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JOINt DISeaSe & injury. Ri Long Jin. Osteoporosis. Osteoporosis Prevalence. Affects 200 million women worldwide 1/3 of women aged 60 to 70 2/3 of women aged 80 or older Approximately 30% of women over the age of 50 have one or more vertebral fractures

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slide3

Osteoporosis Prevalence

  • Affects 200 million women worldwide
    • 1/3 of women aged 60 to 70
    • 2/3 of women aged 80 or older
  • Approximately 30% of women over the age of 50 have one or more vertebral fractures
  • Approximately one in five men over the age of 50 will have an osteoporosis-related fracture in their remaining lifetime

IOF, 2005 (www.osteofound.org)

slide4

Osteoporosis

  • Loss of bone mass
  • Increase bone fragility
  • Increase risk of fractures

Osteoporosis, or porous bone, is a devastating disease that robs its victims of bone mass.

slide5

Osteoporosis

Normal Bone

Osteoporotic Bone

slide7

1.5 Million Fractures Annually

Vertebral Fractures:

700,000+

Wrist Fractures:

200,000+

Hip Fractures:

300,000+

Other Fractures:

300,000+

Source: National Osteoporosis Foundation, 2000

osteoporosis
Osteoporosis

Normal

Spine

Osteoporotic

Spine

Source: National Osteoporosis Foundation, 2000

slide10

Osteoclasts

Osteoblasts

Osteoid

Mineralised

Bone

Bone

Osteoid

Courtesy of Michael Amling

slide11

Excess

Resorption

- menopause

- hyperPTH

Insufficient

formation

- aging

Resorption

Reversal

Bone Loss

Bone Loss

Formation

Quiescence

Unbalanced Remodeling: Bone Loss

osteoporosis types
Osteoporosis - types
  • Postmenopausal osteoporosis (type I)
    • Caused by lack of estrogen
    • Causes PTH to overstimulate osteoclasts
    • Excessive loss of trabecular bone
  • Age-associated osteoporosis (type II)
    • Bone loss due to increased bone turnover
    • Malabsorption
    • Mineral and vitamin deficiency
  • Secondary osteoporosis

(ex, steroid, heparin, hyperthyroidism,

hyperparathyroidism, Cushing’s syndrome, etc)

characterization of the two main types of osteoporosis
Characterization of the two main types of osteoporosis

Age(yr)

Sex ratio(F:M)

Type of bone loss

Rate of bone loss

Bone marker

Fracture sites

Parathyroid function

Calcium absorption

Metabolism of 25OH-D to 1,25(OH)2D

Main causes

51 - 70

6 : 1

Mainly trabecular

Accelerated

Increased

Vertebrae & distal radius

Decreased

Decreased

Secondary decrease

Related to menopause

> 70

2 : 1

Trabecular & cortical

Not accelerated

Not increased

Vertebrae & hip

Increased

Markedly decreased

Primary decrease

Related to aging

Type I Type II

symptoms and warning signs i
Symptoms and Warning Signs I

Persistent, unexplained back pain

Shorter than you used to be

Spinal deformities

symptoms and warning signs ii
Symptoms and Warning Signs II

Recurrent fractures

Fracture from minimal trauma

Experiencing chronic medical problems

factors contributing to osteoporosis i
Factors contributing to osteoporosis I

1) Genetic or constitutional factors

a. white or Asia ethnicity

b. maternal history of fractures

c. small body frame

d. long hip axis length

e. premature menopause (<45 years)

f. late menarche

European Osteoporosis Foundation

slide20

Factors contributing to osteoporosis II

2) Lifestyle and nutritional factors

a. nulliparity

b. prolonged secondary amenorrhea

c. smoking

d. excessive alcohol intake

e. inactivity

f. prolonged immobilization

g. prolonged parenteral nutrition

h. low body weight

European Osteoporosis Foundation

slide21

“Women married to a smoker

have

a 91% greater risk

of heart disease”

slide22

WARNING

TOBACCO USE CAN MAKE YOU IMPOTENT

Cigarettes may cause sexual impotence due to decreased blood flow to the penis. This can prevent you from having an erection.

Health Canada

slide23

Factors contributing to osteoporosis III

3) medical disorders

a. anorexia nervosa

b. malabsorption due to gastrointestinal and hepatobiliary disease

c. primary hyperparathyroidism d. thyrotoxicosis

e. primary hypogonadism f. prolactinoma

g. hypercortisolism (Cushing\'s disease or syndrome)

h. Osteogenesis imperfectai. rheumatoid arthritis

j. chronic obstructive pulmonary disease k. post transplantation

l. chronic neurological disorders m. chronic renal failure

n. mastocytosis o. type I diabetes

European Osteoporosis Foundation

slide24

Factors contributing to osteoporosis IV

4) Drugs

a. chronic corticosteroid therapy

b. excessive thyroid therapy

c. anticoagulants

d. chemotherapy

e. gonadotropin releasing hormone agonist or

antagonist

f. chronic phosphate-binding antacid use

g. anticonvulsant

European Osteoporosis Foundation

diagnosis
Diagnosis
  • BMD test
  • Biochemical markers

- Blood

- urine

slide26

X-ray finding:

1.Mineral loss 30-40%

2. Generalized decreased density of bone

3. Spine –manifested in early stage

Loss trabeculae (transverse >longitudinal), thining of cortex, codfish spine;

Wedging of vertebra caused by compression Fx > round back or kyphotic deformity

4. Widening of medullary canal – loss of both cortical & trabecular bones

5. Bone densitometries

a. Singh’s index

b. Photon absorptiometry

c. Dual energy X-ray absorptiometry DEXA

d. Quantitative computed tomography, QCT

dxa dual energy x ray absorptiometry
DXA ; Dual Energy X-ray Absorptiometry
  • low energy and high energy X-ray
  • lumbar spine A-P & Lat., femoral neck, whole body, ulnar & radius
  • good precision and accuracy
  • low dose X-ray (1/50 of chest X-ray)
  • Most popular
slide31

WHO criteria of osteoporosis

Normal : T-score > -1.0

Osteopenia : -2.5 < T-score < -1.0

Osteoporosis : T-score < -2.5

Servere osteoporosis : T-score < -2.5

with presence of one or more fractures

(established osteoporosis)

T-score ; adult peak bone density와 비교한 score

biochemical markers of bone turnover
Biochemical markers of bone turnover

Bone formation

Osteocalcin (bone gla protein)

Bone-specific alkaline

phosphatase

Procollagen type I propeptides

C-terminal (PICP)

N-terminal (PINP)

Bone resorption

Pyridinoline & Deoxypyridinoline

Type I collagen telopeptide

N-terminal

C-terminal

Hydroxyproline

Tartrate resistant acid phosphatase

Galactosyl hydroxylysine

bone densitometry1
Bone Densitometry

Anyone with a fragility fracture

All women age 65 and older

Postmenopausal younger than 65 with risk factors

Men over 50 with risk factors

slide35

Treatment of Osteoporosis

1. Treament for primary factor or disease & regular exercise

2. medication:

- Enough dose of calcium + activated Vitamin D (1(OH)D3 or 1.25(OH)2D3)

- Estrogen threapy for type I osteoporosis

- Synthectic calcitonin

3. Fracture :

Avoid longterm bed rest

Early ambulation after firm internal fixation

medication
Medication

Bisphosphonates

Fosamax

Actonel

Didronel

Estrogen Replacement Therapy

Medications made from natural hormones

SERMs

Raloxifene (Evista)

Calcitonin

Sodium Flouride

medication under investigation
Medication-Under Investigation

Vitamin D metabolites

Parathyroid hormone

New bisphosphonates

New SERMs

ii chronic arthritis
II. Chronic Arthritis
  • Inflammation of a joint usually accompanied by pain swelling and changes in structure
  • Etiology
    • Degenerative Joint Disease
      • Osteoarthritis, Rheumatoid
    • Metabolic disturbances
      • Gout
    • Infection
      • Gonococcus, TB, Pneumonia
arthritis
Arthritis
  • 1. Classification:

major socio-ecomomic problem

I. Rheumatoid Arthritis (RA)

II. Degenerative arthritis

․Primary osteoarthritis

․Secondary osteoarthritis

III. Others :

Hemophilic Arthritis

Gouty Arthritis

Neuropathic or Charcot Joint

Chondrocalcinosis &Pseudogout

manifestations
Manifestations
  • Pain
  • Stiffness
  • Redness
  • Swelling
  • Knee effusions
  • Crepitus
rheumatoid arthritis1
Rheumatoid Arthritis
  • Chronic, Systemic Autoimmune Disease
    • Inflammation of the connective tissue,
    • Inflammation of the joint
  • Prevalence 0.5-1%
  • 30-50 yrs F>M
reason
Reason
  • unkonwn
  • Infectious : hemolytic and nonhemolytic types streptococci
  • Endocrine: this is suggested by response to adrenocortical steroids.
  • Autoimmune: frequently exhibit various allergic manifestations. = Eosinophilia is frequent.
  • Metabolic:
pathogen
pathogen
  • Diffuse proliferative synovitis

Villous processes hypertrophy -> necrotic &extruded into the joint .

  • Fibrinoid necrosis around withfibroblasts
  • ->fibrous tissue
  • Synovium making->pannus- cover the articular surface withfibrous connective tissue
  • Vascular granulation tissue ->growing from medullary->distruction articular cartilage
manifestations of ra
Manifestations of RA
  • Joint symptoms
    • Pain, swelling, stiffness (↑in morning)
    • Deformity and muscle atrophy
    • Limited ROM
  • Other Symptoms
    • Fatigue
    • Anorexia
    • Low-grade fever
    • Inflammatory changes of heart and lungs
slide49

3. Dx of RA: ACR classification criteria for RA

  • Morning stiffness at least 1 hour
  • Swelling of 3 or more joint
  • Swelling of hand joints (P.I.P M.C.P. or Wrist)
  • Symmetric joint swelling
  • Erosion or decalcification on radiograph of hand
  • Rheumatoid nodule
  • Presence of serum rheumatoid factor

1987 USA RA Association:

4 of more of sever criteria

diagnosis of ra
Diagnosis of RA
  • History and physical exam
  • Labs
    • Rheumatoid factors (RF)
    • ESR (Erythrocyte Sedimentation Rate)
    • Synovial fluid exam
  • X-rays
    • Symmetric periarticular osteoporosis
    • Narrowing joint space
    • Bony trabeculation bridge, obliterate the joint space: ankylosis
laboratory findings
Laboratory findings:
  • ESRî
  • Slight Leukocytosis, ±eosinophlilia (immune reaction)

usually normocytic,hypochromic anemia refractory to iron.

  • Alpha2 fraction of gamma globulin(RF, IgM gamma globulin against Fc portion of IgG) î

Serum albumin

Serum (because of the presence of abnormal macroglobulins called rheumatoid factors) will agglutinate or flocculate suspended particles such as hemolytic streptococci, sheep erythrocytes, latex, and with bentonite sensitized with human gama globulin

Latex fixation test on serum; unknown serum +gamma globulin-latex suspension

Inhibition test : rheumatoid serum of known high agglutinating activity + unknown euglobulin +standard gamma glubulin-latex suspension

slide52

4. RA 的病因和预后

① Pathogenesis of RA.

unknown

Genetic predisposition

Chromic antoimmune responces

② Indications of poor prognosis in RA.

reduced functional states

early radigraphic changes

multiple involved joints

older age at onset

high titiers of rhematoid factor

prolonged elevation of ESR

lower educational level

genetics

treatment of ra
Treatment of RA
  • NO CURE
  • Goals of Treatment
    • Relieve pain
    • Reduce inflammation
    • Stop or slow joint damage and deformity
    • Improve well-being and ability to function
slide54

5. RA medical treatment

  • ․NSAID
  • ․DMARD
  • ․Steroid
  • ․others
slide55

6. RA operative treatment

  • ․Synovectomy
  • ․Arthrodesis
  • ․Arthroplasty
what is gout
What is Gout?
  • Metabolic disorder
  • Inflammation 2° deposits of uric acid crystals in joint
  • Body produces too much uric acid
    • Or
  • Body excretes too little uric acid
what is uric acid
What is Uric Acid?
  • Uric acid is a waste product formed from the breakdown of purines
  • High levels of purines are found in organ meats (liver, brains, kidney), anchovies, herring, mackerel.
    • Alcohol and some drugs may affect purine excretion.
stage 1 asymptomatic hyperuricemia
Stage 1 Asymptomatic Hyperuricemia
  • Uric acid levels elevated to 9-10 range (normals ~ 3 – 6)
  • No symptoms
  • Client may not progress to symptomatic disease
stage 2 acute gouty arthritis
Stage 2Acute Gouty Arthritis
  • Sudden onset, acute pain, redness, swelling
  • Usually hits the big toe, may affect another joint
  • Fever, chills
  • Elevated WBC, sed rate
  • “Attack” lasts hours to weeks
  • 60% have recurrent attack in 1 yr
stage 3 chronic tophaceous gout
Stage 3Chronic Tophaceous Gout
  • Hyperuricemia untreated
  • Tophi (urate crystals deposits) develop in cartilage, synovial membranes, tendons, soft tissues
  • Pain, ulceration, nerve damage
  • Uric acid crystals—>kidney stones
slide62

Symptom:

hyperuricemia ( >7mg%). Several yrs

① acute: 1st metatarsophalangeal joint , sudden onset

* Intercritical Period: weeks -years

recurr factor: meat, high purine diet, drug, fatigue, trauma, surgery

② chronic: continuous slight pain, degenerative arthritis, fibrous ankylosing

slide63

Dx:

  • ① family history
  • ② Repeated attacks with intervals of freedom from pain
  • ③ Renal disturbance as urate calculus
  • ④ Hyperuricemia
  • ⑤ Satisfactory response to adequate doses of colchicine
  • ⑥ Sodium biurate crystals ( rod type, blunt ended, strong negative birefringence under polarized microscope, uricase digested) at joint aspirate ensure.
  • * tophi : subcutaneous tissue ->urate saltdeposit -> ear site ->chalky white material.
treatment of gout
Treatment of Gout
  • Pain
    • Indocin
    • NSAIDS, Narcotics
    • Steroids (po/intra-articular)
  • Interrupt urate crystal formation
    • Colchicine: Does NOT alter uric acid levels
  • Inhibit tubular reabsorption of uric acid
    • Probenecid (Benemid)
  • Reduce the production of uric acid
    • Allopurinol (Zyloprim)
treatment of gout attack continued
Treatment of Gout AttackContinued
  • Dietary Management
    • Drink 3-4 quarts of fluids daily
    • Avoid alcohol
    • Sometimes no diet is prescribed
      • Low purine diet
        • Meats, seafood, yeast, beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower, mushrooms
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