bones and joints Flashcards
inflammatory diseases
CAID
- crystals formation (gout, pseudogout)
- autoimmune (RA)
- infection (septic arthritis/ osteomyelitis)
- degenerative (OA)
OA presentation (3) + pathology
presentation:
- generalised OA - post-menopausal
- erosive inflammatory OA - destructive, quick progression
- hypertrophic OA - ostophyte (bone spurs)
pathology
- eburnation** (bone rub bone)
- subchondral bone cyst
- thickened joint
- inflammation of synovium - synovitis
- degeneration of articular cartilage
- bone spurs
- sclerosis
what is RA+ who is more susceptible
chronic inflammatory autoimmune disease: CD4+ T cells.
RF and ACPA antibodies produced
-> destructive granulation tissue (pannus) formed + synovial inflammation
bone erosion**
affecting joints - esp proximal (UL)
more common in women
RA histology
rheumatoid nodules fibrinoid necrosis (granuloma) in the centre
crystals formation and deposition
- analysis
- location
- 2 types
deposited in joints and soft tissue
gram stain, culture, crystal analysis
- gout + pseudogout
gout pathogenesis + risk factors
caused by increased serum uric acid
-> form urate crystals that deposit in the bone
primary: obesity, alcohol, HTN, fatty diet
secondary: anything that causes hyperuricemia
pathogenesis:
- over-production of purines
- catabolism
- kidney failure: uric acid cannot get eliminated
gout complications
- deformities, erosion of joints
- gouty tophi
- renal stones/ renal failure
gout crystals examintaion
polarised light to examine synovial fluid
birefringent (refractive) needle shaped crystals
pseudogout crystals made of what + shape
- calcium pyrophosphate (chondrocalcinosis)
- rhomboid shaped, weakly birefringent
inflammation caused by infection - osteomyelitis
- common cause of infection
- way of entering the bone
- staph aureus** (most common)
- E.coli, Group B strep, anaerobes
- direct implantation - trauma
- blood (lung TB)*
- contiguous spread (share a border) - middle ear infection
osteomyelitis clinical presentations + where does it happen
tuberculosis
pain, swelling, fever
children: UL/LL
adults: LL, spine
osteomyelitis pathogenesis
bacteria and inflammation spread within shaft of the bone, harversian system and periosteum* (similar to osteosarcoma
(periosteum: impair blood supply -> bone necrosis -> sequestrum (bone within bone)
may also spread to synovium -> septic arthritis
osteomyelitis complications
- fracture and deformity
- amyloidosis
- distal infection
- malignant transformation
TB osteomyelitis
highly destructive - extensive necrosis
chronic inflammation - epithelioid granulomas + caseating necrosis
usually affects the spine
TB osteomyelitis complications
- compression fractures
- severe deformities - kyphosis (hunchback)
- compress spinal cord and nerves -> neurological deficits
metabolic bone diseases (4)
(POOO)
- osteoporosis (reduced bone mass)
- osteomalacia and rickets (mineralisation defects)
- osteitis fibrosa cystica (excessive bone resorption)
- paget’s disease (uncontrolled resorption + uncoordinated osteoblastic effects - formation of new bone)
osteoporosis
- how to measure
- characteristics (serum ca/hormones, mineralisation)
reduced bone mass - BMD <2.5
BMD measurement = X ray absorptiometry at hip/lumbar spine
thinned and reduced trabeculae -> increase risk of fracture
- but normally mineralised!! (osteomalcia has decreased mineralisation)
- normal serum ca/phosphate
- normal ALP (alkaline phosphatase protein: tests liver/bone fn)
- normal PTH hormone
causes of osteoporosis (primary + secondary)
+ site
primary: post-menopause cause of estrogen def
estrogen def
-> increase inflammatory cytokines
-> osteoclast recruitment = bone resorption
increase both bone resorption and formation (but resorption more) = overall bone resorption
secondary: decrease in calcium intake/absorption
- GIT/endocrine, drugs
affects spine, fracture of femur/wrist
osteomalacia cause
defect in mineralisation (calcification) cause of vit D def
- > weak bone: microfactures/softening of bone
children: bowing of legs, may even distort skull
rickets pathogenesis
disturbances of endochondral ossification
-> overgrowth of epiphyseal cartilage - cartilage cells cannot mature
non-calcified, hypertrophied growth plate
vit D def causes
- inadequate dietary intake
- lack of sun exposure
- GI problems -> malabsorption (IBD, bowel resection, celiac disease)
- renal disease: vit D cannot be converted to active form
osteitis fibrosa cystica pathogenesis
- serum calcium/phosphate levels
excessive bone resorption by osteoclasts - because of increased PTH hormones
- high serum calcium (cause of the bone resorption), low serum phosphate
- loss of bone mass
- the bone loss replaced by fibrous tissue
osteitis fibrosa cystica complications
- formation of brown tumour: cystic solid lesion
developed cause of the osteoclasts
Paget’s disease
disorderly bone formation cause of excessive/disorganised bone resorption + formation
-> distorted bone architecture
mosaic pattern of lamellar bone, irregular w/ collagen fibres
Paget’s disease affects who + sites
- elderly and caucasian
- mainly polyostic - pelvis, spine, skull
complication of Paget’s disease
- bone overgrowth -> OA
- chalkstick fractures (affect long bones that become brittle)
- nerve compression
- CVS issues cause of hypervascularity of bone
- osteosarcoma
types of bone tumours
- osteosarcoma - children/young adults** most common
malignant - Ewing sarcoma (EWS)/ PNET** - children/ young
^ respond to chemotherapy - chondrosarcoma** - older pts (malignant)
- chondroma, osteochondroma (benign)
- giant cell tumours
- fibrous/ fibro-osseous tumours
primary malignant bone tumour presentation
pain, swelling
possibly fracture, loss of fn
fever, anemia, weight loss, elevated WBC & ESR (cause of inflammation)
may metastasise: lungs, bone, bone marrow
investigation of bone tumours
- X-ray** first line!!
- MRI - relations: nerves/vessels
- radionuclide scan: detect metastasis
- PET scan: detects spread to see if tumour is malignant
- biopsy
osteosarcoma
- who it affects more
malignant, high grade
produces osteoid from tumour cells
- males high proportion
- 10-25 yrs
osteosarcoma on x-ray
destructive
lytic masses
permeative margins - arises within medullary cortex -> breaks through cortex & periosteum (like septic arthritis)
- tumour: bone formation in soft tissue -> SUNBURST pattern
- affects long bones of LL (femur, tibia, humerus)
- lots of necrosis & hemorrhage -> fleshy appearance
osteosarcoma histology
osteoid** produced by eosinophilic matrix (diagnosis)
EWS
- who it affects more
2nd most common malignant bone tumour in children, esp <10yrs
affects 5-25yrs, more common in males
EWS on x-ray
destructive
poorly marginated + permeative
layered periosteum -> “onion skinning’
EWS on histology
small, round, uniform blue cells
arranged around vessels
+ve w. CD99 stain**
- differentials:
lymphomas, rhabdomyosarcoma, metastatic carcinoma, neuroblastoma, small cell osteosarcoma
chondrosarcoma
- malignant
- produces cartilage
- DOES NOT produce osteoid
- painful, large
chondrosarcoma
- who it affects more
- sites
- reacts to chemo?
males, 30-60yrs (older pts)
sites: long bones/ ribs (>8cm) that grow rapidly during adolescence
does not respond to chemo
macroscopic chondrosarcoma
large lobulated tumour w/ focal calcification
hemorrhagic necrosis present
microscopic chondrosarcoma
cartilaginous matrix
permeation of bone trabeculae
soft tissue and marrow invasion
osteochondroma
benign* - most common benign tumour
arises from long bones
- overgrowth of bone - bone extension containing cortex and periosteum covered by a thin cartilaginous cap
types of chondroma
- enchondroma: medullary cavity
Ollier’s disease; Maffucci syndrome
solitary enchondromas: caused by heterozygous mutations of IDH genes - subperiosteal chondroma: surface of bone
- soft tissue chondroma: inside soft tissue
differences in benign and malignant bone tumour
- permeation of bone trabeculae and marrow
- soft tissue & organ invasion
giant cell bone tumour
benign, but locally aggressive (does not metastasise distally)
most common skeletal neoplasm
giant cell bone tumour
- who it affects more
- site
oriental countries (SEA) affects females more
- affects long tubular bones (knee)
- epiphyseal-metaphyseal region (growth plate)
giant cell tumour characteristics
- NO osteoid formation
- NO malignant transformation
- abundant giant cell w/ numerous nuclei
non-ossifying fibroma
- who it affects
- site
benign
affects children
metaphysis of long bones (esp femur)
micro: cellular lesions, fibroblasts, activated macrophages, giant cells
fibrous dysplasia (FD) \+ 2 polyostotic examples
benign developmental arrest: does not develop into mature bone structure mutation in GNAS1 gene** - Mazabraud syndrome - McCune-Albright
FD microscopy
tan-white and gritty (sandy)
histo:
trabeculae surrounded by fibroblastic proliferation
trabeculae is curvilinear
