chromosome
 Generally affects boys
 Duchenne muscular dystrophy gene
 Encodes for the dystrophin protein
 Dystrophin maintains the structural integrity of
the cytoskeleton

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Duchenne Muscular
Dystrophy(Cont)
 Manifestations of the disorder begin to
appear by approximately 3 years of age:
 Slow motor development
 Progressive weakness
 Muscle wasting
 Sitting and standing are delayed
 The child is clumsy, falls frequently, and has
difficulty climbing stairs