everything you need to know mss
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ONNAZLI0809
Name -
Matric no -
Batch -
Year -
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ONNAZLI0809
OSTEOGENESIS IMPERFECTA/TYPE I COLLAGEN DISEASE/BRITTLE BONE DISEASE
Definition
can be defined as a group of phenotypically related disorder that are caused by deficiencies in the
synthesis of collagen type I. It can be classified to 4 types which the type II is the worst (resulting in
death in the uterus or within days of birth)
Causes
mutation in genes that code α1 and α2 chains of collagen molecules
inherited – autosomal dominant fashion (mostly)
inherited – autosomal recessive fashion (rarely)
Morphology
“too little bone”
Thinning of the cortical part of bone
Attenuation of the trabeculae
Persistent foci of hypercellular woven bone
Clinical features
Multiple fracture from minimal trauma – due to extreme skeletal fragility
Blue sclera – sclera becomes translucent allowing partial visualization of the underlying
choroid due to reduce collagen content of the sclera
Hearing loss – due to both sensorineural deficit and impaired conduction because of the
abnormalities of the middle and inner ear bones
Dental imperfections – due to deficiency in dentin
Heart valve disorder – less collagen component
Hypermobility of joints
Treatments
Bisphosphonates – to enhance the bone cortical thickness
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ONNAZLI0809
DEVELOPMENTAL (GENETIC) AND ACQUIRED ABNORMALITIES IN BONE CELLS, MATRIX AND
STRUCTURES
It can be classified to;
1.
Defects in nuclear proteins and transcriptional factors Failure of developmental of the bone (phalanx, rib, clavicle)
Formation of extra bones
Fusion of adjacent digits
Craniorachischissis (failure of closure of spinal column and skull)
2. Defects in hormones and signal transduction
Achondroplasia
Thanatophoric dwarfism
3. Defects in extracellular structural proteins
Type I collagen diseases
Type 2, 10 and 11 collagen disease
4. Defects in folding and degradation of macromolecules
Mucopolysaccharidoses
5. Defects in metabolic pathway (enzymes, ion channels and transporters)
Osteopetrosis
6. Decrease in bone mass
Osteoporosis
7. Osteoclast dysfunction
Paget disease
8. Abnormal mineral homeostasis
Rickets and osteomalacia
Hyperparathyroidisme
Renal osteodystrophy
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ONNAZLI0809
OSTEOPETROSIS/MARBLE BONE DISEASE/ALBERT-SCHONBERG DISEASE
Definition
is a rare genetic disease characterized by reduction in osteoclast activity resulting in diffuse
symmetrical skeletal sclerosis
Causes
Autosomal recessive – malignant type
Autosomal dominant – benign type
Pathogenesis
1. Deficiency in Carbonic Anhydrase II (CA II)
2. Mutation of CIC-7 chloride channel gate
Morphology
Gross morphology
1. Lack of medullary canal
2. Bulging end of long bone and misshapen
3. Small neural foramina, compressing the nerve
4. Bones formed are not remodelled and usually woven in architecture
Histology
1. Normal number of osteoclast
1. Osteoclast use CA II to acidify and resorp
bones. Deficiency in CA II prevent
osteoclast to acidify resorption pit and
solubilising hydroxyapatite crystal
2. CIC-7 chloride channel gate located at
ruffled borders of osteoclast. It is
important for proton pump H+/ATPase
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Clinical features
1. Malignant type
Fracture occurs commonly – due to woven bone architecture
Anaemia – lack of medullary canal
Hydrocephalus – due to anaemia
Hepatosplenomegally – increase extramedullary erythropoiesis
Mental retardation
Infections
2. Benign type
Repeated fracture
Infections
Increase level of acid phosphate
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Morphology
1. Postmenopausal osteoporosis
- Usually affects bone that have high surface area – e.g. cancellous compartment of
vertebrae commonly affected
- Thinned osteoporotic trabeculae and lose interconnections (loss of horizontal trabeculae
– thickens of vertical trabeculae)
- Progressive micro fractures – leads to vertebral collapse
2. Senile osteoporosis
- Thinning of osteoporotic cortex by subperiosteal and endosteal resorption
- Widened Harvesian system
Clinical features
1. Fracture2. Vertebral crush fracture leads to severe back pain, radiating to front. Increase kyphosis,
height loss and abdominal protuberance
Investigations
1. Dual energy X-ray absorptiometry – reliable to measure bone density (mineral per surface
area)
2. Quantitative ultrasound of calcaeneum
3. Quantitative CT scanning – allows true assessment and distinct between trabecular and
cortical bone
Treatment
1. Exercise
2. 700 – 1000 mg Calcium diet daily
3. Cessate smoking
4. Estrogen replacing agents
5. Bisphophonates
6. Recombinant PTH
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ONNAZLI0809
PAGET DISEASE/OSTEITIS DEFORMANS
Definition
Is a chronic focal disorder of bone remodelling
Causes
- Paramyxovirus
- Subacute sclerosing leukoencephalitis
- Measles
Pathogenesis
Morphology
Histological features1. Mosaic pattern of lamellar bone – represent jigsaw puzzle
2. Initial phase – waves of osteoclastic activity and numerous resorption pit
3. Mixed phase – bone surfaces are lined by prominent osteoblast. Marrow contains numerous
blood vessels as well as loose connective tissue (osteoprogenitor cell)
4. Osteosclerotic phase – fills with coarsely trabeculae and cortical that are soft and porous
and lack of structural stability
Measles virus/paramyxovirus/subacute sclerosing
leukoencephalitis infections
1. Initial osteolytic phase – infected cells secrete cytokines
(IL-6) and Pagetic bone produce M-CSF
Both IL-6 and M-CSF are chemotactic to osteoclast leading to
increase in osteoclastic activity
The osteoclast are hyperactive (predispose locus on
chromosome 18q)
2. Mixed phase – compensatory mechanism to increase in
new bone formation, increase in local blood flow as well
as fibrous tissue
Ends with predominantly osteoblastic activity
3. Burnt out quiescent osteosclerotic phase – new bone
formed but structurally abnormal
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Clinical features
1. Bone pain – caused by microfractures and bone overgrowth that compress spinal and cranial
nerve
2. Compression fracture – shows sign like kyphosis or lordoisis
3. Pathological fracture
4. Deformities – anterior bowing of femur and tibia, distorts femoral head leading to arthritis
5. Cardiac hypertrophy – owing to increase blood supply to the bone
Investigation
1. X –ray – 1) in lytic phase – central and endosteal cortical resorption and replacement by less
compact new bone 2) in sclerotic phase – thickened trabeculae, loss of distinction between
cortex and trabeculae
2. Bone scans
3. Serum alkaline phosphatase - increase
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ONNAZLI0809
RICKETS AND OSTEOMALACIA
Definition
Rickets (in children) and osteomalacia (in adults) is an inadequate mineralization of bone matrix due
to defects in vitamin D availability or metabolisme.
Causes
Vitamin D deficiency Renal disease Others
Skin synthesis
Malabsorption
Malnutrition
Chronic renal failure
Dialysis
Tubular disorder (ATN, APN)
Vitamin D dependant rickets
Tumor
Pathogenesis
Vitamin D deficiency
Reduce substrate for renal α1 hydroxylase
Reduce formation of 1,25-dihydroxycholecalciferol
Reduce absorption of calcium and phosphate in the gut
Reduce serum level of calcium and phosphate
Activates parathyroid hormone
Increase calcium absorption in the renal but promotes
phosphate excretion via urine
Serum calcium level normal but phosphate level decrease
Impaired mineralization for bone formation
Bone formation abnormal
Rickets (children) and osteomalacia (adults)
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Clinical features
1. Pathological fractures
2. Waddling gait
3. Neonatal – thin deformed skull
4. Widened epiphyses at wrist
5. Beading at costochondral junction
6. Groove in the rib cage (Harrison’s sulcus)
Investigations
1. Increase serum alkaline phosphatise – increase osteoblastic activity
2. Serum phosphate reduce – increase PTH
3. Serum 1,25-DHCC decrease
4. X-ray – showing Looser’s zones (linear area of reduce density surrounded by sclerotic body)
Treatment
1. Oral vitamin D supplement
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ONNAZLI0809
OSTEOMYELITIS
Definition
Is an inflammation of bone and bone marrow due to infections. It can be local or systemic
Causes
In adults In neonates
Staphylococcus aureus
Escherichia coli
Pseudomonas sp
Klebsiella sp
Mycobacterium tuberculosis
Haemophilus influenza
Group B streptococci sp
Pathogenesis
Bacteria enters the bones via
1. Direct penetration
Bacterial organism introduced directly into the bone by penetrating the wounds,
fractures or surgery
Staphylococcus sp and streptococcus sp are common
2. Haematogenous spread
Arise from focus (skin pustules, infected teeth and gums etc) elsewhere in the body
and through bloodstream, it reaches the bone.
Likely to spread to the metaphyses of the long bones such as ankle, knee, hip etc
Tuberculosis is the commonest bacteria causing osteomyelitis via haematogenous
spread (non-neoplastic metastasis)
3. Direct seeding
Pulmonary tuberculosis affecting the lung and give rise to the formation of
pulmonary focus. This focus can directly transfer the bacteria to the bones such as
ribs and thoracic vertebra.
Morphology
Pyogenic osteomyelitis
1. Cloaca – hole formed in the bone during formation of a draining sinus
2. Sequestrum – fragments of necrotic bones that are embedded in the pus
3. Brodie abscess – reactive bone from periosteum and endosteum whic surrounds and
contains the infections
4. Involucrum – lesion in which periosteal new bone formation forms a sheath around the
necrotic sequestrum
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Morphology
Tuberculous osteomyelitis
1. Granuloma produce caseous necrosis of the bone marrow
2. Slow resorption of bony trabecullae
3. Formation of cystic spaces in the bone
Clinical features
Pyogenic osteomyelitis
1. Fever with chills and rigors
2. Malaise
3. Leukocytosis
4. Throbbing pain at the affected site
Tuberculous osteomyelitis
1. Pain in motion
2. Localize tenderness
3. Low grade fever
4. Loss of appetite
5. Kyphotic and scoliotic deformities – compression fracture of vertebra
Treatment
1. Cloxacillin
2. Fusidic acid
3. Immobilization
Complications
1. Septicaemia – infection disseminated to the blood stream
2. Acute bacterial arthritis – direct ‘digestion’ (cytokines effect) by inflammatory cells destroy
srticular cartilage, producing osteoarthritis
3. Pathological fracture
4. Squamous cell carcinoma
5. Amyloidosis
6. Chronic osteomyelitis
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ONNAZLI0809
BONE TUMORS
Character
Diverse in their gross and morphologic features
Behavior – biological innocuous to rapidly fatal
Target group – Benign (10 – 30 years old)
Malignant (later in adult life)
Risk factor
Li Fraumeni syndrome and hereditary retinoblastoma genes (mutations in p53 and RB gene). Bone
infarcts, chronic osteomyelitis, Paget disease, radiation and metal prostheses.
Classification
Base on normal cell tissue of origin (as stated below)
1. Bone forming tumors
2. Cartilage forming tumors
3. Fibro-osseous tumors
4. Miscellaneous tumors
Bone forming tumors Cartilage forming
tumors
Fibro-osseous tumor Miscellaneous tumors
Osteoma
Osteoid osteoma
Osteoblastoma
Osteosarcoma
Osteochondroma
Chondroma
Chondroblastoma
Chondromyxoid fibroma
Chondrosarcoma
Fibrous dysplasia Giant cell tumor
Ewing sarcoma
Metastatic tumor
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Pathogenesis of Bone Tumors
Normal cell
DNA damage
DNA mutation
Mutation in Genome
Activation of Growth Promoting
Oncogenes* (oncogenic product class
1, 2 and 3)
Carcinogenic agents
Acquired DNA
damaging substance
Apoptosis Gene Alteration*
(hereditary)Cancer suppressing gene alteration*
(hereditary)
Oncogenic product class 4 and 5
Expression of altered gene product
Loss of regulatory gene product
Malignant Neoplasia
Successfully repaired
Alteration in gene that
regulates DNA repair*
CANCER RELATED GENES
1. Oncogenenic Products – class 1 to class 5
2. Tumour Supressing genes – p53,pRb genes
3. Genes regulates apoptosis – Bax, Bcl-2, bad, Bcl-xL
4. Genes regulates DNA repairAny defect in this gene, commonly inherited will increase the chances of getting
cancer 4-5 folds
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ONNAZLI0809
BONE-FORMING TUMORS
OSTEOMA
Definition A benign bone tumor, an exophytic mass from skull and paranasal sinuses
Character - Most often arise on or inside the skull or facial bones
- Often affecting middle age adults (30-50 years old)
- Always associated with Gardner syndrome
Gross morphology Bosselated, round to oval sessile tumors that project from the subperiosteal or
endosteal surfaces of the cortex
Histopathology - Composed of lamellar and woven bone – frequently deposited in a
cortical pattern with Harvesian-like system
- Compact lamellar cortical bone
- Small amount of fibrofatty stromaClinical features - Usually asymptomatic
- Symptomatic if the tumors pressed adjacent structure such as sinus
obstruction, extracranial extension and nerve compression
Radiologic
findings
- Sharply demarcated mass protruding from the bone surface
- No bone destruction and periosteal reaction
- Periosteal osteoma may mimics periosteal osteosarcoma
Prognosis Never change or transform to malignant
Treatment Simple excision
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ONNAZLI0809
OSTEOID OSTEOMA AND OSTEOBLASTOMA – benign bone tumors that have identical histologic
features but differ in size, sites of origin and symptoms
OSTEOID OSTEOMA
Definition Tumors which the size of less than 1 cm in greatest dimensionCharacter - Usually occurs in teens or twenties
- Most often rise from appendicular skeleton
- Mostly at tibia, femur and spine
Gross morphology - Is a well circumscribed tumor
- Mostly round to oval masses of gritty tan tissue
Histopathology - Well circumscribed tumor cells
- Composed of randomly interconnecting trabeculae of woven bone
rimmed by fibroblast
- loose vascular stroma
Clinical features - localized pain usually worse at night
- relieved by aspirin
Radiologic
findings
- intracortical nidus
- sclerotic rim of bone reaction
Prognosis Never change or transform to malignant
Treatment - Complete resection
- Removal of nidus
- Bone grafting may needed
OSTEOBLASTOMA
Definition A tumor of bone arises from the osteoblast
Character - Mostly arise from the axial skeleton
- Mostly affecting spine, femur and jaw
Gross morphology - Is a well circumscribed tumor
- Mostly round to oval masses of gritty tan tissue
Histopathology - Well circumscribed tumor irregular cells
- Composed of randomly interconnecting trabeculae of woven bone
rimmed by fibroblast
- loose vascular stroma
- presents of hyaline cartilage mimics the osteosarcoma
Clinical features - dull achy pain
- localize
- not responsive to salicylates
Radiologic
findings
- well-circumscribed tumor cell (irregularly demarcated)
- well defined by a surrounding shell of mature bones
- small extracortical mass
- Radiolucent lesion (20 -100 mm diameter)
- expansile lesion
- variable ossification
- may be aggressive with cortical destruction and soft tissue extension
Prognosis Less than 1 % recorded to be malignant transformation
Treatment Enbloc resection
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CARTILLAGE FORMING TUMORS
OSTEOCHONDROMA
Definition also known as exostosis is a benign cartilage-capped outgrowth that is attached
to the underlying skeleton by a bony stalk
Character - Can be solitary or multiple
- Men are predominantly affected (3:1)
- developed only in bones of endochondral origin
- arise from metaphysis of the growth plate of long tubular bones, about
the knee
Gross morphology - mushroom-shaped (1-20 cm in size)
- cortex of the stalk continuous with the medullary cavity of the
osteochondroma are in continuity
Histopathology - cap of the tumor composed of hyaline cartilage
- appearance of the disorganized growth plate
- echondral ossification occurs at the growth plate
Clinical features - slow growing mass
- pain of the affected area – due to tumor impinge on the nerve or the
stalk of the tumor fractured
- bowing and shortening of bone due to disturbance in epiphyseal
growth
Radiologic
findings
- outgrowth of the bone from normal cortex – which is continuous
- Cap cannot be seen initially. As age increase, the cap undergoes
calcification in a punctuate or nodular fashion
- well-defined peripheral margin without localize bone destruction
Prognosis The stalk usually stop growing at the time of growth plate closure, <1% give rise
to osteosarcoma
Treatment Removal of loose body, synovectomy
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CHONDROMA
Definition Benign tumor of hyaline cartilage. The terms enchondroma implicate the tumor
arise from the medullary cavity while subperiosteal/juxtacortical chondroma
denotes the tumor arise from the surface of the bone
Character - most common intraosseous cartilage tumor
- commonly diagnosed in patient between age 20-50
- no sex predominant
- solitary and often located in the metaphyseal region of the tubular
bones
- multiple chondroma is called chondromatosis occurs in the Oller
disease
Gross morphology - smaller than 3 cm
- enchondroma are gray blue, translucent and have a nodular
configuration
Histopathology - nodules of the cartilage are well circumscribed and have hyaline matrix
- neoplastic chondrocytes that reside in the lacunae are cytologically
benign
- nodules characteristic – peripheral undergoes enchondral ossification,
central undergoes calcification and dies
Clinical features - usually is asymptomatic
- local pain
- pathological fracture
- deformities occurs when the cartilage tumor is numerous and large
Radiologic
findings
- presence of ‘O ring sign’, an unmineralized nodules of cartilage produce
well circumscribed oval lucencies surrounded by thin rim of dense bone
- expansile growth of the cortex with size between 10 – 30 mm
Prognosis Tumor growth usually stable, if associated with chondromatosis, it has high
probability to become sarcomatous
Treatment Complete excise (but may recur)
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ONNAZLI0809
CHONDROBLASTOMA
Definition A tumor derived from chondroblast which is very rare and accounts for less
than 1 % of the primary bone tumors
Character - occurs in young patients in their late teens
- male to female ratio 1:2
- mostly occurs at knee, in older patient, the tumor may occurs at pelvis
and ribs
Gross morphology - not stated
Histopathology - cellular tumor which composed of sheets of compact polyhedral
chondroblast that have well defined cytoplasmic border
- highly cellular lesion which is composed of chondroblast and giant cell
- nuclei are hyperlobulated with longitudinal groove
- moderate amount of pink cytoplasm
- surrounded by scanty amount of hyline matrix which are deposited in a
lace-like configuration
- prominent haemorrhagic cystic degeneration
Clinical features - local pain – if joint are affected
- joint effusion
- reduce joint (affected) range of movement
Radiologic
findings
- well-defined geographic lucency that has spotty calcifications
- round and well-defined calcific margin
Prognosis Rarely distant metastases to lung, recurrence common after surgical excision
Treatment Surgical excision
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ONNAZLI0809
CHONDROMYXOID FIBROMA
Definition Is a rare benign tumor that accounts of less than 0.5 % of biopsied primary
tumor of the bones which composed of various tissue combination; fibrous,
cartilaginous and myxoid
Character - mostly occurs between 10-30 years old patient
- male are predominantly affected
- Usually arise in the metaphysis of long tubular bones – proximal 3rd
of
tibia (25 %), bones of leg and distal femur (50 %)
Gross morphology - tumor size 3-8 cm in greatest dimension
- well circumscribed, solid and glistening tan gray
Histopathology - nodules of poorly formed hyaline cartilage and myxoid tissue
delineated by fibrous septa
- cellularity varies, greatest at the periphery nodules
- tumor cell located in the lacunae at the cartilaginous region
- tumor cells are stellate and their delicate cell processes extend through
the mucinous ground substance and in contact with neighbouring cell
- varying degree of cytologic atypia – presence of large hyperchromatic
nuclei
- small foci of calcification of the cartilaginous matrix and scattered non-
neoplastic osteoclast-type giant cell
Clinical features - localize dull and achy pain
Radiologic
findings
- eccentric geographic lucency that is well delineated from adjacent bone
by a rim of sclerosis
- punched out lesion involving cortex and medulla
- presence of soap bubble appearance
Prognosis Tumor may recur but it doesn’t pose a threat for malignant transformation
Treatment Simple curettage
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ONNAZLI0809
CONVENTIONAL CHONDROSARCOMA
Definition A malignant tumor of cartilage cell in which the cancerous cell produce
cartilage matrix and occurs in the bone
Character - occur at patient age 40 and above
- affecting male twice than female
- risk factor are enchondroma, osteochondroma, chondroblastoma,
fibrous dysplasia and Paget diseae
Gross morphology - composed of malignant hyaline and myxoid cartilage
- myxoid is viscous and gelatinous and the matrix oozes from the cut
surface
- presence of spotty calcification and central necrosis creating cystic
spaces
- adjacent cortex is thickened and eroded
Histopathology - poorly differentiated sarcoma – dedifferentiated chondrosarcoma
- sheets of large malignant chondrocytes that have abundant clear
cytoplasm, numerous osteoclast-tyoe giant cell and intralesional
reactive bone formation – clear cell chondrosarcoma
- island of well differentiated hyaline cartilage surrounded by sheets of
small round cell
- cellular anaplasia, bizarre shaped nuclei, chromatin clumping and
mitoses
Clinical features - painful lesion
- progressively enlarge masses
Radiologic
findings
- poorly demarcated between normal and abnormal bones
- presence of calcification which may be stippled, nodular or
englomerate (‘popcorn’) in a pattern of flocculent density
- nodular growth pattern of cartilage produces prominent endosteal
scalloping
Prognosis Depends on the grading, higher the grade and larger the size, poorer the
prognosis (chance of survival reduce)
Treatment Chemotherapy
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ONNAZLI0809
OSTEOARTHRITIS
Definition
Is a degenerative joint disease characterized by progressive erosion of articular cartilage
Classification
Classify based on the causes of osteoarthritis
Primary Secondary
Idiopathic Metabolic
Ochronosis
Acromegaly
Haemochromatosis
Calcium crystal deposition
Anatomic
Slipped femoral epiphysis
Epiphyseal dysplasia
Congenital dislocation of the hip
Leg length inequality
Hypermobility syndrome
Traumatic
Motor vehicle trauma
Fracture through joint or osteonecrosis
Joint surgery
Inflammatory
Acute inflammatory arthropathy Septic arthritis
Pathogenesis
Idiopathic caused
Degeneration of chondrocytes
Decrease local synthesis of collagen
type II, proteoglycan produced is withinnormal range
Water absorption normal (PG normal)
but collagen network production less
Unstable osmolarity between collagen
network and water content leads to
increase breakdown of the pre-existing
collagen
Osteoarthritic cartilage produce
molecular messenger (IL-1, TNF-α and
nitric oxide)
PRIMARY OSTEOARTHRITIS
Erosion of the articular cartilage
Production of molecular messenger
predominate the compensatorymechanism
Compensatory mechanism –
chondrocytes in the deeper layers
proliferate and attempt to repair the
destroyed cartilage
Reduction of functional chondrocytes
Apoptosis increase
Trigger inflammatory reaction as well as
apoptosis
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Morphology
Gross morphology
1. Vertical and horizontal fibrillation and cracking of the matrix at the superficial layers of the
cartilage which are degraded2. Granular articular surface softer than normal
3. Bone eburnation – friction smoothes and burnish the exposed bones
4. Mushroom shaped osteophytes (bony outgrowth) develop at the margins of articular
surface which capped by fibrous and hyaline cartilage
Histology
1. Synovium is congested and fibrotic
2. Scattered chronic inflammatory cell
Clinical features
1. Joint pain and tenderness
2. Joint swelling (stiffening and pain after immobility)
3. Joint instability
4. Crepitus on movement
5. Limitation of range of movement
6. Joint effusion
7. Heberden nodes – prominent osteophytes at DIP joint
Investigation
1. X-rays – abnormal only when the damage is advanced
2. MRI – demonstrate early cartilage and subchondral bone change
3. Arthroscopy – reveals each fissuring and surface area of the cartilage
Treatment
1. NSAID
2. Total replacement arthroplasty
3. Realignment osteotomy of knee and hip
4. Weight loss and exercise for strength
5. Local heat, ice packs and massage
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ONNAZLI0809
RHEUMATOID ARTHRITIS
Definition
Chronic systemic inflammatory disorder which principally attacks the joint, producing a non-
suppurative proliferative and inflammatory synovitis that often progresses to destruction of thearticular cartilage and ankylosing of the joint
Pathogenesis
Morphology
1. Synovial edematous, thickened and hyperplastic forming villous configuration2. Infiltration by dense perivascular inflammatory cells such as B-cells, T-cells, plasma cell and
macrophages
3. Increase vascularity
Unknown antigen
Bind to MHC class II (genetic susceptibility)
Induce CD4+ T cells to release cytokines
B-cell activation
Formation of rheumatoid factor
Immune complex formation and
deposition inside joint cavity
Joint injury
Induce macrophage to release
cytokines
Proliferation of fibroblasts,
chondrocytes and synovial cells
Release of collagenase,
stromelysin, elastase, PGE2, and
other enzyms
Endothelial activation
Expression of adhesion
molecules
Accumulation of inflammatory
cells
Pannus formation; destruction of bone,
cartilage leading to fibrosis and
ankylosing
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Clinical course
1. slowly progressive, symmetrical and peripheral polyarthritis evolving over a period of few
weeks and months
2. pain and stiffness of small joints of hands – PIP, DIP and feet (MTP)
3. pain and stiffness in the morning improve with physical activity
Investigations
1. Blood count – anaemia
2. Increase in ESR
3. Increase in C-reactive protein
4. Serology test – Presents of Rheumatoid factor and ANA at low titre
5. X-rays – soft tissue swelling
6. Aspiration – effusion presents and cloudy owing to white cells
Treatment
1. NSAID
2. Disease modifying anti-rheumatic drugs that inhibit cytokines and reduce inflammatory
response – TNF-a, corticosteroid, methotrexate etc