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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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Joint disease injury

JOINtDISeaSe& injury

Ri Long Jin

Joint disease injury

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 (

Joint disease injury


  • 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.

Joint disease injury


Normal Bone

Osteoporotic Bone

Joint disease injury

1.5 Million Fractures Annually

Vertebral Fractures:


Wrist Fractures:


Hip Fractures:


Other Fractures:


Source: National Osteoporosis Foundation, 2000






Source: National Osteoporosis Foundation, 2000

Joint disease injury








Courtesy of Michael Amling

Joint disease injury



- menopause

- hyperPTH



- aging



Bone Loss

Bone Loss



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


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



Vertebrae & distal radius



Secondary decrease

Related to menopause

> 70

2 : 1

Trabecular & cortical

Not accelerated

Not increased

Vertebrae & hip


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

Joint disease injury

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

Joint disease injury

Women married to a smoker


a 91% greater risk

of heart disease”

Joint disease injury



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

Health Canada

Joint disease injury

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

Joint disease injury

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


f. chronic phosphate-binding antacid use

g. anticonvulsant

European Osteoporosis Foundation


  • BMD test

  • Biochemical markers

    - Blood

    - urine

Joint disease injury

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

Joint disease injury

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


Procollagen type I propeptides

C-terminal (PICP)

N-terminal (PINP)

Bone resorption

Pyridinoline & Deoxypyridinoline

Type I collagen telopeptide




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

Joint disease injury

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






Estrogen Replacement Therapy

Medications made from natural hormones


Raloxifene (Evista)


Sodium Flouride

Medication under investigation
Medication-Under Investigation

Vitamin D metabolites

Parathyroid hormone

New bisphosphonates


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


  • 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


  • 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


  • 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:


  • 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

Joint disease injury

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

Joint disease injury

4. RA 的病因和预后

① Pathogenesis of RA.


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


Treatment of ra
Treatment of RA


  • Goals of Treatment

    • Relieve pain

    • Reduce inflammation

    • Stop or slow joint damage and deformity

    • Improve well-being and ability to function

Joint disease injury

  • 5. RA medical treatment

  • ․NSAID

  • ․DMARD

  • ․Steroid

  • ․others

Joint disease injury

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

Joint disease injury


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

Joint disease injury


  • 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