Curiculum Vitae

Nama : dr. Agus P Sambo, SpPD - KEMD

Tempat & tgl Lahir : Rantepao 4 Agustus 1951
Status : Nikah dengan 3 orang putri dan putra
Agama : Kristen
Pendidikan
SMA : Rantepao 1971
Dokter umum : FK Universitas Indonesia 1977
Ahli Penyakit Dalam : FK Universitas Indonesia 1989
Konsultan Endokrinologi : PAPDI 2006
Pekerjaan : Tugas di RS Luramay, RS Stella Maris RS
Hermina, Makassar
OSTEOPOROSIS

Agus P Sambo
 Introduction to Osteoporosis
During bone turn-over, osteoclastic activity > osteoblastic
activity
WHO : A disease characterised by
low bone mass and
micro-architectural deterioration of bone tissue, leading to
enhanced bone fragility and a consequent
increase in fracture risk

3
 Introduction to Osteoporosis

Bone mass:

Increases till late 20’s or

early 30’s

Relatively constant between

30-50 years of age

Accelerated bone loss in females around menopause (3-5% per year), subsequent
slower decline (1-2%)

4
Introduction to Osteoporosis
Bone Mass decreases with age after 50
Osteoporosis prevalence increases with age

Women between age

50-59, = 4%
60-69, = 8%
70-79, = 25%
> 80, = 48%

5
 Introduction to Osteoporosis
Projected
Hip Fracture Incidence is Increasing to reach
3.250 million
Projected worldwide increase
in Asia
by 2050
800
700
Total no of hip fractures:
600
1950 = 1.66 million
500
2050 = 6.26 million
400 1950
2050
Estimated no of hip 300
fractures: (1000s) 200

100

0
North Europe Latin
From Cooper C. et al, 1992, America America
Asia 6
Osteoporos Int. 2(6):285-289.
Age-related bone development
in men and women
I Men
1,500

I III
Bone mass (g/calcium)

Women
1,000
II

III

500
I Peak bone mass
II Rapid bone loss (menopause)
III Age-related bone loss
0
0 20 40 60 80 100
Age (years)
Factors affecting bone strength:
bone mass and bone quality

Bone Bone Bone

quality + mass = strength

Osteoporosis is defined as a skeletal disorder

characterised by compromised bone strength
predisposing to an increased risk of fracture

Osteoporosis prevention, diagnosis and therapy.

NIH consensus statement 2000;17:9
Determinants of Peak Bone Mass

Genetics

PEAK BONE MASS

Nutrition Hormones
20-22 years of age

Lifestyle
Normal bone remodelling
Pre- Pre- 6H, PTH, IL-1
osteoclast osteoblast IL-6, -E2, T3
IL-6

Growth factors
IL-6 Osteoblast Binding protein
Osteoclast

60µm H+ Proteases

Binding Growth Binding Growth

protein factors protein factors
30µm

Resorption Formation
20 days 160 days

Rosen C. In: Marcus R, et al. Ed. Osteoperosis, Atlas of Clinical

Endocrinology, volume 3. Blackwell Science Publisher 2000.
 Bone remodeling
Bone marrow precursors
Mesenchymal cells Hematopoietic cells

Osteoclast
Osteoblast Lining cells
Pathogenesis of osteoporosis

Resorbed cavity Newly formed packet

too large of bone too small

Formation does not Increased numbers of

match resorption remodeling units

INCREASED BONE LOSS

 WHAT ARE
THE CLINICAL RISK FACTORS?
Previous fractures – serious risk factor
Sex
Age
Ethnic
Smoking
Caffeine
Drug therapy
Other diseases
 What Causes Osteoporosis?
Lifestyle - Sedentary lifestyle; too little exercise
- Vitamin D AND Calcium-poor diet
- Smoking
- Excessive alcohol intake
Medication - steroids, excessive thyroxine, anti-convulsants

Medical illnesses
- early natural/surgical menopause
- Hyperthyroidism, hyper-parathyroidism, Cushing’s
- CRF, COPD, RA, liver disease, malabsorption syndromes
- Serious illness with prolonged bed rest, anorexia nervosa

Family history of osteoporosis

14
CLASSIFICATION OF OSTEOPOROSIS

Primary osteoporosis
Most common types of fractures
– spine, forearm, hip – no identified cause

Secondary osteoporosis
Osteoporosis occur in the setting of an illness or a
recognized cause of osteoporosis
(Cushing, multiple myeloma)
 Age-related bone loss
Dietary calcium intake Vitamin D intake and synthesis

Calcium absorption Estrogen deficiency

Plasma calcium PTH secretion

Bone turnover and resorption

BONE LOSS
 Secondary osteoporosis

Endocrine Nutritional Drug-induced Immobilization Others

Hyperthyroidism Glucocorticoids Rheumatoid A.

Hypogonadism Immunosuppressly Diabetes
Cushing Syndrome Anticonvulsants Tumors
(Myeloma, etc.)
Symptoms
Osteoporosis is asymptomatic
: silent disease
Osteoporosis are usually
symptomatic of fracture

Age 40 Age 60 Age 70

Progression of vertebral
fractures in osteoporosis

http://www.osteofound.org
 PMO

1959 1989 1996

Inger Lundegaardh, Sweden

http://www.osteofound.org
DIAGNOSIS
OF OSTEOPOROSIS
DIAGNOSIS OF OSTEOPOROSIS

CLINICAL HISTORY AND PHYSICAL FINDINGS

BIOCHEMICAL MARKERS
BONE IMAGING
DIAGNOSIS
CLINICAL HISTORY – PHYSICAL FINDINGS
Able to diagnose only in its advanced stages
Often the diagnose is not made until the occurrence of
the first fracture
The first fracture is a major risk factor for subsequent
fractures
The goal is to diagnose osteoporosis before the first
fracture occurs
Although clinical risk factors correlate with BMD,
osteoporosis can not be diagnosed by risk factors

Conclusions
“clinical history and physical findings
can not be used for the diagnosis of osteoporosis”
DIAGNOSIS
BIOCHEMICAL MARKERS

At present cannot be used to diagnose osteoporosis

The primary use for biochemical markers is for monitoring
the response to treatment
DIAGNOSIS
BONE IMAGING

At present the mostly used bone imaging are

Quantitative ultrasound (QUS)

Dual energy X-ray absorbtiometry (DEXA)
No single technology is likely to be ideal, particularly with
respect to cost an availability (Johnston CC, Amer J Med 1995)

DEXA is now the gold standard for the diagnosis

of osteoporosis
Quantitative computed Tomography (QCT)
DEXA – “gold standard” untuk diagnosis osteoporosis
DEXA – “gold standard” untuk diagnosis osteoporosis
Diagnotic osteoporosis with USG
Diagnotic osteoporosis with USG
 CLASSIFICATION OF
BONE MINERAL DENSITY LEVELS

DESCRIPTIONS MEANING

Normal BMD BMD above – 1 SD from the

young normal mean

Low BMD or osteopenia BMD between - 1 SD and –

2.5 SD
Osteoporosis BMD is reduced < – 2.5 SD

Severe or established BMD is reduced < – 2.5 SD in

osteoporosis the presence of fractures

WHO Technical Report Series. Geneva: WHO, 1994

DIAGNOSIS
BONE IMAGING

Normal Osteoporosis
 Scanning electron microscopy
of normal and osteoporotic bone
Normal Osteoporotic

Dempster DW, et al. J Bone Miner Res 1986;1:15–21

http://www.helenhayeshospital.org/rbcmain.html
WHY SHOULD WE TREAT
OSTEOPOROSIS
WHY SHOULD WE TREAT OSTEOPOROSIS ?

BP Cholesterol BMD

Stroke CHD Fractures

Neurologist Cardiologist Surgeon

“Like hypertension, hypercholesterolemia,

osteoporosis is preventable and treatable”
WHEN TO TREAT
 Risk Assessment

BMD Osteopaenia consider prevention

alone If asymptomatic, unsuitable or
undecided, consider repeat BMD
after 1-2 yrs to assess rate of bone
loss.
< -2.5 consider treatment
Some Clinical Risk Factors to consider before initiating medication

Factors Tend to treat if Tend to defer if

Fracture risk high low
Past fracture present absent
BMD low (T-score <-2.5, ?-2.0) high
Age older (e.g. >65 years) younger
Falls risk / bone loss high low 36
 Treatment objectives
Osteoclast Osteoblast

Inhibition of resorption Stimulation of formation

Treatments of osteoporosis
• Calcium and vitamin D
• HRT Hormonal agents
• SERMs (raloxifene)
• Calcitonin
• Bisphosphonates
– ibandronate Anti-resorptive
– etidronate agents
– alendronate
– risedronate
• PTH (1–34)
Anabolic agents
• Fluoride
• Strontium ranelate
Dual mechanism of
• Combination action
• Denosumab SERMs = selective oestrogen receptor modulators
PTH = parathyroid hormone
PREVENTION

• Smoking cessation

• Exercise

• Calcium and vitamin D