wk 12, lec 3 Flashcards
osteopenia t score
-1 to -2.4
Causes of osteopenia
more osteoclasts
decrease estrogen in menopause or testosterone in men
vit d and calcium deficient
old age
genes
testosterone impacts on bone
increase osteoblast, inhibit osteoclast, muscle mass and strength
clinical features of osteopenia
- Asymptomatic
- Height Loss
- Bone Pain
- Fractures (MC: vertebrae, hips,
wrists, metatarsals, and ribs) - Decreased Grip Strength
labs for osteopenia
serum BUN,
creatinine, albumin, calcium,
phosphate, alkaline phosphatase,
and 25-OH vitamin D
check DXA every 1-2 year if T score
below 2
and if using prednisone./ corticosteroid
osteoporosis t score
< -2.5
causes of osteoporosis
nutrient deficient
age
genes
change in osteoporosis
decrease BMD
microartchitectral changes (thin trabecular, increased porosity, decreased connectivity of bone tissue)
imbalance in bone formation and resorption
which bone effected in osteoporosis
trabecular (spongy) and cortical (bone) – trabecular more metabolically active and effected more
features of osteoporosis
- Fractures (hip, wrist, spine)
- Back Pain
- Loss of Height (kyphosis)
- Decreased Mobility and Function (hip fracture)
- Risk of Secondary Complications. (pneumonia, DVT, pressure ulcers)
- Asymptomatic Osteoporosis
- Reduced Grip Strength and Muscle Weakness
pagets disease of the bone (osteitis deforming)
abnormal bone remodelling, excess breakdown and formation = large and weak bones
causes of pagers disease of bone
genes, viral (paramyxoviruses i.e. measles and respiratory synctitial virus)
features of pagets disease of bone
excess bone resorption via osteoclast
disorganized bone formation (weak)
increase vascularity; hyperemia
abnormal bone architecture ( mixture of lamellar and woven bone, with
disorganized trabeculae and irregular cement lines)
phases of pagets disease of bone
- initial osteolytic phase = bone resorption and hypervascularization
2.s Econ phase= bone formation and resorption - replace normal lamellar bone with woven bone
- sclerotic phase; bone resorption declines and leads to hard, dense, less vascular bone (burn out phase)
-all 3 phases can happen at same time in different bones
symptoms of pagets disease
asymptomatic
bone pain
bone deformtion
fractures
neurolgocail if compress nerves (headache, hearing)
arthritis
labs in pagets disease of bone
elevated alkaline phosphatase levels
a marker of increased bone turnover
scoliosis
abnormal lateral curvature
of the spine
usually in childhood
4 categories of scoliosis
- idiopathic (80%)
- congenital
- neuromuscular (associated with neuropathy or musclular disease)
- syndromic (associated with other syndrome)
scoliosis features
spinal curvature C or S shape
vertebral rotation
imbalance of muscles and ligaments
- Visible Curvature
- Asymmetry of the Shoulders, Hips, or Waist
- Uneven Leg Length
- Back Pain
- Reduced Range of Motion
- Breathing Difficulties (thoracic spine, reduce lung capacity)
osteogenesis imperfecta (brittle bone disease)
fragile bones
genetics
mutrations in which gene for osteogenesis imperfecta (brittle bone disease)
mutations in the genes responsible for producing
type I collagen
osteogenesis imperfecta features
type I collagen synthesis mutation
abnormal bone matrix; weak
blue sclera (from CT abnormalities)
dentinogenesis imperfecta (tooth discoloured and weak)
short stature
skeletal deformities; bowed limbs, scoliosis,
joint hypermobile (lax ligaments)
hearing loss (from collagen dysfunction)
pulmonary (pneumonia, restrictive or obstructive lung disease)
cardiovascular (collagen in cardiac valves and aortic wall deformed) i.e. mitral regurgitation
osteomyltiits
bone infection; usually bacteria
mainly in vertebrae; hematogenous spread
secondary infections if neuropathy or vascular insufficient
body tries to make new bone; sclerosis; but is irregular
bone pain, warm and swollen, fever and chills, limited ROM, drainage or sinus tracts
systemic: septicemia (bloodstream infection), septic arthritis, or even spread to
distant organs, posing a risk of life-threatening complications
multiple myeloma
cancer that affects plasma cells (a WBC that makes antibodies)
causes them to profligate in bone marrow and crowd out normal blood cells and make abnormal antibodies
myeloma common in
among farmers,
wood workers, leather workers, and those exposed to petroleum products
multiple myeloma cells involved
MM cells bind via cell-surface adhesion molecules to bone marrow stromal cells (BMSCs)
and extracellular matrix (ECM)
- Triggering MM cell growth, survival, drug resistance, and migration in the bone marrow
milieu
cytokines: IL6, IGF1, VEGF, SDF-1a
ras/raf/protein kranse, PI3K/.Akt, PKC
Immune cells such as plasmacytoid dendritic cells (pDC), myeloid-derived
suppressor cells (MDSC), and T helper 17 (TH17) cells are increased in number and
support myeloma growth
multiple myeloma feature
plasma cell proliferate via monoclonal immunoglobulins (m proteins)
infiltrate bone marrow and crowd out normal hematopoietic cells
osteolytic lesions, stimulate osteoclasts
monoclonal protein production
bone pain
anemia
renal dysfunction (proteinuria, hematuria)
hypercalcemia (ca in blood- N/V, constipation, confusion, dehydration)
recurrent infections
neurological (weak, numb, tingle if compress spinal cord)
akylosing spondylitis
cause
infalmmation of spine and sacroiliac joints
HLA-B27 gene
features of ankylosing spondylitis
infalmamtion’ ossification
TNFalpha
bone formation; ossification –> syndesmophyte formation –> fusion of adjacent vertebrae and lose spinal mobility –> bamboo spine
SI joint most effected (sacroilitis)
back pain, morning stiffness >30min, reduce spine mobility, enthesitis (inflamed ligament andtendons) esp achilles and chest/costochondral, fatigue, system (fever, weight loss, malaise), extra articular (uveitis, IBD, CVD)
joints for anklosing spondylitis
mostly sacroiliac
osteomalacia and rickets
soften and weaken bones from impaired mineralization of bone matrix
inadequate deposition of calcium and phosphorus
osteromalacia= adults
rickets= kids during rapid growth (before epiphyseal fusion, vitamin D deficiency)
rickets cause
in children during periods of rapid growth
* Before epiphyseal fusion, vitamin D deficiency results in growth
retardation associated with an expansion of the growth plate known as
rickets
features of osteomalacia and rickets
mineralization defect
inadequate intake or absorb phosphorus and calcium and vitamin D
hypercaleamia (muscle cramp, tetany, numb, tingle, seizure)
other: fatigue, weak, secondary hyperparathyroidism
causes of osteomalacia and rickets
- Inadequate dietary intake of vitamin D or calcium
- Malabsorption disorders (such as celiac disease or inflammatory bowel
disease) - Renal disorders affecting vitamin D metabolism
- Liver disorders impairing vitamin D activation
- Insufficient sunlight exposure.
osteomlalcia in adults features
bone pain
muscle weak
secondary hyperparathyroid from low serum calcium
fractures
skeletal deformities; bowed legs, pelvic
rickets (kids) features
delayed growth and development
skeletal deform; bowed legs (genu varum), knock knees (genu valgum), and
deformities of the chest (e.g., pigeon chest or Harrison’s groove)
delayed dentition (teeth)
muscle weak
fracture repair steps
- Hematoma Formation (blood vessels rupture and make blood clot for inflammatory cells to come)
- Inflammatory Phase (heal hematoma; TNFa, IL1, IL6, IL11, IL18, TNFa)
- Granulation Tissue Formation (mesenchymal stem cells differentiate to chondroblasts or fibroblasts) (chrondroblasts form temporary cartilaginous callus and fibroblasts make collagen)
- Callus Formation (cartilage is apoptosis, then VEGF from osteoblasts comes in; M-CSF, RANKL, OPG, TNFa) (replace cartilaginous callus with bony callus and osteoblasts make new bone matrix, osteoid)
–> chondrocytes hypertrophy and calcify ECM
–>ca2+ binds phospahte and make hydroxyapatite crystals
–>type 1 collagen bind hydroxyapatite - Bone Remodelling (osteoclasts resorb excess bone tissue, osteoblast make new deposits, hard callus woven bone replaced by lamellar bone, haversian system, IL1 and TNFa)
fracture repair steps
- Hematoma Formation
- Inflammatory Phase
- Granulation Tissue Formation
- Callus Formation
- Bone Remodelling
frature repicar in osteoporosisi
reduced bone density and altered bone metabolism
associated with osteoporosis, the healing process may be slower and less
robust compared to fractures in individuals with normal bone density
- The formation of a stable callus and subsequent bone remodelling may
take longer in osteoporotic fractures
support via nutrition, weight bearing, smoking cessation, less alcohol
