Pathology of

musculoskeletal system
By
Faisal Mehboob

Introduction

Bone cells
Osteocyte (maintain bone tissue)
Osteoblast (form bone matrix)
Osteogenic cell (stem cell )
Osteoclast (resorb bone )

Advances in musculoskeletal biotechnology

Advances in molecular biology tech have extended the potential for
understanding musculoskeletal disorders from microscopic level to the
molecular levels.
Orthopedic surgery has been revolutionized by tissue engineering, including
biologic manipulation for spinal fusion, synthetic skeletal substitute materials,
preservation and restoration, transplantation or fabrication of avascular tissue.
E.g. meniscus, articular cartilage.
In addition the first nerve tubes for repair and regeneration of peripheral
nerves is now available for clinical use.
Training and conditioning differently during different times of the month may
help protect from injury
Men inc their muscle volume about twice as much in response to strength
training compared with women. Men also experience larger losses in response
to detraining than women.

Aging and musculoskeletal system

Sarcopenia occur in muscle with aging
Sarcopenia is an age related loss in muscle mass, strength and endurance
accompanied by changes in the metabolic quality of skeletal muscle.
The etiology is multifactorial , involving changes in muscle metabolism,
endocrine changes (low testosterone level), nutritional factors , mitochondrial
and genetic factors.
Pathogenesis of sarcopenia refer as the loss of function appear due to dec total
fibers, dec number of muscle fibre size, impaired excitation-contraction
coupling mechanism or dec high-threshold motor units. Selective loss of motor
unit number or atrophy of fast twitch muscle fiber may occur.Type 2 fibers are
preferentially affected by aging and that fiber 2 atrophy is associated with a
decline in satellite cells
Effects of sarcopenia are it dec basal metabolic rate which contribute to
metabolic disorders like type 2 diabetes and osteoporosis, and dec muscle
strength and activity level which in turn dec energy requirement of aging adult.

Effects of aging on joints and connective tissues

Increased stiffness and decreased flexibility
Changes in articular cartilage (friction increases) (proteoglycan aggregation
dec)
Tendon exhibit a lower metabolic activity associated with aging that has
implication for injury and healing in the aging population .
With age , presence of osteoarthritis seems to make joint proprioception even
worse.
Effects of aging on bones
Around the time of menopause for women , resorption, the process by which
bone is broken down and calcium is released from the bone for use of the body
inc, while formation , the bone rebuilding process fails to keep pace.
The same progressive dec of calcium can occur in men , only at a reduced and
slowed rate.

Genetic and
developmental
disorders

1. Down syndrome
Down syndrome was first genetic disorder attributed to a chromosomal
aberration and referred to as trisomy 21.
Down syndrome is characterized by *muscle hypotonia *cognitive delay
*dysmorphic facial features and other distinctive physical abnormalities.
Etiology of down syndrome is with trisomy 21 produces three copies of
chromosomes 21 instead of normal two because of faulty meiosis of the
ovum or sperm.
Alzheimer disease is also more common in people with down syndrome.
The increased rate of Alzheimer disease in individuals with down
syndrome is a result of abnormally high production of B-amyloid that
makes up the extracellular plaques seen in individuals with down
syndrome.

Clinical characteristics of Down syndrome

Most frequently observed
manifestations

Flattened nasal bridge

Almond eye shape
Flat occiput
Muscle hypotonia
Joint hyperextensibility
Short limbs
Short ,broad hands and feets

Associated manifestation

Absence of kidney
Duodenal atresia
Visual impairments
Hearing loss
Myopia
Cataracts
Conjunctivitis
Diabetes

2. scoliosis
Abnormal lateral curvature of the spine. The curvature may be towards the right (more common in
thoracic curves) or left (more common in lumber curves)
Scoliosis is often associated with kyphosis and lordosis.
Scoliosis is classified as 1..Idiopathic (unknow cause) 2..Osteopathic (as a result of spinal disease or
bony abnormality) 3..Myopathic (as a result of muscle weakness) 4.Neuropathic (as a result of CNS)
Scoliosis can be functional or structural. Functional or postural scoliosis may be caused by factors
other than vertebra involvement such as pain, poor posture, leg length discrepancy, or muscle spasm
induced by a herniated disk or spondylolisthesis. Structural scoliosis is a fixed curvature of the spine
associated with the vertebral rotation and asymmetry of the ligamentous supporting structures. It can be
caused by deformity of the vertebral bodies and my congenital, musculoskeletal, neuromuscular,
idiopathic.
The pathogenesis of scoliosis remains unclear but may be better understood in relation to the underlying
cause. Abonormal embryonic formation and segmentation of the spinal column are possible pathologic
pathways in congenital scoliosis. Neuromuscular scoliosis is often the result of an imbalance or
asymmetry of muscle activity through the truck and spine.
Curvatures less than 20degree rarely cause significant problems.
Severe untreated scoliosis curvature greater than 60degree may produce pulmonary insufficiency and
reduced lung capacity, back pain and degenerative spinal arthritis.
Common charecteristics of scoliosis are asymmetric shoulder and pelvic postion.

3.Kyphoscoliosis
Scheuermann disease (juvenile kyphosis, vertebral epiphysitis) is a structural
deformity characterized by
Anterior wedging of 5 degrees or more of three adjacent thoracis bodies affecting
adolescents b/w the ages of 12 and 16 years.
Scheuermann disease is most common cause of structural kyphosis.
Adolescent khyposis is asymptomatic but shows prominent vertebral spinous
processes. Mild pain at the apex of the curvature in addition to faigue , and
tenderness or stiffness in the involved area or along the entire spine.

4
Spina bifida occulta results in only a bony defect, with the spinal cord, meninges,
spinal fluid intact.
Meningocele involves the bifid vertebra, with only a CSF filled sac protruding, the
spinal cord or cauda equine(depending on the level of the lesion) remains intact.
Myelomeningocele is the most severe form because the spine is open the protruding
sac contains CSF, the meninges , and the spinal cord or cauda equina.
Symptoms >
Sac sticking out of the mid to lower back.
Loss of bladder or bowel control
Partial or complete lack of sensations
Partial or complete paralysis of legs.
Weakness of hips, legs or feet of a newborn

Myelomeningocele : clinical features

Clinical features

Hydrocephalus
Arnold-chiari malformation
Bowel and bladder incontinence
Sensory impairment below the
lesion
Absence of deep tendon reflexes

Associated charecteristics

90% have intelligence within the

normal range
Increased incidence of learning
disabilities
Inc CSF pressure
Weakness, pain , sensory changes,
vertigo, ataxia ,diplopia
Small spastic bladder
Large flaccid bladder
Lack of response to pain
Altered biomechanics

Sign and symptoms of hydrocephalus

Full, bulging, tense soft spot on top of the childs head.
Large , prominent veins in the scalp
Setting sun sign
Behavioral changes
High pitched cry
Seizures
vomiting

5. Developmental dysplasia of hip

Also term as congenital hip dislocation.
DDH can be unilateral or bilateral and occurs three forms
1. Unstable hip dysplasia (in which hip is positioned normally but can be
dislocated by manipulation).
2. Subluxation or incomplete dislocation (in which the femoral head remains in
contact with acetabulum but the head of the femur is partially displaced or
uncovered
3. Complete dislocation (in which the femoral head is totally outside the
acetabulum.

6. Neuromuscular disorders
Muscular dystrophies
Congenital myopathies
Spinal muscular atrophy

Muscular dystrophies
Types
Duchenne muscular dystrophy (pseudohypertrophies)
Becker BMD (x-linked, recessive, mutation in dystrophin gene)
Facioscapulohumeral FSHD (autosomal dominant, arise from mutation)
Limb-girdle LGMD (autosomal recessive or dominant )
Myotonic dystrophy (autosomal dominant )
Congenital muscular dystrophy (autosomal recessive)
Congenital myopathies (autosomal recessive or dominant)

Pathogenesis
of DMD
Steps
Dystrophin deficiency
Nnos down regulation
Satellite cell hyperactivation
Expenditure of satellite /stem cell
pool
Progressive damage and decline in
success of regeneration
Decline in function

Morphology of Muscular dystrophy

Congenital myopathy
A group of disorders with somewhat
similar phenotype course, including
central core disease, nameline
myopathy, multicore-minicore
disease and myotubular myopathy.

Pathogenesis
Nemaline myopathy is a
heterogeneous disease with a
number of genetic loci identified.
The genes, loci, and protein
products responsible for the
resulting pathology include alphatropomyosin slow, B-tropomyosin,
troponin 1, nebulin and alpha-actin.
These genes can have either
autosomal dominant or recessive
inheritance.

Classification

Myotubular myopathy
Nemaline myopathy
Non-specific congenital myopathy
Minicore myopathy
Central core desease

Spinal muscular atrophy

A neuromuscular disease characterized by progressive weakness and
wasting of skeletal muscle resulting from anterior horn cell degeneration.
SMA type 1, the more severe or acute form, referred to as WerdninHoffmann disease and causes respiratory failure and early death, typically in
the first few years of life, if respiratory support is not provided.
SMA type 3 is the mildest form. These individuals learn to walk without
assistance, a relatively slow progression is noted in type 3.
SMA type 2 represent an intermediate form affected individuals
demonstrate the ability to sit independently at some point, but significant
functional impairment and reliance on power mobility in typical.

7. Torticollis

Twisted neck and is contracted state of the sternocleidomastoid

muscle, producing head tilt to the affected side with rotation of the
chin to the opposite side.
clinically it is seen as nontender, palpable enlagement of SCM often
reffered to as a sternocleidomastoid tumor of infancy.
If the torticollis left untreated, the deformity can become severe,
the infants face, ear and head flatten from resting on the affected
side, a condition refered to as plagiocephaly(oblique head) this
cranial asymmetry gradually worsens.

8. Brachial plexus birth palsy

A paralysis of the upper limb typically resulting from a traction injury
to the brachial plexus at birth.
Erbs palsy is made up of three distinct types of brachial plexus palsies
1. Erb-Duchenne palsy (affecting the C5 to C6 nerve roots)
2. Whole arm palsy affecting C5 to T1
3. Klumpke palsy affecting the C8 and T1 nerve roots.
Pathogenesis
Plexus injury at birth is usually due to stretch of plexus.
The degree of disability depends on the site and severity of injury.

Erbs palsy IMP points

Typical posture is shoulder in internal rotation, adduction , finger flex
Strength losses of deltoid, supraspinatus, teres minor, biceps,
brachialis, bronchioradialis, supinator.
Sensory losses are C5-C6 deficits.
Skeletal changes include flattening of glenoid fossa/humeral head ,
elongating deformity of coracoid process hooking down and latera,
scapular winging.

9.Osteogenesis imperfecta
Also term as brittle bone disease
A hereditary defect leading to abnormal syn of type 1 collagen.
Patient have generalized osteopenia(brittle bones) which results in
recurrent fractures and skeletal deformity
Patient have abnormally thin sclera with blue hue.
Laxity of joints ligaments leads to hypermobility.
Inolvement of the middle ear bones produces deafness.
Some patients have Dentinogensis which is characterized as small
fragile and discolored teeth due to a deficiency of dentin.

Clinical manifestations of osteogenesis

imperfect

Blue sclera
Triangular facies
Macrocephaly
Hearing loss
Defective dentition
Barrel chest
Scoliosis
Limb deformity
Fractures
Joint laxity

10. Arthrogryposis multiplex

congenita
The presence at birth of multiple congenital contractures resulting
from dec fetal movement in an intact skeletan.
There are three types of AMC exist
1. Contracture syndrome
2. Amyoplasia (lack of muscle formation or development)
3. Distal arthrogryposis (primarly affecting hands and feet)
Clinical features include joint contractures, articular rigidity, muscle
weakness, and in some cases replacement of muscle with fibrous and
fatty tissue.

Metabolic
disorders

1. osteoporosis
Dec bone mass (osteopenia), resulting in thin, fragile bones susptebile to
fracture.
Pathogenesis :: primary cause of osteoporosis include estrogen deficiency
(postmenopausal) genetic factors (low density of original bone) lack of
exercise , old age, and nutritional factors. Secondary causes include
immobilization, endocrinopathies (Cushing disease, thyrotoxicosis)
malnutrition (deficiency of vit c and D)
Clinical features. *bone pain and fracture

Osteoporosis Risk factors

Alcohol use
Corticosteroid use
Calcium low
Estrogen low
Smoking
Sedentary lifestyle

Pathogenesis
Postmenopausal bone loss
Age related bone loss
Leads to
Low bone mass
Which lead to
Fractures (low BMD)

2. Osteomalacia
Caused by deficiency of vit D with
specific causes including dietary
deficiency of vit D, intestinal
malabsorption , lack of sun light and
renal and liver disease.
it occurs in adults
Bone becomes fragile, thin , more
suspetible to fracturs.
Clinically paitent present with bone
pain and fracture.
Labortary studies shows .low serum
phosphorus and high alkaline
phosphatase.

Pathogenesis

Vitamin D (deficiency Occur due

to GI malabsorption)
25 OH D (occur due to liver
disease and anticulsant therapy)
1,25 (OH)2 D (occur due to
osteodystrophy, and parathyroid
disorders)
These three leads to
OSTEOMALACIA.

3. Paget disease
Also term as Osteitis deformans
A localized disorder of bone remodeling, resulting in excessive bone resorption followed by
disorganized bone replacement producing thickened but weak bone that is sustible to fracture.
It could be related to the slow-virus infection (paramyxovirus) and also have genetic
predisposition.
Paget disease begins after 40 years of age.
Paget disease develop in three stages
1) The osteolytic stage (osteoclastic activity predominate)
2) The mixed osteolytic osteoblasstic stage
3) The osteosclerotic stage (osteoblastic activity predominates in this burnout stage.
Skull involvement leads to inc head size and foraminal narrowing that can impinge cranial
nerves.
Clinical features..*Most cases are asymptomatic *Bone pain and deformity *Fractures *x.rays shows bone enlargement with lytic and sclerotic areas.

Bones effected in Paget disease

Pathogenesis of Paget disease

Skull
Spine
Pelvis
Femur
Tibia

Steps
Hypervascular/osteolytic phase
Initial phase (bone resorption by
osteoclast)
Intermediate phase
Osteoclast and osteoblast activity
Exhaustive stage (burn out stage)
Abonrmal matrix persist but cellular
activity is nearly absent
PAGET DISEASE

Infectious diseases
of musculoskeletal
system

1.osteomyelitis
1) pyogenic osteomyelitis
Most cases are caused by bacteria and
bacteria reach the bone by three routes
a) through blood b) extension from an
infection from the adjacent joint c)
traumatic implantation afrer compound
fracture
Staph aureous infection is related to
bone expression
E.coli and group B streptococci are
involve in neonates.
Salmonella is common pathogen in
persons with sickle cell disease.

2..Tuberculous osteomyelitis
Occurs 1% of cases of TB
Patient presents with pain ,
tenderness, and fever, night sweat,
weight loss.
Biopsy shows caseating
granulomas with extensive
destruction of bones.
Common sites of involvement are
thoracic and lumber vertebrae
(POTT DISEASE)
Complications include vertebral
compression fractures, psoas
abcessses and secondary
amyloidosis.

2. Infections of prosthesis and implants

Over the past decade , joint replacement surgery has become common place ,
which is largely attributed to the success of these procedure in restoring functions.
Implant infections remains the primary cause of prosthetic failure, which either
occur within the month or year after surgery.
80% of these infection are caused by Staphlococus organisms, which enter
perioperative, hematogenous or contiguous means.
Other types of prosthesis and implants suspetible to infection are include *internal
fixation of spine *breast implants *penile implants *dental implants *cardiac
implants *other orthropedic devices and hardware, shunts and even contact lenses.

3. Diskitis
It is a range of conditions from a self-limiting
inflammatory process to a pyogenic infection.

The intervertebral disk is the most common site

for a spinal infection.
These infections affecting the annulus nucleus
, or the vertebral endplates.
S.aureous & Mycobecterium Tuberculosis is
commonly found in this type of the infections

4.Infectious (septic arthritis)

Articular structures can also
become infected by direct
inoculation or by contiguous
spread from osteomyelitis or soft
tissue abscess.
Imp agents are staph aureous
, Nisilia gonorrhea, E.coli
Causes *septic *gonochocal
*viral *fungal *TB *lyme
Risk factors *old age *RA *DM
*immunosuppresion

Ways of infection
Hematogenous spread
Direct inoculation and
penetrating injury
Direct extension (periarticular
osteomyelitis)

Causative agents of infectious arthritis

Bacterial

Viral

Gonococcal
Infectious endocarditis
Lyme disease
Syphilis
TB

Reactive

Fungal
candida

Epstein Barr virus

Hepatitis
Human immunodeficiency virus
Mumps
Rubella
Acute rheumatic fever
Chlamydial infection
Enteric infection
Reiter syndrome

5.Infectious (inflammatory) muscle disease

Myositis
Inflammation of muscle that can be an
autoimmune condition or directly caused by
viral , bacterial, and parasitic agents
Infection induced myositis is most often caused
by S.aureous and parasites such as Trichinella
and tape worm larva Taenia Solium.
The most common form are Dermatomyositis ,
polymyositis and body myositis.

Musculoskeletal
Neoplasm

Connective tissue
Fibrous :: Benign (Fibroma) Malignant (Fibrosarcoma, Malignant fibrous
histiocytoma,chondrosarcoma)
Cartilage :: Benign(chondroma,echondroma,Chondroblastoma,osteochondroma)
Malignant (chondrosarcoma)
Bone :: Benign (osteoma, osteoblastoma) malignant (osteosarcoma )

Bone marrow :: malignant (leukemia ,multiple myeloma Ewing sarcoma)

Adipose :: Benign (lipoma) malignant (liposarcoma)
Synovium:: Benign (ganglion, giant cell of tendon sheath ) malignant (synovial
sarcoma)
Muscle (le o rehab karany aya ha)

Smooth muscle:: Benign (leiomyoma) Malignant (leiomyosarcoma)

Striated muscle:: Benign (Rhabdomyoma) Malignant (Rhabdomyosarcoma )

Endothelium

Lymph vessels :: Benign (lymphangioma) Malignant (Lymphangiosarcoma)

Blood vessels :: Benign (Angioma,Hemangioma) Malignant (angiosarcoma)
Neural tissue

Nerve fibers and sheaths :: Benign (Neurofibroma, neuroma) Malignant

(neurofibrosarcoma, neurogenic sarcoma)
Glial cells :: Benign (Giosis ) Malignant (Glioma)
Epithelium

Skin and mucous membrane :: Benign (papilloma) malignant (squamous

cell carcinoma, basal cell carcinoma)
Glandular epithelium :: Benign (Adenoma) malignant (adenocarcinoma)

Benign tumors of bone

Osteoma
*involves skull and facial bones, osteoma
can be associated with gardner syndrome.
HYPEROSTOSIS FRONTALIS INTERNA
is an osteoma that extends into the orbit or
sinuses.

Osteoid sarcoma
*benign painful growth of diaphysis of a long
bone often tibia or femur. Affects males more
than females.microscopically these tumors
shows lesion of <2cm fo the cortex.

Osteoblastoma
*similar to osteoid osteoma but is larger than
>2cm and involve vertebra.

Osteochondroma
*benign bony metaphysial growth capped
with cartilage that originates from epiphyseal
growth plate. Found in adult male .it may be
asymptomatic

Echondroma
*benign cartilaginous growth within in the
medullary cavity of bone . Usually involve
hands and feets. Asymptomatic

Osteoclastoma (giant cell tumor of

bone)
*uncommon . Benign tumor containing
multinucleated giant cells adminxed with
stromal cells. More fund in females .
Clinically , tumor form a bulky mass with
pain and fracture. Pathogenesis .. Tumor
causes a red brown mass with cystic
degenration that often involves the epiphyses
of long bones usuaaly around the knees.

Malignant tumors of bone

Osteosarcoma

Ewing sarcoma

*most commonly occurring primary tumor

of bone
*occur more in male at teenage
*clinically :: localized pain and swelling
*x-ray shows codman triangle, sun burst
pattern
*secondary osteosarcoma occurs in elderly
persons
*associated with paget disease , irridation
, Chronic osteomyelitis

*undifferentiated cells arising within

the marrow cavity. Males affected
more and in teenage.
*clinically pt present with pain ,
swelling and tenderness.
Pathogenesis :: this tumor affect
diaphysis of long bones , most
commonly femur , pelvic and tibia.

Chondrosarcoma
*malignant tumor of chondroblasts which
arise denovo or sec to other disease like paget
disease.
*patient present with enlarging mass with pain
and swelling

Metastasis of bone
*Common than primary bone tumors
*Common primary sites include
prostate, breast , lung , thyroid and
kidney.

Soft tissue, joint

and bone
disorders

1..Soft tissue disorders

Strains
Sprains
Laceration
Tendon reputure
Muscle injuries
Myofacial compartment
syndrome
Dislocation
Subluxation

Imp point
Heterotopic ossification
*bone formation in nonosseous
tissue (usually in muscles and
other soft tissues)

1.Chondrolysis
A process of progressive cartilage degeneration
resulting in narrowing of joint space and loss of
motion.
It is seen most often as a complication of slipped
capital femoral epiphysis, but can occur in
association with infection, trauma and prolong
immobilization.
The hip is the most likely location for
chondrolysis to occur but cases have been
reported affecting knees , shoulder and ankle.
Affect more often in females than males.

2.Osteoarthritis

Radiographic
a joint degeneration with loss of articular cartilage with no to minimal
finding of OA.
inflammation. It is the most common form of arthritis. The risk increases
with age.
Joint space
Clinically, there is an insidious onset of joint stiffness; deep, aching joint wide(early)
pain, which worsens with repetitive motion; decreased range of motion;
Subchondral bone
crepitus; and joint effusions and swelling. Osteophytes may cause nerve
compression.
sclerosis
X-ray studies show narrowing of the joint space due to loss of cartilage;Subchondral bone
osteosclerosis and bone cysts.
cysts
The pathogenesis involves both biomechanical factors (aging or wear and
tear of articular cartilage) and biochemical factors (chondrocyte injury and Osteophytes
abnormal collagen activity).
Joint space
Predisposing factors include obesity, previous joint injury, ochronosis,
narrowing
diabetes, trauma, and hemarthrosis. Pathology. Osteoarthritis affects weightbearing joints (knees, hips, and spine), often with asymmetrical involvement.
There is degeneration and loss of articular cartilage with eburnation
(exposed bone becomes pol ished) and subchondral bone sclerosis.

Pathogenesis of osteoarthritis
Steps
Obesity, aging, trauma genetic
and metabolic disorders leads to
Abnormal stress on cartilage
Biophysical changes like
proteoglycan unraveling and
biochemical changes like
proteolytic enzymes inc , leads
to
Cartilage breakdown.

Morphology of osteoarthritis
Early stage
Inc in chondrocytes
Cracking of matrix
Gross
Granular surface
Small fracture (joint mice)
Osteophytes formation

3. Degenrative intervertebral disc

disease
Degenerative joint changes are not limited to synovial joints ,
they also occur in spine (particulary in lumber spine) in the
intervertebral discs..
The process of disk degeneration is an aberrant , cell-mediated
response to progressive structural failure.
Mechanism
First (nucleus in the center of disk begins to lose its ability to
absorb water. Disc becomes dehydrated. Then nucleus
becomes thick and fibrous, so that it looks like annulus) then
(nucleus is not able to absorb shock . Routine stress and strain
begin to take a toll on the structures of spine. Tears from
around the annulus. The disc weakens and it start to collapse
and bones of the spine gets compress.

4.Rheumatoid arthritis
a systemic,chronic,autoimmune, inflammatory disease characterized by progressive
arthritis, production of Rheumatoid factor, and extra articular manifestations.
Females are affected four times more frequently than men.

Clinical features. Hand, wrist, knee, and ankle joints most commonly
involved, and the involvement tends to be symmetrical involvement. There is often
morning stiffness that improves with activity. There is typically fusiform swelling,
redness, and warmth of the proximal interphalangeal (PIP) joint.
The joint deformities can include radial deviation of the wrist and ulnar
deviation of the fingers swan neck deformity (hyperextension of PIP and flexion of
distal interphalangeal (DIP)) and boutonniere deformity (flexion of PIP and
extension of DIP joints). Baker cysts (synovial cysts in the popliteal fossa) may
be present.

Extra-articular manifestations may be prominent. Systemic symptoms

include low-grade fever, malaise, fatigue, lymphadenopathy, and weakness.
Arteries may show acute necrotizing vasculitis due to circulating antigen antibody
complexes.

Pathogenesis of RA
Induction (cell recruitment
marrow cytokines)
Inflammation (cytokines network ,
antigen presentation, autoinbodies,
innate immunity , prostaglandins,
proteases)
Destruction (pannus formation ,
osteoclast activation , somatic
mutations, proteases)

5.Neuroarthropathy
An articular abnormality related to
neurologic deficit, regardless of the nature of
primary disease. Other terms applied to this
disorder are Charcot joint, neurotropic or
neuropathic joint disease, and neuropathic
osteoarthropathy.

6. Fractures
Any defect in the continuity of a bone,
ranging from a small crack to a complex
fracture with multiple segments.
Classification
1. Fractures by sudden impact (traumatic)
2. Stress or fatigue fracture
3. Insufficiency fracture
4. Pathologic fractures

Imp terms of fractures

Colles fracture (fracture of distal radius and ulnar styloid in which the
lower fragment is displaced posteriorly, usually from a fall on an outstretched
hand.)

Galeazzi fracture (fracture of middle third and distal third of the radius
accompanied by dislocation of the distal radioulnar joint at the wrist)

Jones fracture (fracture of the base of the fifth metatarsal)

Maisonneuve fracture (tear of the ant and interosseous tibiofibular
ligaments and a fracture of fibula 3 to 4 inches above the ankle mortise.

Nightstick fracture (fracture of the ulna alone, usually midshaft)

Piedmont fracture (fracture of the radial shaft)
Pott fracture (oblique fracture of the lat. Malleolus)
Torus fracture (localized cortical expansion but little or no displacement)

8.Osteochondrosis
Number of clinical disorders of ossification
centers (epiphysis) in growing children
share the common denominator of avascular
necrosis and its squelae.
These disorders are grouped together and
referred as OSTEOCHONDROSIS with
multiple synonyms (epiphysistis,
Osteochondritis, aseptic necrosis, ischemic
epiphyseal necrosis)

9.Osteonecrosis
Death of bone and bone marrow cellular
components as a result of loss of blood supply
in the absence of infection.
Femoral head is the most common site of this
disorder (sometimes called as Chandler
disease), but other site can include scaphoid,
talus, proximal humerus, tibial plateau, and
small bones of wrist and foot.

Pathogenesis
Fat embolism leads to intravascular
coagulation which leads to osteonecrosis.

10. Pathogenesis of GOUT

Morphology of GOUT

 Thanks