Flashcards in day 2 - pathology of bones and joints Deck (18):
Higher in Caucasian and Asian!
One of the most common conditions of the elderly!
￼￼￼￼Affects more than 75mil. people
Estimate to cause 8.9 million fractures/year
￼(EUA, EU, Japan- WHO) !
localised / regional
osteogenesis imperfecta , Turner syndrome, rheumatoid arthritis, glucocorticosteroid use, systemic mastocytosis, hyperthyroidism, adrenal disease, malignancy, steroid or anticoagulant therapy, chronic alcoholism, multiple myeloma, and immobilisation!
Women with bone mineral density values of more that 2.5 standard deviation (SD) below
that of normal adult mean value ! are at risk of fracture = Osteoporosis!
Women with bone density values of more that 1 SD below that of normal adult mean value = osteopenia!
most likely sites of fractures in osteoporosis
hip = neck of femur!
explain RANKL pathway
￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼Receptor activator of nuclear factor kappa-B
RANK (receptor) is expressed on the surface of osteoclast precursors and mature osteoclasts.
RANKL, produced by osteoblasts (and other cells) interaction with its receptor, RANK, promotes osteoclast differentiation, increased bone resorption by mature osteoclasts and extension of osteoclast survival via suppression of apoptosis.
Osteoprotegerin (OPG) is a glycoprotein, secreted by osteoblasts and bone marrow stromal cells, is a natural inhibitor of RANKL. OPG blocks the interaction of RANKL with RANK by acting as a ‘decoy receptor’.￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼
￼￼Oestrogene limits the amount of RANK ligant expression by ostoblasts.
effect of menopause on bone loss
Rapid bone loss at menopausal period – 3% / year in the spine for 5 years
0.5% per annum subsequently
Women may lose up to 40% of bone mass
Presentation of disease 20 years after the menopause
If bone loss occurs in all women after the menopause, why does everyone not get osteoporosis?
Peak bone mass – 20 – 30 years of age
More bone available to lose before reaching fracture threshold
Genetic / familial
risk factors for lower bone density
Life style / exercise! Smoking! Alcohol!
Diet – low calcium!
Endocrine diseases – ! hyper and hypothyroidism!
Addison disease - Adrenal
prevention of bone loss drugs
cancer risk – breast and endometrium
value of lower levels ?
RANKL inhibitors (denosumab)
types of joint disease
Osteoarthritis / degenerative joint disease
INFLAMMATORY / AUTOIMMUNE
MAY REPRESENT ONE MANIFESTATION OF A MULTI-SYSTEMIC DISORDER
what is osteoarthritis
Degenerative changes in the articular cartilage (biochemical / metabolic).
Reactive change in the subchondral bone and the synovium.
Males and females are equally affected with exponential increase in prevalence after age 50.
Monoarticular / polyarticular Weight-bearing joints: knee, hip, spinal joint
Non weight-beating joints: hands and feet (more frequent in women)
Joint pain, stiffness and function impairment Loss of quality of life
OSTEOARTHRITIS / DEGENERATIVE JOINT DISEASE causes
Primary (90%): unknown cause
Changes in proteogycan and collage II lead to altered load-bearing properties.
Secondary (10%): as a consequence of pre-existing joint disease that predisposes to the joint failure.
(ex. deformity, RA, metabolic disorder, crystal deposition disease)
structure of articular cartilage
Lamina splendens: -superficial flat chondrocytes
Middle layer:-round chondrocytes
Calcified cartilage: -chondrocytes organised in clusters
Subchondra compact bone
cartilage structure in osteoarthritis
￼Roughened cartilage with erosion, depression & linear grooves
Whitish areas of fibrous and cartilage repair !
Loss of cartilage with exposure of bone that becomes marble-like (EBURNATION)
what are osteophytes in osteoarthritis
Osteophytes - new bone formation at edge of joint !
cause is not understood !
can compress nerves and inflict pain
what might you see on an X-ray of an osteoarthritic joint
Narrowing of articular space