Problem-Based Learning (PBL)

Tutorial 1
Scenario 1
Group 4
Member :
1. Mellyana 2. Febriana Qolbi 3. Aisyah Triansari 4. Feblin Versiliantina 5. Ginda Chitra Puspita 6. Tiara Anggita Q 7. Aulia Shahnaz 8. Gerry Irawan 9. Likoh 10. Joande Necisa 11. Nevinia Ann A/P Robert 54081001002 54081001015 54081001027 54081001029 54081001030 54081001034 54081001064 54081001095 54081001099 54081001102 54081001110

Medical Faculty Sriwijaya University

2008 - 2009

Scenario D Mrs. Fatimah, 70 years old, 43 kilograms body weight, 165 centimeters height, came to your practice room with complaints of pain to spine for 7 days duration. There were no recognizable factors which might have precipitated the pain, and the symptoms seemed to appear spontaneously. No definite history of antecedent trauma or pre-existing disease was obtained. The episode of pain began gradually. The pain became more severe over a period of 2 weeks to a month. Morning stiffness was not present. She still lives alone and always consumed coffee. I am a smoker so I must drink coffe more than common people. She had got menopause since 20 years ago. From physical examination is completely notrmal. Her lumbosakral radiologic examination was compresi fracture on L2-L5. Densitometri from femur : T Score -4, from radius : -3.7

I. Term Clarification Pain to spain Pain in vertebral coloumn Antecedent trauma / pre existing disease A trauma / disease yang di dahului trauma sebelumnya Morning stiffness Difficulty in moving the joint or stretching a muscle in the morning Menopause The time in a womans life when the ovaries cease to produce an egg cell every 4 weeks Lumbosakral Radiologic Radiology of relating to part of the spine composed of the sacrum Densitometri An imaging techique that uses low-dose X-rays to measure bone density Compresi fracture

II. Problem Identification

1.

Mrs. Fatimah, 70 years old, 43 kilograms body weight, 165 centimeters height, complaints of pain to spine for 7 days duration, pain spontaneously, no recognizable factors which might have precipitated the pain, no definite history of antecedent trauma, the pain became more severe over a period of 2 weeks to a month.

2. 3. 4.

She still lives alone and had got menopause since 20 years ago She always consumed coffee and a smoker From physical examination is completely notrmal. Her lumbosakral radiologic examination was compresi fracture on L2-L5. Densitometri from femur : T Score -4, from radius : -3.7

III. Problem Analysis 1. a. What is the BMI of Mrs. Fatimah? Berat badan normal = TB 110 (untuk TB > 160cm) = 165 110 = 55kg Berat badan ideal menurut Broca = (TB - 100) 10% (TB - 100) = (165 - 100) 10% (165 - 100) =58.5 kg (dengan batas ambang 10%) BMI = BB / TB2 = 43 kg / 1.65 = 26.06 b. What is the correlation between her age and complaint of pain to spine? Pertambahan usia, fungsi organ tubuh menurun. Pada wanita usia 75 85 tahun, wanita memiliki risiko dua kali lipat dibandingkan pria dalam mengalami kehilangan tulang trabekular karena proses penuaan, penyerapan kalsium menurun, fungsi hormon paratiroid meningkat dan hormon estrogen menurun c. Mengapa sakit datang dan pergi? d. mengapa dalam waktu 7 hari sakitnya berlanjut? e. apa mekanisme pain dalam kasus ini ? f. mengapa pain terjadi secara spontan tanpa sebab yang jelas? Answer for all : Fraktur adalah terputusnya kontinuitas jaringan tulang dan/atau tulang rawan. Fraktur juga berarti pemecahan suatu bagian terutama tulang atau kerusakan pada

tulang. Fraktur yang terjadi biasanya di daerah vervical dan lumbal, tempat yang mungkin dilakukan tarikan maximal dari columna vertebralis. Di daerah cervical, dengan leher yang lurus, sebuah gaya vertikal yang berlebihan dari atas dapat menyebabkan arcus atlantis cedera dan massa lateralis atlantis terdorong ke lateral (fraktur Jefferson). Jika leher sedikit fleksio, vertebra cervicalis bagian bawah tetap berada dalam garis lurus dan beban kompresi diteruskan ke vertebra yang lebih bawah, tetapi tidak menyebabkan cedera discus invertebralis dan pecahnya corpus vertebrae. Fraktur kompresi tanpa cedera atau fraktur patologis terjadi pada kasus osteoporosis. Ketika terjadi fraktur tersebut sakit bisa datang dan pergi secara spontan tanpa sebab yang jelas dikarenakan bentuk fraktur kompresi yang pada tulang spongiosa dan garis patah fraktur lebih dari satu yang saling berhubungan, fraktur kominutif. Terjadi juga fraktur undisplaced (tidak bergeser) yang menyebabkan garis patah komplit tetapi kedua fragmen tidak bergeser, periosteumnya masih utuh yang menyebabkan rasa sakit yang semakin menjadi selama tujuh hari. 2. a. Apakah normal menopause saat berumur 50 tahun?

b. Apa hubungan menopause dengan sakitnya? c. Apa hubungan tidak menikah dengan sakitnya? d. Apakah orang yang menikah mempunyai kesempatan lebih besar terkena menopause daripada yang tidak menikah? 3. a. Apa hubungan antara konsumsi lebih kopi dan merokok dengan

sakit yang dirasakannya? b. Hormon apa yang terganggu pada konsumsi kopi dan merokok? c. Kandungan apa saja yang ada di kopi dan merokok yang menyebabkan sakit yang dirasakannya? d. Cara kerja dari kopi dan merokok yang menyebabkan sakit yang dirasakan? Answer for all : 1. Merokok Rokok bisa meningkatkan risiko penyakit osteoporosis. Perokok sangat mudah terkena osteoporosis, karena zat nikotin dan TAR di dalamnya mempercepat penyerapan sel tulang. Selain penyerapan tulang, nikotin juga membuat kadar dan aktivitas hormon estrogen dalam tubuh berkurang

sehingga susunan susunan sel tulang tidak kuat dalam menghadapi proses pelapukan. Rokok juga membuat penghisapnya bisa mengalami hipertensi, penyakit jantung, dan tersumbatnya aliran darah ke seluruh tubuh. Kalau darah sudah tersumbat, maka proses pembentukan tulang sulit terjadi. 2. Minum kopi Unsur utama dalam kopi adalah kafein konsumsi kafein berlebih berkontribusi pada meningkatnya kehilangan kalsium dari tubuh. Asupan kafein lebih dari 2 cangkir sehari seumur hidup berhubungan dengan rendahnya densitas (kepadatan) massa tulang wanita usia lanjut. Dampak negatif kafein pada masa tulang lebih besar pada wanita yang tidak minum susu. Wanita yang berisiko tinggi terhadap osteoporosis dan kurang asupan kalsium perlu membatasi kafein. 4. a. examination? b. apa working diagnosis, diagnosis, prognosis, complication, management and risk factor dari hasil physical examination and radiologic examination? c. apa mekanisme pain yang dirasakan? d. apa penyebab keropos dan physiology tulang? e. hormon yang berpengaruh? f. bagaimana nutrisi dan metabolismenya? g. bagaimana prevention di semua usia? h. bagaimana sistem neuromuscularskeletal? IV. Hypothesis Mrs. Fatimah, 70 years old, came with complaint of pain to spine 7 days due to osteoporosis V. Learning Issue a. Lumbosakral and compression fracture b. Osteoporosis c. Hormon and nutrition Apa interpretasi dari physical examination and radiologic

VI. Synthesis 1. Lumbosakral and compression fracture The human spinal cord is divided into 31 different segments. At every segment, right and left pairs of spinal nerves (mixed; sensory and motor) form. 68 motor nerve rootlets branch out of right and left ventro lateral sulci in a very orderly manner. Nerve rootlets combine to form nerve roots. Likewise sensory nerve rootlets form off right and left dorsal lateral sulci and form sensory nerve roots. The ventral (motor) and dorsal (sensory) roots combine to form spinal nerves(mixed; motor and sensory), one on each side of the spinal cord. Spinal nerves, with the exception of C1 and C2 form inside intervertebral foramen (IVF). Note that at each spinal segment the border between the central and peripheral nervous system can be observed. Rootlets are a part of the peripheral nervous system. There are 31 (Some EMS text say 26, counting the sacral as one solid piece) spinal cord nerve segments in a human spinal cord:

8 cervical segments forming 8 pairs of cervical nerves (C1 spinal nerves exit spinal column between occiput and C1 vertebra; C2 nerves exit between posterior arch of C1 vertebra and lamina of C2 vertebra; C3-C8 spinal nerves through IVF above corresponding cervica vertebra, with the exception of C8 pair which exit via IVF between C7 and T1 vertebra)

12 thoracic segments forming 12 pairs of thoracic nerves (exit spinal column through IVF below corresponding vertebra T1-T12) 5 lumbar segments forming 5 pairs of lumbar nerves (exit spinal column through IVF, below corresponding vertebra L1-L5) 5 (or 1) sacral segments forming 5 pairs of sacral nerves (exit spinal column through IVF, below corresponding vertebra S1-S5) 1 coccygeal segment forming 1 pair of coccygeal nerves (exit spinal column through the sacral hiatus)

Because the vertebral column grows longer than the spinal cord, spinal cord segments do not correspond to vertebral segments in adults, especially in the lower spinal cord. In the fetus, vertebral segments do correspond with spinal cord segments. In the adult, however, the spinal cord ends around the L1/L2 vertebral level, forming a structure known as the conus medullaris. For example, lumbar and sacral spinal cord segments are found between vertebral levels T9 and L2. Although the spinal cord cell bodies end around the L1/L2 vertebral level, the spinal nerves for each segment exit at the level of the corresponding vertebra. For the nerves of the lower spinal cord, this means that they exit the vertebral column much lower (more caudally) than their roots. As these nerves travel from their respective roots to their point of exit from the vertebral column, the nerves of the lower spinal segments form a bundle called the cauda equina. There are two regions where the spinal cord enlarges:

Cervical enlargement - corresponds roughly to the brachial plexus nerves, which innervate the upper limb. It includes spinal cord segments from about C4 to T1. The vertebral levels of the enlargement are roughly the same (C4 to T1).

Lumbosacral enlargement - corresponds to the lumbosacral plexus nerves, which innervate the lower limb. It comprises the spinal cord segments from L2 to S3, and is found about the vertebral levels of T9 to T12.

Vertebral Fractures : An accurate assessment of the incidence of vertebral fracture is difficult as most patients do not necessarily get admitted to hospital and the criteria for diagnosis are not clearly defined. It is generally believed that only about a third of all vertebral deformities noted on x-rays come to medical attention, and less than 10% necessitate admission to hospital. The data from the United States and Europe, in women over the age 60 years demonstrate a two to three fold greater incidence of vertebral fracture than men. The lifetime risk of a clinically diagnosed vertebral fracture is about 16% in white women compared with just 5% in white men. A recent study on the Chinese population suggest the risk of vertebral fracture among post menopausal women in Beijing is about 25% lower than that noted in Minnesota even though incidence of hip fractures in China is just one eighth of that in women from Minnesota. As anticipated the cause of fractures in the vertebra are much less related to falls and it is estimated that only a quarter of such vertebral fractures result from falls and most are precipitated by routine everyday activities of daily living21. The likelihood of fracture of a vertebra depends on the compressive strength of a vertebral body and is partly determined by the bone density and each standard deviation drop is associated with twice the risk of fracture. It is also believed that occurrence of one vertebral fracture, even in asymptomatic individuals detected incidentally on a routine radiograph increases the likelihood of additional fracture by at least fourfold. This increased risk is apparently not dependent on bone density, which suggests the quality of the bone may be more important in the pathogenesis of these fractures in the vertebra rather than the bone density alone. Lumbar Vertebrae The spine is made up of three groups of bones called "vertebrae." There are five "lumbar vertebrae" in the small of the back (loins). Since the lumbars must support more weight than the vertebrae above them, they have developed larger and stronger bodies. The transverse processes of these vertebrae project backward at sharp angles, while their short, thick spinous processes are directed nearly horizontally.

Lumbar Spine Fracture of the lumbar spine can occur whenever forces applied to the lower spinal column exceed the strength and stability of the spinal column unit. Common injuries resulting in fractures of the lumbar spine include fall from a height; motor vehicle and motor vehicle and pedestrian accidents; and penetrating trauma, including gunshot wounds and stabbings. Unstable injuries to the pelvis often are associated with injury to the sacral plexus and the lower lumbar spine. The spine is one of the strongest and of the most important parts of the body. Every organ relies on the support of the spine like the chassis of a car. The wellness of the body is based on the right posture of the spine and alignment of the spine, since eighty-five percent all of symptoms are due to spinal blockages. The spine consists of seven cervical, twelve vertebra, five lower lumbers, five sacral, and four coxies including the tailbone. Each and every joint of the spine represents a different organ. For instance if any nerves or veins due to wrong posture is blocked in vertebrae four. You will have problems with your speech. In the same way if vertebrae one through four and five have blockages, it will affect your lower back, you will suffer from tremendous back pain, noticing difficulty in walking and sitting due to the pain. The spinal cord is lubricated with the cerebral fluid starting from the lower lumber to cervical. This natural lubricant must be flowing without obstruction to enable the spine functioning properly. Seventy-three nerves are parallel to the spine, which assists, in the proper circulation to all the parts of the body. It is imperative that the nerves are free of blockages and plaque since they carry the required minerals and vitamins to every system of the body. Wherever the nerves are blocked, for example, your lower back hurts then your lower back it is not receiving the proper circulation resulting in the minerals and vitamins unable to nourish your lower back. The chemistry of the body is changed, symptoms and disease occur until the nerves are unblocked. Sacrum The sacrum is a large triangular bone at the base of the lower spine. Its broad upper part joins the lowest lumbar vertebrae and its narrow lower part joins the coccyx or "tail bone". The sides are connected to the iliums (the largest bones forming the pelvis). The sacrum is a strong bone and rarely fractures. The five vertebrae that make up the sacrum are separated in early life, but gradually become fused together between the eighteenth and thirtieth years. The spinous processes of these fused bones are represented by a ridge

of tubercles. The sacrum is wedged between the coxal bones of the pelvis and is united to them by fibrocartilage at the sacroiliac joints. The weight of the body is transmitted to the legs through the pelvic girdle at these joints. What are the symptoms of a compression fracture of the spine? Back pain is by far the most common problem in patients with a compression fracture. Patients with osteoporosis who sustain multiple compression fractures may begin to notice a curving of the spine, like a hunchback, called a kyphotic deformity. The reason for this is the vertebrae are compressed in front, and usually normal in back. This wedge shaped appearance causes the spine to curve forward. When enough compression occurs, this may become a noticeable curvature. Patients with compression fractures also often notice a loss of their overall height because of the decreased size of the spinal column. Nerve complaints are unusual in compression fractures because the spine and its nerves are behind the vertebra, and, as mentioned above, the front of the vertebra is compressed and the back remains normal. In some serious traumatic fractures, called "burst fractures," the compression occurs around the spinal cord and nerves. This is more serious and may require immediate treatment to prevent or relieve pressure on the spinal cord or nerves. 2. Osteoporosis What is osteoporosis? Osteoporosis means porous bones. It is a condition where the skeleton becomes fragile and results in broken bones under normal use. Osteoporosis is a silent condition that happens slowly over years. The rate of bone loss resorption exceeds the rate of new bone formation acretion. Many times neither a person nor a doctor is aware of weakened bones until one breaks unexpectedly. What are the symptoms of osteoporosis? Because of mineral loss, osteoporosis can cause progressive breaks in a persons back. This causes a person to lose height and get shorter and shorter. This spinal compression causes a gradual decrease in height due to forward bending of the upper spine. This eventually results in a painful, stooped back, commonly referred to as a dowagers hump. And, loss of height can also result in a pot belly or a prominent abdomen even with no increase in weight.

What happens to bones with osteoporosis? Most people think of their bones as completely solid and unchanging. This is not true. Your bones are constantly changing as they respond to the way you use your body. As muscles get stronger, the bones underneath them get stronger, too. As muscles lose strength, the bones underneath them weaken. Changes in hormone levels or the immune system can also change the way the bones degenerate and rebuild themselves. As a child, your bones are constantly growing and getting denser. At about age 25, you hit your peak bone mass. As an adult, you can help maintain this peak bone mass by staying active and eating a diet with enough calories, calcium, and vitamin D. But maintaining this bone mass gets more difficult as we get older. Age makes building bone mass more difficult. In women, the loss of estrogen at menopause can cause the bones to lose density very rapidly. The bone cells responsible for building new bone are called osteoblasts. Stimulating the creation of osteoblasts helps your body build bone and improve bone density. The bone cells involved in degeneration of the bones are called osteoclasts. Interfering with the action of the osteoclasts can slow down bone loss. In high-turnover osteoporosis, the osteoclasts reabsorb bone cells very quickly. The osteoblasts cant produce bone cells fast enough to keep up with the osteoclasts. The result is a loss of bone mass, particularly trabecular bone--the spongy bone inside vertebral bones and at the end of long bones. Postmenopausal women tend to have highturnover osteoporosis (also known as primary type one osteoporosis). This relates to their sudden decrease in production of estrogen after menopause. Bones weakened by this type of osteoporosis are most prone to spine and wrist fractures. In low-turnover osteoporosis, osteoclasts are working at their normal rate, but the osteoblasts arent forming enough new bone. Aging adults tend to have low-turnover osteoporosis (also known as primary type two osteoporosis). Hip fractures are most common in people with this type of osteoporosis. Secondary osteoporosis describes bone loss that is caused by, or secondary to, another medical problem. These other problems interfere with cell function of osteoblasts and from overactivity of osteoclasts. Examples include medical conditions that cause inactivity, imbalances in hormones, and certain bone diseases and cancers. Some medications, especially long term use of corticosteroids, are known to cause secondary osteoporosis due to their impact on bone turnover.

Osteoporosis creates weak bones. When these weak bones are stressed or injured, they often fracture. Fractures most often occur in the hip or the bones of the spine (the vertebrae). They can also occur in the upper arm, wrist, knee, and ankle. What is characteristic of osteoporosis?
Umur : kerusakan tulang Bone turnover Lokasi fraktur Fungsi paratiroid Fungsi estrogen Etiologi utama Tipe 1 50 75 6:1 Terutama trabekular Tinggi Vertebra, radius distal Menurun Terutama skeletal Defisiensi estrogen Tipe 2 >70 2:1 Trabekular dan kortikel rendah Vertebral, kolum femoris meningkat Terutama ekstraskletal Penuaan, defisien estrogen

Patogenesis osteoporosis tipe 1 Setelah menopause, maka reabsorpsi tulang akan meningkat, terutama pada dekade awal setelah menopause sehingga insiden fraktur, terutama fraktur vertebra dan radius distal meningkat. Penuaan densitas tulang terutama pada tulang trabekular, karena memiliki permuakaan yang luas dan hal ini dapat dicegah dengan terapi sulih estrogen. Petanda resorpsi tulang dan fromasi tulang keduanya meningkat menunjukkan ada bone turnover. Estrogen juga berperan menurunkan produksi berbagai sitokin oleh bone marrow stromal cell dan sel sel mononuklear, seperti IL-1, IL-6, dan TNF yang berperan meningkatkan kerja osteoklas. Dengan demikian penurunan kadar estrogen akibat menopause akan meningkatkan produksi berbagai sitokin tersebut sehingga aktivitas osteoklas meningkat. Menopause Estrogen Bone marrow stromal cell + sel mononuklear osteoblas Sel endotel osteoklas Reabsorpsi kalsium Reabsorpsi di ginjal

TGF

NO Hipokalsema

HIL-1, TNF , IL6, M-CSF

 reabsorpsi tulang osteoporosis Patogenesis osteoporosis tipe 2 Selama hidupnya seorang wanita akan kehilangan tulang spinalnya sebesar 42 % dan kehilangan tulang femurnya sebesar 58 %. Pada dekade kedelapan dan sembilan kehidupannya, terjadi ketidakseimbangan remodeling tulang, dimana resorpsi tulang meningkat, sedangkan formasi tulang tidak berubah atau menurun. Hal ini akan menyebabkan kehilangan massa tulang, perubahan mikroarsitektur tulang dan peningkatan risiko fraktur. Peningkatan resorpsi tulang merupakan risiko fraktur yang independen terhadap BMD. Peningkatan osteokalsin seringkali didapatkan pada orang tua, tetapi hal ini lebih menunjukkan peningkatan turnover tulang dan bukan peningkatan formasi tulang. Defisiensi kalsium dan vitamin D sering didapatkan pada orang tua. Hal ini disebabkan oleh asupan kalsium dan vitamin D yang kurang, anoreksia, malabsorpsi dan paparan sinar matahari yang rendah. Aspek nutrisi yang lain adalah defisiensi protein yang akan menyebabkan penurunan sintesis IGF-1. Defisiensi vitamin K juga akan menyebabkan osteoporosis karenan akan meningkatkan karboksilasi protein tulang, misalnya osteokalsin. Defisiensi estrogen adalah salah satu penyebab osteoporosis. Pada laki laki estrogen berfungsi mengatur resorpsi tulang, sedangkan estrogen dan progesteron mengatur formasi tulang. Kehilangan massa tulang trabekular pada laki laki berlangsung linier, sehingga terjadi penipisan trabekula tanpa disertai putusnya trabekula seperti pada wanita. Putusnya trabekula pada wanita disebabkan karenan peningkatan resorpsi yang berlebihan akibat penurunan kadar estrogen yang drastis ketika menopause. Faktor lain yang juga ikut berperan pada kehilangan massa tulang pada orang tua adalah faktor genetik dan lingkungan (merokok, alkohol, obat obatan, imobilisasi lama). Dengan bertambahnya umur, remodelling endokortikal dan intrakortikal akan meningkat, sehingga kehilangan tulang terutama terjadi pada tulang kortikal dan meningkatkan risiko

diferensiasi dari muturasi osteoklas

fraktor tulang kortikal, misalnya pada femur proksimal. Total permukaan tulang untuk remodelling tidak berubah dengan bertambahnya umur, hanya berpindah dari tulang trabekular ke tulang kortikal. Risiko fraktur karena terjatuh juga harus diperhatikan. Usia lanjut Defisiensi vitamin D, aktifitas 1- hidroksilase, resistensi terhadap vitamin D reabsorpsi Ca di ginjal sekresi GH dan IGF 1 aktifitas fisik sekresi estrogen Hiperparatiroidosme sekunder absorpsi Ca di usus

osteoporosis

Fraktur

terjatuh

What are the risk factors for osteoporosis you cant control? Unchangeable risk factors are: gender: being female; women are five times more likely to develop osteoporosis than men. lack of exercise: bedridden people lose bone faster than people who exercise regularly having a thin, small-boned frame family history of older family members with broken bones or stooped posture, especially women, which suggests osteoporosis history of disordered eating that may have contributed to a loss of regular menstrual cycles an early menopause in women before age 45 due to estrogen deficiency, either naturally or resulting from surgical removal of the ovaries and not treated with hormone replacement therapy race: Caucasian and Asian women are at highest risk while African and Hispanic women are at lower risk

 prolonged use of some medications such as glucocorticoids (prednisone) used as an antiinflammatory to treat asthma or arthritis, excessive thyroid hormone, and some antiseizure medications; and antacids that contain aluminum age: the risk of osteoporosis increases with age low testosterone level (in men) not treated with hormone therapy Those listed above are risk factors you cant control. Are there other risk factors that you can control? Yes, you can control these risk factors with lifestyle changes. Here are some suggestions: get foods that are rich in calcium and vitamin D dont smoke or quit smoking if you drink alcohol, do so in moderation get regular weight bearing and resistance exercise avoid excess protein intake avoid extreme dieting that can lead to loss of regular mestrual cycles avoid excessive soda pop intake which contains phosphoric acid How is osteoporosis diagnosed? Dual energy X-ray absorptiometry (DXA, previously DEXA) is a means of measuring bone mineral density (BMD). Two X-ray beams with differing energy levels are aimed at the patient's bones. When soft tissue absorption is subtracted out, the BMD can be determined from the absorption of each beam by bone. Dual energy X-ray absorptiometry is the most widely used and most thoroughly studied bone density measurement technology. A T-score equal to or less than -2.5 is indicative of osteoporosis. This test is very reliable. Special considerations are involved in the use of DXA to assess bone mass in children. Specifically, comparing the bone mineral density of children to the reference data of adults (to calculate a T-score) will underestimate the BMD of children, because children have less bone mass than fully developed adults. This would lead to an over diagnosis of osteopenia for children. To avoid an overestimation of bone mineral deficits, BMD scores are commonly compared to reference data for the same gender and age (by calculating a Z-score). Also, there are other variables in addition to age which are suggested to confound the interpretation of BMD as measured by DXA. One important confounding variable is bone size. DXA has been shown to overestimate the bone mineral density of taller subjects and underestimate the bone mineral density of smaller subjects. This error is due to the way in

which DXA calculates BMD. In DXA, bone mineral content (measured as the attenuation of the X-ray by the bones being scanned) is divided by the area (also measured by the machine) of the site being scanned. Because DXA calculates BMD using area (aBMD: areal Bone Mineral Density), it is not an accurate measurement of true bone mineral density, which is mass divided by a volume. In order to distinguish DXA BMD from volumetric bone-mineral density, researchers sometimes refer to DXA BMD as an areal bone mineral density (aBMD). The confounding effect of differences in bone size is due to the missing depth value in the calculation of bone mineral density. Despite DXA technology's problems with estimating volume, it is still a fairly accurate measure of bone mineral content. Methods to correct for this shortcoming include the calculation of a volume which is approximated from the projected area measure by DXA. DXA BMD results adjusted in this manner, are referred to as the bone mineral apparent density (BMAD) and are a ratio of the bone mineral content versus a cuboidal estimation of the volume of bone. Like aBMD, BMAD results do not accurately represent true bone mineral density, since they use approximations of the bone's volume. BMAD is used primarily for research purposes and is not yet used in clinical settings. Other imaging technologies such as Computed Quantitative Computer Tomography (QCT) are capable of measuring the bone's volume, and are therefore not susceptible to the confounding effect of bone-size in the way that DXA results are susceptible. DXA uses X-rays to assess bone mineral density. However, the radiation dose is approximately 1/10th that of a standard chest X-ray What can you do to prevent osteoporosis? Osteoporosis cant be prevented outright. However, the onset of this condition can be delayed and the severity reduced. Calcium intake is critical in childhood as well as young adulthood. Calcium cant build bone by itself; vitamin D is also required. And a lifelong habit of weightbearing exercise such as walking or resistance exercise, also helps build and maintain strong bones. Is there a cure for osteoporosis? There is no cure for osteoporosis. However, the onset of this condition can be delayed. And, early intervention can prevent bone fractures. What kinds of treatments are available for a person with osteoporosis? Drug treatments?

For many years, the only choices for drug treatment of osteoporosis were the hormones estrogen and calcitonin. Estrogen replacement therapy (ERT) is the best prevention for the drop in bone mass at menopause. Estrogen not only helps prevent osteoporosis, but also protects against heart disease. However, some 3050% of women are concerned about taking estrogen. These women may have risk factors which make them more likely to get cancer if they take estrogen. They now have other treatment options. A non-hormonal treatment, Alendronate marketed as Fosamax, slows down bone breakdown by inhibiting osteoclast activity. Its been shown to increase bone mass as much as 8% and reduce fractures by 30-40%. Studies are still ongoing to determine its effectiveness and side effects. Non-drug treatments or supplements? Calcium and vitamin D supplements are an integral part of all treatments for osteoporosis. Calcium carbonate supplements are best (e.g., Oscal, Caltrate, Tums) absorbed in doses of 500 milligrams or less taken with meals. Calcium citrate (e.g., Citrical) can be taken between meals. In addition, diet and exercise are important not only for treatment but for prevention. What foods can I eat to prevent osteoporosis? Bone health requires a lot of nutrients and youre likely to get most of them in dairy products. For those concerned with lowering the fat in their diet, low fat and nonfat dairy products are still excellent sources of calcium and vitamin D. The best recommendation for overall good health includes a balanced and varied diet with foods adequate in calcium, protein, vitamins and minerals, and eating in moderation. Other ways to get CALCIUM into your diet especially if you dont consume dairy productsis to eat foods fortified with calcium, such as orange juice, or take calcium supplements. Other good sources of calcium are: broccoli dark-green leafy vegetables like kale tofu, calcium fortified canned fish with bones fortified bread and cereal products How much calcium do I need each day? The recommended dietary reference intakes from the National Academy of Sciences for adults is 1,000 to 1,300 milligrams a day with hormone replacement and 1500 mg a day

without hormone replacement. The recommendation is aimed at decreasing the risk of chronic disease through nutrition. The National Osteoporosis Foundation recommends 1,500 milligrams a day for men over 65 (as well as for women over age 50)-the amount in five glasses of milk. In addition for healthy bone, adults need 400 international units (IUs) of vitamin D daily, the amount in 1 quart of milk or 10 minutes of sun exposure, weightbearing exercise, and good lifestyle habits. (Too much vitamin D can result in vitamin D toxicity and can cause health problems so more vitamin D is NOT better). Clinical Diagnosis and Management : Osteoporosis is undetectable until the onset of fractures just as hypertension may remain undetected until a serious consequence of untreated hypertension occurs. Both hypertension and Osteoporosis are asymptomatic, but, if left untreated and undetected they can lead to their respective clinical consequences. Therefore detection of the disease is paramount before the consequences manifest clinically.

Increased bone resorption Loss of bone mass poor bone quality trauma Progressive increase in fracture risk
DD Osteoporosis Nyeri Nyeri pada punggung / tulang belakang Kadang nyeri radiculopathic Biasa terjadi pada vertebral column, Osteomalasia hip and wrist Tidak ada nyeri, hanya ketidakmampuan tulang yang parah Fraktur Beresiko terjadi fraktur karena berkurangnya kepadatan tulang, spinal cord compression atau cauda equina syndrome Dapat terjadi fraktur bila ada riwayat injury Defisiensi vitamin D Defisiensi sinar matahari Penyebab Berkurangnya kepadatan tulang Menopause Keterangan Penyakit degeneratif Tidak ada symptom yang spesifik

Osteoarthritis

Nyeri pada otot dan tendon (tangan, kaki, spine dan paha)

Tidak ada fraktur tulang kecuali jika pernah

Penyakit degenerative, alergi, infeksi,

Biasanya menyerang pada orang gemuk, tidak berhubungan dengan usia tua, ada spur / osteophytes

mengalami injury fungi

3. Hormone and nutrition 1. Calcium and Vitamin D Calcium and Vitamin D intake modulates age related increases in parathyroid hormone (PTH) levels and bone resorption. Adequate intake of Calcium have been proven to be useful in randomised clinical trials and such supplements in diet increases the Bone Mineral Density of spine and reduce the vertebral and non vertebral fractures. Low levels of 25 hydroxy Vitamin D are quite common in the ageing population and significant reduction in hip and other non vertebral fractures have been observed in patients receiving this therapy in prospective clinical trials. The maximum effective dose of Vitamin D is uncertain but thought to be around 400 1000 IU per day. There is consensus about the fact that Vitamin D. Supplements in adequate amounts together with Calcium intake are required for good bone health. The therapeutic effects of most of the clinical trials of various drug therapies for Osteoporosis have been achieved in the presence of Calcium and Vitamin D supplementation among the control of our patients in the interventional studies. Optimal treatment of Osteoporosis with any drug therapy also requires Calcium and Vitamin D intake meeting recommended levels. The preferred source of Calcium is dietary and Calcium supplements should be available in an absorbable state. A few epidemiological studies have shown that treatment with Vitamin D was associated with a reduction of Hip fracture by 55 % amongst elderly women with low Body Mass Index. Indeed, parental vitamin D may be worthwhile particularly in patients in the developing world where a lot of social bias exists about Hormone replacement therapy and also some

newer drugs. It will have also a significant effect on the savings to health service as well as personal expenses, which is usually the case in the so-called Developing world. 2. Bisphosphonates Systematic review and metanalysis of various randomised placebo controlled clinical trialson Bisphosphonates have revealed that all of these Bisphosphonates increase bone density at the spine and hip in a dose dependent manner. They consistently reduce the risk of vertebral fractures by about 30 50%. Alendronate and Risedronate reduce the risk of subsequent non-vertebral fractures in women with Osteoporosis and adults glucocorticoid induced Osteoporosis. There is uncertainty about the effect of anti resoptive therapy in reducing non-vertebral fracture in women without Osteoporosis. In randomised clinical trials the relative risk of discontinuing medication due to an adverse event with each of the three Bisphosphonates was not very statistically significant. The safety and efficacy of this therapy in children and young adults has not been evaluated as subjects in clinical trials may not always be representative and reflective of the real clinical practice. The recent data of the effect of Risedronate is very promising with the improvement in bone density occurring within six months at all sites. 3. Hormone Replacement Therapy (HRT) This is an established treatment for Osteoporosis in postmenopausal women particularly in those who have significant postmenopausal symptoms. It is essentially an approach to both prevention and treatment and many short term studies and some long term studies with Bone Mineral Density has a primary outcome have in fact shown its efficacy. Observational studies also had demonstrated reduction in hip fracture in cohorts of women who maintain HRT therapy and it has also been shown to reduce the vertebral fracture risk although there is some posity of studies on the prevention of hip fracture by Oestrogen. The development of selective Oestrogen receptor modulators (SERM) has been an important new thrust in Osteoporosis research projects and the goal of these agents is to maximise the beneficial effect of Oestrogen on bone and to minimise or antagonise the deleterious effects on the breasts and endometrium. Raloxifene, a SERM product for the treatment and prevention of Osteoporosis has been shown to reduce the risk of vertebral fracture by 30 40% in large prospective clinical trials. Tamoxifen, often

used in the treatment and prevention of breast cancer, can maintain bone mass in postmenopausal women. However, its effects on fracture rates are yet unclear. 4. Natural Oestrogens There is a great deal of public interest in natural Oestrogens, particularly plant derived Phyto-Oestrogens. These compounds have weak Oestrogen like effects and although some animal studies are promising, no effects on fracture reduction in humans have yet been shown. 5. Calcitonin Salmon Calcitonin has demonstrated positive effects on Bone Mineral Density at the lumbar spine, but this effect is less clear at the hip. Other than a recently completed randomised controlled trial of nasal Calcitonin, no analysis of fracture risk is yet available. The PROOF study revealed a significant reduction in vertebral fracture risk at the 200 IU dose but not at the 100 IU or 400 IU dose. The absence of dose response and the lack of strongsupporting data from Bone Mineral Density and markers decrease confidence in the fracture risk data from this trial. Data on the effects of Calcitonin on fracture rates have been summarised in a recent published systematic reviewin which 14 randomised trials, including 1309 men and women, were identified and all but one of these studies used symphetic Salmon Calcitonin and the root of administration varied. The relative risk of any fracture for individuals taking Calcitonin, when compared to those not taking the drug, was 0.43 (95% CI.0.38-0.50). The effect was apparent for both vertebral fracture (relative risk equal to 0.45; 95% CI 0.39 0.53) and non-vertebral fractures (relative risk equal to 0.34; 95% CI 0.17 0.68). When same studies were analysed identifying patients with fracture rather than numbers of fractures the magnitude of effect was somewhat less (relative risk equal to 0.74; 95% CI 0.60 0.93), and the separate effects on vertebral and non vertebral fractures became non significant. This data suggests that Calcitonin treatment was associated with a significant decrease in the number of vertebral and non vertebral fractures but that dose benefits might be lower than those observed in the trials of Bisphosphonates 6. Parathyroid Hormones Most conventional agents described so far, in our experience, has shown that the bone density increases year after year for the first two three years and thereafter it tends to

plateaus. Although anti resorptive agents do reduce the fracture by about 40-60 % in spine compared to placebos, they never normalise the bone density. It is possible that in these scenarios an additional agent such as Parathyroid hormone (PTH) act as an anabolic agent. PTH exerts most of its effects on bone through the PTH 1 receptor, which it shares with the PTH receptor protein (PTH r P). These receptors are absent on Osteoclasts but are abundantly present in the stromal cells of the Osteoblastic lineage. Increased Osteoclastic resorption, driven by PTH, is believed to be a consequence of secondary signalling from bone cells. Further activation of the PTH receptors is likely to include recruitment to the osteoblastic phenotype, prevention of apoptosis of osteoblasts besides augmentation of the capacity of the osteoblasts to form new bone. In clinical trials, it is possible to synthesise the whole PTH molecule by recombinant technology, only active fragments of PTH, made (like calcitonin) by solid state technology, were available when the human studies began. Initial studies with human PTH (1-34) were undertaken for two simple reasons i.e. it was thought to be a natural cleavage product and secondly it all retained all the bioactivity of natural PTH in the chich hypercalcemia assay. Very recently human PTH (1-36 & 1-38) has been found which may well have a greater potency than the h PTH (1-34). PTH has been studied and found active in Postmenopausal osteoporosis, Glucocorticoid induced osteoporosis and Idiopathic Osteoporosis of men and GnRh induced Osteoporosis. 7. Testosterone and Anabolic Steroids As early as 1941, Albright first reported the efficacy of androgens in the treatment of osteoporosis. Several anabolic steroids have been tried in humans including Stanozolol and Nandrolone; the former given by mouth and the latter given by intra muscular injection .The effects of these steroids on bone mass are essentially consistent with a preferential effect of these agents on the cortical bone mass. It is associated with an increase in total body calcium and this increase can continue over years. We do not have any major reservation for its used in the elderly men who have a number of fragility fractures and are intolerant to more conventional drug regimens. 8. Teriparatide

Teriparatide (Forteo) is an injectable form of human parathyroid hormone. It is approved for postmenopausal women and men with osteoporosis who are at high

risk for having a fracture. Unlike the other drugs used in

osteoporosis,

teriparatide acts by stimulating new bone formation. Side effects include nausea, dizziness, and leg cramps. Teriparatide is approved for use for up to 24 months.

REFERENSI
www.nhlbi.nih.gov/health/public/heart/other/sp_smok

Kamus Kedokteran Dorland. 2006. EGC : Jakarta. Price, Sylvia A. and Wilson. 2006. Patofisiologi Konsep Klinis Proses-Proses Penyakit Volume 1 dan 2. EGC : Jakarta. Robbins, Cotrans, and Kumar. 1995. Buku Saku Dasar Patologi Penyakit. edisi 5. EGC : Jakarta. Staf pengajar IKA FK UI. 1985. Ilmu Penyakit Dalam. INFOMEDIKA : Jakarta Harrison's Principles of Internal Medicine, McGraw-Hill, edited by Eugene Braunwald, et. al., 2001. F. Rauch. What is new in neuro-musculoskeletal interactions?.literature review Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride. Institute of Medicine, Food and Nutrition Board, National, Academy Press, 1997. http://www.niams.nih.gov/Health_Info/bone/default.asp

Coffee and Calcium Loss. By Robert H. Shmerling, M.D., Harvard Medical School, for MSN Health & Fitness www.wikipedia/DXA www.eOrthopod.com Osteoporosis: Detection, Prevention and Treatment with Chiropractic Care.by Dr. Ailin Oishi-Stamatiou. Literature review www.bethanymedical.pdf/osteoporosis.com