Definition & Etiology
Prognosis
Definitions
OSTEOPOROSIS (OP)
1. Primary: idiopathic
2. Secondary: caused by identifiable conditions such as: nutritional def, endocrine pathologies (thyroid, parathyroid, KI dis), BM or CT disorders, drug related
- m/c metabolic origin  ↓ in
density & quality of bone
- general, regional or local
- #1 fracture site – vertebral
fractures, #2 – hip
Etiology:
- extremely common (1 in 4 women
> 50years)
- 40% lifetime fracture risk in
Caucasian women at 50
- 1 in 2 Caucasian women will suffer
from osteoporotic fracture risk in
their lifetime
Clinical Risk Categories:
1) Extremely High: prior OP fracture
2) Very High: Glucocorticosteroid
3) High: post menopausal w/ >1 of:
>65yrs, Hx fracture w/out trauma
>40yrs, FxHx fracture >50, current
smoker, wt < 127lbs, Frailty
4) Moderate Risk: post meno, no
HRT, no other factors, FxHx OP
Medications: cyclosporine, GnRH tx,
anticonvulsants, heparin, tacrolimus,
tamoxifen b/f menopause, inhaled
GC
Conditions w/ association:
- alcoholism, Cushings, gastrectomy,
hypogonadism, hemochromatosis,
hyperPTH, IBD, LV dz, multiple
myeloma, malabsorption, RA,
premonopausal amenorrhea
Pathogenesis &
OSTEOARTHRITIS (OA) & OSTEOPOROSIS (OP)
- Osteopenia: ↓ bone mass; appears as loosened bone on x-ray
- Osteomalacia: insufficiency of bone matrix mineralization (↓ quality)
- Osteoporosis: loss of total bone mass (↓ quantity); characterized by low bone mass & microarchitectural deterioration of bone T  ↑ bone fragility, ↑ risk of
fracture with less P DEXA T- score < - 2.5 SD
RISK FACTORS /EPIDEMIOLOGY:
1) Age: post menopausal, 5x
increase risk/decade, idiopathic OP
in pre-menopausal & juvenile = rare
2) Gender: females 2x more, 25%
fracture in men
3) Race: Caucasians & Asians
increased risk
4)Genetics: 80% bone mass
genetically determined, Vit D &
estrogen receptors
Causes:
- estrogen(females)/ testosterone
(males) deficiency
- increased age
- glucocorticosteroid use
- Cushings, hyperPTH,
hyperthyroidism, malabsorption,
severe LIV disease, herparin Tx,
Immobility, Vit D deficiency
Increase bone: calcitriol (active
vitD), Calcitonin, Estrogen,
testosterone, GH, GF, PTH
Decrease bone: PTH, Thyroid
hormone, cortisol
2o Causes:
- lymphoma, leukemia, multiple
myeloma, tumor secreting PTH-
related peptide (or PTH), Addison’s
disease, amyloidosis, congenital
porphyria, hemochromatosis,
hemophilia, thalassemia
Prognosis/Outcomes:
- 70% respond to tx & stabilize
- 20-30% w/ hip fracture (femoral
neck) institutionalized / die
- Men die > hip fracture
Signs & Sx
- Asymptomatic – first presentation
fracture (hip, wrist, vertebrae m/c)
- back pain, loss of ht, kyphosis from
fracture
Sx:
- asymptomatic until fracture
- pain, disability, poor mobility
- abdominal complaints
(compression)
- pulmonary s  restrictive LU dz
- back/ soft tissue pain
Ss:
- tenderness @ fracture site
- bony deformity
- kyphosis & loss of ht w/ fractures
- lax ab muscles w/ protuberant ab
Fracture threshold:
- BMD below which fracture risk ↑
Physiological activity of bone:
- balance btwn osteoblastic &
osteoclastic activity
- bone turnover = 100% in infants,
18% in adults per yr
- influenced by calcitonin (from
thyroid gland), PTH (from para-
thyroid gland), 1,25-dihydroxl-
cholecalciferol (vit D, skin), &
estrogen
- affected by: extracellular fluids &
mechanical stress
Dx & DDx Tx & Other
Physical Exam Allopathic therapeutic options:
- most ppl at risk of OP completely - lifestyle recommendations, CA & Vit
normal clinical exam D, Bispohosphonates, HRT,
- measure height, examine spine, Raloxifene, Calcitriol, Calcitonic,
Teriparatide
fracture site, proximal muscle
weakness
Primary prevention is ultimate
therapeutic goal
DDX:
- most tx only puts back 5-10% of
- sex hormone deficiency (M/C)
bone over 5 yrs
- glucocorticoid XS
- reduction of modifiable risk factors
- osteomalacia
is vital
- hyperparathyroidism
- once bone has been lost it is
- osteogenesis imperfecta
impossible to replace it with
(deficiency of osteoclasts)
structurally normal bone
- multiple myeloma
Lab Tests:
1o tests to dx 2o causes:
- Serum Ca2+, serum Phosphate,
total ALP/bone ALP, LIV/KI function
tests, CBC, thyroid function tests,
25-H vit D level (elderly), serum
testosterone (men)
2o tests to dx causes:
- PTH levels (w/ ABN Ca2+& P-),
serum PRO & electrophoresis(w/
ABN CBC), 24 hr urine Ca &
Creatinine & free cortisol, urine
PRO electrophoresis & Bence
Jones PRO, XRAY(past/present
fracture)
Testing for Dx & monitoring:
DEXA (Dual Energy Xray
absorptiometry)
- single photon xray absorptiometry,
CT, QUS
 Definition & Etiology Pathogenesis &
Prognosis
- Repeat DEXA to monitor Tx
- Continue CS tx
OSTEOARTHRITIS (DJD)
- Definition: degenerative disease in which degeneration & loss of articular cartilage occur together with new bone formation at the jt surfaces & margins, leading to pain & deformity.
1. Primary: idiopathic
2. Secondary: dt trauma, prior inflammation, arthritis, endocrine pathologies & metabolic disorders (see OP)
- Cartilage: is physiologically active so disruptions in biomechanics  disruptions in normal synthesis & degradation  ↓ in tensile strength and ↓ ability to deform; surface becomes less tolerant to
stress  cartilage erosion
- 2 main functions:
1. Absorbing stress by deforming
2. Provides a smooth, frictionless surface for mvmt in the joint
- m/c joint disorder Epidemiology:
1) Age: by 40 radiographs show
- affects synovial, wt bearing joints; 90% have OA changes to wt bearing
w/ focal areas of cartilage loss & jts, <45 m/c in men, > 55 m/c in
remodeling of subchondral bone women
- knee joint m/c’ly affected 2) Race: knee OA higher in African
- predilection for distal & proximal American women, Hip OA higher in
Europeans/ Caucasian American
ITP joints; zygopopheal (facet) jnts
3) Gender: equally affected, pattern
of spine; hip
of jt involvement similar Women 
Etiology: DIPs, PIPs 1st carpometacarpal jts;
- 2-6% of popl’n Men  hips
- Begins asymptomatically in 20-30s 4) Genetics: FxHx of herberden’s
and common by 70 nodes (female side of family),
- 33-90% of ppl > 65 show evidence mutation in type II collagen gene
of OA seen with 1o OA
5) Geography: closer to equator, but
Sx less severe in warm climates
6) SES: mech. Stress related to
Prognosis: occupation/ activity
- progressive process, leading to
continual loss of articular cartilage, Pathophysiology of OA
pain & eventual loss of ROM in - Change in force vectors across jnt
advanced stages w/ full loss of surfaces effects the cartilage of the
cartilage joint
- ligaments become lax, jt becomes  Micro: synovial fluid pushes into
less stable subchondral bone  geode
- jt enlargement & osteophyte  Metaplasia: ↑ stress at the
formation can cause locking of jt capsule insertion  osteophyte
- continual deformity, muscle atrophy formation
& pseudocysts
- occasionally know to stop or Cartilage breakdown dt:
reverse - repetitive/excessive impulse
loading
- immobility (↓ nourishment to the
jnt)
- developmental disorders
Signs & Sx
Sx:
- aching pain in jts (<use, >rest)
- stiffness on waking/ inactivity
(<30 min)
- pain w/ ROM
- jt enlargement, jt buckling
/instability
- referred pain away from affected jt
- loss of function of jt, flexion
contractures
Ss:
- crepitus w/ motion
- limited / pain w/ motion
- bony enlargement of affected jts
(Herberden’s nodes, Bouchards
nodes)
- Misalignment / jt deformity
Features:
- Bony spur, no ankylosis,
subchondral cyst, subchondral
sclerosis, osteophyte, thinned &
fibrillated cartilage
Dx & DDx
Lab Testing
- generally noncontributory
- normal ESR, CBC, negative ANA,
absent RF
- Dx of exclusion
- Synovial Fluid analysis (WBC, %
PMN)
Dx Evaluation:
- radiography may confirm OA &
assess severity
- Pain: >rest, <movt/ wt bearing
- Previous trauma/injury / fracture /
surgery
- P/E: distinguish b/w
inflammatory & non-inflamm
condition
XRAY  decrease in jt space d/t
decreased articular cartilage (may
see pseudocytes, osteophytes
DDX:
- Infective arthritis
- RA (chronic inflamm. RF, > am)
- Bursitis, tendonitis,
- Psoriatic arthritis
- Polymyalgia rhematica
Tx & Other
Treatment (allopathic):
1. Education / exercise/ wt loss
2. Paracetamol (Tylenol tx)
3. Glucosamine (oral/topical),
Topical NSAIDS or capsaicin
4. COX inhibitors / Opiods (jt
injections) / NSAIDS
Risk Factors (complications)when
taking NSAIDS:
- upper GI complications
- age > 65ys
- Co-morbid med conditions
- Use of oral glucocorticoids
- Hx of peptic ulcer disease
- Hx of upper GI hemorrhage
- Renal complications
- Raised serum Creatinine levels
- Hypertension
- CHF
- Use of ACE inhibitors
- Use of diuretics
#1 Tx for OA is exercise  maintain
ROM
Recommendations:
- exercise regularly, control wt, eat
healthy, know limits, avoid strain on
jts, spread wt over jts, stretch, good
posture, use strong muscles, apply
HEAT, apply cold for flare ups,
orthodics, relaxation, positive attitude
Definition & Etiology Pathogenesis & Signs & Sx Dx & DDx Tx & Other
Prognosis

- jnt surface incongruity & instability