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1. Osteoporosis

OSTEOPOROSIS

Oleh Dr H Subagyo SpB - SpOT

 

BAB 1 – PENDAHULUAN

Osteoporosis merupakan sebuah penyakit yang berjalan kronik dan progresif, dan memiliki  berbagai faktor penyebab. Penyakit ini dianggap pencuri yang biasanya tidak nampak secara klinis sampai terjadi fraktur.Osteoporosis adalah sebuah kondisi dimana massa tulang rendah dan terjadi kerusakan mikroarsitektur jaringan tulang, yang menyebabkan kerapuhan tulang dan peningkatan risiko fraktur. Osteoporosis dapat disebabkan  kegagalan membentuk tulang dan mencapai puncak massa tulang saat dewasa muda dan akibat hilangnya tulang di usia tua. Peningkatan kecepatan hilangnya tulang dapat terjadi pada wanita perimenopause dan orang tua dan dapat terjadi sebagai akibat sekunder dari berbagai keadaan penyakit dan medikasi.

Osteoporosis merupakan sebuah masalah serius di Amerika Serikat dan diseluruh dunia. Penderita osteoporosis dilaporkan semakin bertambah. Beban ekonomi dari penyakit ini cukup signifikan dan hanya akan bertambah seiring dengan bertambahnya populasi orang tua, padahal penyakit ini dapat dicegah.

Menopause adalah saat dimana terjadi berhentinya menstruasi secara permanen akibat berkurangnya atau hilangnya aktivitas ovarium. Postmenopause adalah masa setelah menopause sampai senium setelah 12 bulan amenore.

Estrogen menyebabkan meningkatnya aktivitas osteoblast. Sesudah menopause, hampir tidak ada estrogen yang diekskresikan oleh ovarium. Kekurangan ini akan menyebabkan berkurangnya osteoblast pada tulang, berkurangnya matriks tulang dan berkurangnya deposit kalsium dan fosfat tulang.

Diagnosis dapat menggunakan pemeriksaan laboratorium, biopsi tulang, penanda biokimia dari bone turnover, radiografi dengan x-foto, MRI, bone scanning, dan berbagai metode pengukuran massa tulang. Alat yang dipakai untuk mengukur massa tulang adalah Densitometri. Densitometri ini tersedia beberapa macam, seperti Dual-energy x-ray absorptiometry (DXA / DEXA), quantitative computed tomography (QCT), dan Quantitative Ultrasound (QUS). Dengan DEXA dapat diukur T-score, yang merupakan  perbandingan dari BMD (bone mineral density) pasien saat pemeriksaan dengan BMD saat puncak massa tulang. Hasil T-score kemudian dibandingkan dengan WHO densitometric classification, untuk menentukan diagnosis osteoporosis. Selain untuk diagnosis osteoporosis, pengukuran BMD juga berguna untuk menilai resiko fraktur yang akan datang dan untuk monitoring terapi.

Rencana manajemen yang komprehensif untuk osteoporosis termasuk evaluasi pasien dengan risiko tinggi, eksklusi penyebab sekunder dari rendahnya bone mineral density, perubahan gaya hidup, rehabilitasi medik dan pemilihan terapi yang tepat. Pengobatan medis termasuk hormon replacement therapy, kalsium, vitamin D, dan obat-obatan anti-osteoporotik seperti bisphosphonate, Selective Estrogen-Receptor Modulator (SERM) raloxifene, calcitonin,strontium ranelate,  denosumab, agen anabolik teriparatide.  Waktu optimal dan tipe terapi preventif masih belum ditetapkan secara jelas. Terapi pembedahan pada tulang punggung termasuk vertebroplasty dan kyphoplasty. Selain itu juga ada upaya pencegahan dini untuk osteoporosis.

Pada makalah ini akan dibahas mengenai osteoporosis, khususnya osteoporosis pasca menopause. Pembahasan akan meliputi definisi, epidemiologi, patofisiologi klasifikasi, gambaran klinis, pemeriksaan untuk menegakkan diagnosis, dan pemilihan tatalaksana yang sesuai.

 

BAB 2 –STRUKTUR TULANG

Secara garis besar tulang dikenal ada dua tipe yaitu tulang korteks (kompak) dan tulang trabekular (berongga = spongy = cancelous). Bagian luar kedua tulang tersebut merupakan tulang padat yang disebut korteks tulang dan bagian dalamnya adalah tulang trabekular yang tersusun seperti bunga karang(Buckwalter, 1995; Riis, 1996). Tulang korteks merupakan bagian terbesar (80%) penyusun kerangka,mempunyai fungsi mekanik, modulus elastisitas yang tinggi dan mampu menahan tekanan mekanik berupa beban tekukan dan puntiran yang berat. Tulang korteks terdiri dari lapisan padat kolagen yang mengalami mineralisasi, tersusun konsentris sejajar dengan permukaan tulang. Tulang korteks terdapat pada tulang panjang ekstremitas dan vertebra. Tulang spongiosa atau canselous atau trabekular mempunyai elastisitas lebih kecil dari tulang korteks, mengalami proses resorpsi lebih cepat dibandingkan tulang korteks. Tulang spongiosa terdapat pada daerah metafisis dan epifisis tulang panjang serta pada bagian dalam tulang pendek (Buckwalter, 1995; Cusharon, 1998).

 

Tulang Kortikal dan Trabekular

Secara makroskopis tulang dibedakan menjadi tulang woven dan tulang berlapis lamellar. Tulang woven adalah bentuk tulang yang paling awal pada embrio dan selama pertumbuhannya terdiri dari jaringan kolagen berbentuk ireguler. Setelah dewasa tulang woven diganti oleh tulang berlapis yang terdiri dari tulang korteks dan trabekular (Lane, 2001; Rachman, 2006).

 

 Tulang Woven dan Lamellar

                                                                                                         

Histologi Tulang Woven dan Lamellar

Korteks tulang tersusun seperti osteon, yaitu lapisan konsentris dari tulang yang dikelilingi oleh kanal dengan panjang > 2 mm dan lebar 2 mm dimana di dalamnya terdapat osteosit dan pembuluh darah untuk nutrisi. Trabekular tulang terdiri dari unit tulang struktural. Pada kedua tempat ini yaitu bagian trabekular tulang dan permukaan dalam korteks tulang merupakan bagian yang rentan terhadap pengeroposan tulang (Lane, 2001; Rachman, 2006).

 

Susunan Tulang

Terdapat sistem havers yang merupakan susunan melingkar berbentuk silinder yang dihubungkan oleh saluran havers.  Saluran ini berisi kapiler, arteriola, venula, nervi dan limfe. Tulang mendapat nutrisi melalui sirkulasi intraoseus (Buckwalter, 1995; Compston, 2001).

Sistem Havers

Selama perkembangannya tulang membutuhkan kalsium yang tinggi dansetelah mencapai masa pubertas kematangan hormon estrogen pada wanita dankematangan hormon testoteron pada laki-laki, karena pengaruh anabolik dan prekusor estrogen terjadilah proses remodeling tulang. Keterlambatan dankegagalan pembentukan gonad (sindroma Turner, sindroma Klinefelter), faktornutrisi dan aktivitas fisik berat terutama saat puber sebelum menarche (atlitberperestasi merupakan faktor yang menyebabkan tidak tercapai puncak massatulang dan ancaman terjadinya osteoporosis dini) (Rachman, 2006).

Komposisi tulang

Unsur yang membentuk tulang adalah mineral sekitar (65%), matriks(35%), sel-sel osteoblast, osteoclast, osteosit dan air.Matriks tulang korteks dantrabekula tersusun atas matriks organik dan anorganik. Komponen anorganik merupakan 65% dari seluruh masa tulang sedangkan, komponen organik sekitar 20% dan air 10%.Kolagen tulang merupakan komponen organik terbesar yangmembentuk dan memungkinkan tulang menahan regangan sedangkan anorganik atau mineral berfungsi menahan beban tekanan (Compston, 2001).

Asal mula sel-sel tulang berasal dari stem sel tulang yang berkembangmenjadi mesoderm progenitor kemudian membentuk jalur mesenkim(preosteoblast, osteoblast, osteosit danbone lining cells) dan jalur hemopoetik (preosteoclast, osteoclast). Stem sel ini definisinya masih sulit dipahami, beberapapendapat mendefinisikan stem sel merupakanunspesifieddanundifferentiated cellsyang berfungsi memperbaharui sel-sel tubuh termasuk didalamnya sel-seldarah, kulit, intestinal, dan seterusnya. Pada awal pembentukannya diawali oositteraktifasi, menjadi zigot membelah berbentuk blastokis yang berisi DNA donor(Compston, 2001; Morgan, 2001; Rosenberg, 2005; Kumar, 2005).Blastokis akan terurai menghasilkan sel-sel embrionik / stem cellembryonic.Sel-sel ini terdiri dari beberapa tipe sel-sel pluripoten terbagimenjadi tiga yaitu endoderm, mesoderm (progenitor sel mesoderm dan progenitorsel hematopoesis) dan ektoderm yang akan berdiferensiasi sebagai sel-selprogenitor dan mempunyai kapabilitas berdiferensiasi menjadi berbagai jaringantubuh nantinya, seperti proses pembentukan sumsum tulang. Sumsum tulang adalah tempat terpenting dari 6 sampai dengan 7 bulankehidupan janin dan selama masa anak dan dewasa normal, sumsum tulang adalahsatu-satunya sumber sel darah baru serta lingkungan yang cocok untuk perkembangan stem sel. Di dalamnya terdapat sel stromal, sel lemak dan jaringanmikrovaskuler. Sumsum tulang juga merupakan tempat asal utama limfositmanusia dan ada bukti untuk sel prekursor sama dari kedua sistem hemopoetik dan limfoid. Stem sel hemopoetik juga membentuk osteoclast yang merupakanbagian sistem fagosit monosit dan berfungsi sebagai resorpsi tulang. Didalamaspek umum hemopoesis, stem sel sumsum tulang (pluripoten stem sel) setelahpembelahan sel dan langkah diferensiasi, menjadi urutan sel progenitor untuk tigajalur berfungsi membentuk sel sumsum tulang utama yaitu : a. eritroid ; b.granulositik dan monosotik ; c. megakariositik (Hoffbrand, 1996; Kumar, 2005).

Diferensiasi Sel

Sel Tulang

a.       Osteoblast

Osteoblast berasal dari jalur sel mesenkim stroma sumsum tulang.Osteoblastmemproduksi osteoid atau matriks tulang, berbentuk bulat, oval atau polihedral,terpisah dari matriks yang telah mengalami mineralisasi. Osteoblast berfungsimensintesis dan mensekresi matriks organik tulang, mengatur perubahan elektrolitcairan ekstraselular pada proses mineralisasi. Osteoblast mengandung retikulumendoplasmik, membran golgi dan mitokondria. Pematangan osteoblastmemerlukanfibroblast growth factor (FGF),bone morphogenic proteins(BMPs),core binding factor-1(CBFA-1) dan osteoblast specific cis acting element (OSE-2). Osteoblastmemiliki reseptor estrogen, sitokin, paratiroid hormon (PTH), insulin derivated growth factor (IGF), dan Vitamin D3.Osteoblast salingberhubungan melalui gap junction.Osteoblast yang menetap pada permukaantulang bentuknya pipih yang dinamakanbone lining cells / restingosteoblastt.(Compston, 2001; Morgan, 2001; Rosenberg, 2005).

b.      Osteoclast

Osteoclast berasal dari jalur hemopoetik yang juga membuat makrofag dan monosit. Sel ini berpindah dari sumsum tulang lewat sirkulasi atau migrasidirek. Sel prekursor osteoclast terdapat pada sumsum tulang dan sirkulasi darah. Sel ini ditemukan pada permukaan tulang yang mengalami resorpsi dan kemudianmembentuk cekungan yang dikenal sebagai lakunaHowship. Osteoclast dalamsitoplasmanya akan terisi oleh mitokondria guna menyediakan energi untuk proses resorpsi tulang. 

Osteoclast merusak matriks tulang, melekat pada permukaan tulang, memisahkan sel dengan matriks,menurunkan pH7 menjadipH4. Keasaman ini akan melarutkan mineral dan merusak matriks sel sehinggaprotease keluar. Osteoclast memiliki reseptor yaitu RANK-ligand (RANK-L)untuk maturasi sel dan apoptosis (Manolagas, 1995; Compston,2001;Morgan, 2001).

c.       Osteosit

Osteosit berasal dari osteoblast dimana pada akhir proses mineralisasi akantersimpan pada matriks tulang. Osteosit mempunyai satu inti, jumlah organelabervariasi dan sel ini menjangkau permukaan luar dan dalam tulang, membuattulang menjadi sensitif terhadap tekanan, mengontrol pergerakan ion sertamineralisasi tulang (Compston, 2001; Drajad, 2002).Osteosit merupakan 90% dari sel tulang terletak diantara matriks tulangyang mengalami mineralisasi. Osteosit mempunyai satu inti, jumlah organelabervariasi. Jaringan sel ini menjangkau permukaan luar dan dalam tulang,membuat tulang menjadi sensitif terhadap pengaruh tekanan, mengontrolpergerakan ion serta mineralisasi tulang. Osteosit berasal dari osteoblast yang padaakhir proses mineralisasi terhimpit oleh ekstraselular matriks. Osteosit merupakansel yang sensitif terhadap tekanan mekanik, berperan dalam pemeliharaan massa dan strukturtulang (Compston, 2001; Drajad, 2002; Van Essen, 2007).

 

BAB 3 - PEMBENTUKAN TULANG

 

Homeostasis tulang, sebuah jaringan hidup,dipertahankan oleh osteoclast, yang bertanggung jawab untuk resorpsi tulang, dan osteoblast, yang bertanggung jawab untuk pembentukan tulang. Osteoblast berasal dari mesenchymal stem cell.Sedangkan osteoclast berasal dari prekursor hematopoietik. Kedua tipe sel bergantung satu sama lain untuk produksi. Bahkan pembentukan osteoclast dari prekursor hematopoietik tidak dapat dicapai kecuali terdapat sel-sel mesenkimal.

Sel-sel mesenkim dengan potensi untuk menjadi osteoblast juga memiliki potensi untuk menjadi fibroblas, kondrosit, adiposit, atau sel otot. Potensi untuk diferensiasi ini membuat osteoblast mampu mensekresikan sitokin dan colony-stimulating factors yang sama dengan yang diproduksi oleh fibroblas.

Hematopoietic granulocyte-macrophage colony-forming units (CFUs) memproduksi osteoclast dan melahirkan monosit dan makrofag.Oleh karena itu, osteolas memproduksi sitokin-sitokin yang sama seperti monosit. Interleukin (IL)-6 diproduksi sebgian oleh osteoblast yang menstimulasi aktivitas osteoclasttik. Fenomena ini adalah sebuah mekanisme yang diperkirakan untuk suatu penyakit tertentu yang berciri peningkatan resorpsi tulang. Dua contoh penyakit yang mengakibatkan osteoporosis dengan mekanisme ini adalah multiple myeloma dan rheumatoid arthritis.

Tulang mengalami remodeling secara terus menerus seumur hidup karena tulang senantiasa mengalami mikrotrauma. Remodeling tulang terjadi pada lokasi-lokasi tertentu didalam kerangka dan berjalan mengikuti urutan tertentu.

Kaskade Yang Menyebabkan Resorpsi Tulang

Resorpsi tulang selalu diikuti pembentukan tulang, sebuah fenomena yang disebut sebagai coupling. Pada osteoporosis, mekanisme coupling ini diduga tidak mampu mengikuti mikrotrauma konstan yang diderita tulang trabekular. Pada orang dewasa, diperkirakan 25% tulang trabecular diresorpsi dan diganti setiap tahun, dibandingkan dengan hanya 3% tulang kortikal.

Osteosit, yang merupakan diferensiasi terakhir osteoblast tertanam didalam tulang yang termineralisasi, menentukan waktu dan lokasi remodeling. Osteoblast tidak hanya mengeluarkan dan memineralisasi osteoid, tapi juga diduga mengendalikan resorpsi tulang yang dilakukan oleh osteoclast. Osteoclast membutuhkan berminggu-minggu untuk meresorpsi tulang, sedangkan osteoblast memerlukan berbulan-bulan untuk membentuk tulang baru. Oleh karena itu, proses apapun yang meningkatkan kecepatan remodeling tulang berakibat hilangnya tulang seiring waktu.

Proses Metabolisme Tulang

Lebih jauh lagi, pada periode dimana remodeling terjadi dengan cepat (misalnya setelah menopause), tulang mengalami peningkatan risiko fraktur karena tulang yang baru dibentuk lebih sedikit kepadatan mineralnya, lokasi resorpsi sementara tidak terisi, dan isomerisasi dan maturasi kolagen terganggu.

Para ahli biologi molekular sudah mulai mampu membuka mekanisme-mekanisme remodeling tulang. Contohnya, sekarang sudah dimengerti bahwa Receptor Activator of Nuclear factor-Kappa B Ligand (RANKL) / Receptor Activator of Nuclear factor-Kappa B (RANK) / osteoprotegerin (OPG) system adalah jalur akhir untuk resorpsi tulang.

Ikatan RANKL dan RANK Menyebabkan Diferensiasi Osteoclast

Osteoblast dan activated T cell didalam sumsum tulang menghasilakan RANKL cytokine. RANKL terikat pada reseptor RANK yang diekspresikan oleh osteoclast dan prekursor osteoclast untuk mempromosikan diferensiasi osteoclast. Osteoprotegerin adalah sebuah soluble decoy receptor yang menghambat RANK-RANKL dengan mengikat dan melakukan sekuesterasi RANKL.

 

OPG Sebagai Decoy Receptor Sehingga Menghambat Differensiasi

Massa tulang mencapai puncaknya pada dekade ketiga kehidupan, setelah itu menurun secara perlahan.  Kegagalan mencapai kekuatan tulang yang optimal pada titik ini adalah salah satu faktor yang berkontribusi terhadap osteoporosis. Oleh karena itu, nutrisi dan aktivitas fisik penting saat pertumbuhan dan perkembangan. Namun, faktor-faktor herediter memainkan peran penting dalam menentukan puncak kekuatan tulang seorang individu. Bahkan, genetik bertanggung jawab sampai sebanyak 80% dari variasi puncak

Massatulang diantara individu.

Pertumbuhan dan Berkurangnya Kepadatan Tulang Dalam Siklus Kehidupan Manusia

BAB 4 –OSTEOPOROSIS

Osteoporosis merupakan sebuah penyakit yang berjalan kronik dan progresif, dan memiliki  berbagai faktor penyebab. Osteoporosis merupakan penyakit metabolik tulang yang paling sering dijumpai di Amerika Serikat. Penyakit ini paling banyak dijumpai pada wanita tua berkulit putih (ras kaukasia),  namun dapat terjadi pada kedua jenis kelamin, semua ras, dan semua usia.

Penyebab Fraktur Pada Wanita

Penyebab Fraktur Pada Pria

Penyakit ini dianggap pencuri yang biasanya tidak nampak secara klinis sampai terjadi fraktur.Oleh karena itu, dibutuhkan screening pada populasi yang memiliki risiko.

Osteoporosis dapat mengenai hampir seluruh tulang. Penyakit ini merupakan penyakit sistemik yang memiliki ciri massa tulang yang rendah dan kerusakan mikroarsitektur daripada jaringan tulang, sehingga menyebabkan peningkatan kerapuhan tulang.

 

 

Tulang Osteoporosis

 

  • Definisi lama dari osteoporosis adalah penurunan massa tulang tanpa terjadi penurunan kualitas tulang.
  • Definisi   osteoporosis menurut World Health Organization (1991) adalah: osteoporosis adalah penyakit yang ditandai dengan rendahnya massa tulang dan disertai kerusakan mikroarsitektur jaringan, kelainan ini menyebabkan kerapuhan tulang sehingga terjadi peningkatan resiko fraktur.
  • Definisi modern dari osteoporosis adalah penyakit tulang dengan ciri penurunan massa tulang dan kerusakan mikro arsitekturnya sehingga menyebabkan tulang mudah patah.
  • Definisi terbaru dari osteoporosis adalah penyakit tulang dimana terjadi penurunan kekuatan tulang sedemikian sehingga meningkatkan resiko patah tulang. Kekuatan tulang terdiri dari dua bagian: densitas tulang (kuantitas) dan kuaitas tulang.

 

 

Gambaran Tulang Osteoporosis Dengan Mikroskop Elektron

Osteoporosis merupakan sebuah masalah serius di Amerika Serikat dan diseluruh dunia. Penderita osteoporosis dilaporkan semakin bertambah. Beban ekonomi dari penyakit ini cukup signifikan dan hanya akan bertambah seiring dengan bertambahnya populasi orang tua.

 

 

Projeksi Peningkatan Jumlah Penderita Osteoporosis

Walaupun osteoporosis memiliki komplikasi yang mengerikan, kondisi ini seringkali terlewat dan tidak diobati. Hal ini diakibatkan sifat penyakit ini yang tersembunyi sampai terjadi fraktur.

Sebuah survei Gallup yang dilakukan oleh National Osteoporosis Foundation menemukan bahwa 75% dari semua wanita berusia 45 – 75 tahun tidak pernah membicarakan osteoporosis dengan dokter mereka. Kegagalan mengidentifikasi pasien yang berisiko,untuk mengedukasi mereka, dan untuk menerapkan langkah preventif, dapat menimbulkan akibat yang besar.

 

Pengobatan medis termasuk kalsium, vitamin D, dan obat-obatan anti-osteoporotik seperti bisphosphonate, Selective Estrogen-Receptor Modulator (SERM) raloxifene, calcitonin dan denosumab.Selain itu juga ada sebuah agen anabolikteriparatide.Terapi pembedahan termasuk vertebroplasty dan kyphoplasty.

Osteoporosis adalah sebuah penyakit yang dapat dicegah, yang dapat menimbulkan akibat yang berat pada segi fisik, psikososial, dan ekonomi.Pencegahan dan pengenalan dari penyebab sekunder osteoporosis merupakan langkah pertama untuk mengurangi akibat dari penyakit ini.

 

Patofisiologi

Osteoporosis adalah sebuah kondisi dimana massa tulang rendah dan terjadi kerusakan mikroarsitektur jaringan tulang, yang menyebabkan kerapuhan tulang dan peningkatan risiko fraktur. Hal ini terjadi akibat faktor-faktor herediter dan lingkungan yang mempengaruhi massa tulang dan kualitas tulang.

Secara tradisional, osteoporosis dibagi menjadi tipe I (postmenopause) atau tipe II (senilis).Osteoporosis postmenopausal terjadi terutama karena defisiensi estrogen; osteoporosis terutama akibat dari penuaan tulang dan defisiensi kalsium. Namun, semakin diketahui bahwa berbagai mekanisme patogenesis berinteraksi dalam perkembangan keadaan osteoporotik, tanpa melihat usia.

Ciri osteoporosis adalah penurunan massa kerangka yang disebabkan oleh ketidakseimbangan resorpsi tulang dan pembentukan tulang. Pada kondisi fisiologis, pembentukan dan resorpsi tulang berada pada keseimbangan yang baik.  Adanya perubahan keseimbangan ini, yaitu baik karena meningkatnya resorpsi tulang atau menurunnya pembentukan tulang, menyebabkan terjadi osteoporosis.

Osteoporosis dapat disebabkan  kegagalan membentuk tulang dan mencapai puncak massa tulang saat dewasa muda dan akibat hilangnya tulang di usia tua. Peningkatan kecepatan hilangnya tulang dapat terjadi pada wanita perimenopause dan orang tua dan dapat terjadi sebagai akibat sekunder dari berbagai keadaan penyakit dan medikasi.

 

Hilangnya fungsi gonad dan penuaan adalah 2 faktor paling penting yang menyebabkan terjadinya osteoporosis. Studi menunjukkan bahwa hilangnya tulang pada wanita bertambah cepat dengan cepat pada tahun pertama setelah menopause. Kurangnya hormon gonad diduga menyebabkan up-regulation dari sel-sel progenitor osteoclast.

Defisiensi Estrogen tidak hanya mempercepat hilangnya tulang pada wanita postmenopause namun juga berperan dalam berkurangnya tulang pada pria.Defisiensi estrogen dapat menyebabkan resorpsi tulang berlebih yang disertai dengan tidak cukupnya pembentukan tulang.Osteoblast, osteosit, dan osteoclast semua mengekspresikan reseptor estrogen.Selain itu, estrogen mempengaruhi tulang secara tidak langsung melalui sitokin dan faktor pertumbuhan lokal.Keadaan  penuh estrogen dapat meningkatkan apoptosis osteoclast melalui meningkatnya produksi transforming growth factor (TGF)-beta.

Dalam kondisi tidak adanya estrogen, sel T mendatangkan osteoclast, menyebabkan diferensiasi, dan memperpanjang usianya melalui IL-1, IL-6, dan tumor necrosis factor (TNF)-alpha.

Sebuah studi membandingkan tikus yang dikeluarkan ovariumnya dan yang menjalani operasi palsu, menemukan bahwa tingkat IL-6 dan granulocyte-macrophage CFU jauh lebih tinggi pada tikus yang mengalami ovariectomy.Penemuan ini membuktikan bahwa estrogen menghambat sekresi IL-6, dan IL-6 berperan dalam mendatangkan osteoclast dari jalur sel monosit, sehingga berkontribusi terhadap osteoporosis.IL-1 juga ditunjukkan terlibat dalam produksi osteoclast.Produksi IL-1 meningkat di dalam sel mononuklear sumsum tulang dari tikus yang ovariectomy.Memasukkan antagonis reseptor IL-1 pada hewan ini mencegah stadium lanjut dari kerusakan tulang yang diinduksi oleh hilangnya fungsi ovarium, namun tidak mencegah stadium awal kerusakan tulang.Peningkatan IL-1 di dalam sumsum tulang kelihatannya bukan merupakan suatu kejadian yang dipicu, namun merupakan hasil dari disingkirkannya efek inhibitor dari steroid sex pada IL-6 dan gen-gen lain yang diregulasi langsung oleh steroid sex.

Sel T juga menghambat diferensiasi dan aktivitas osteoblast dan menyebabkan apoptosis prematur dari osteoblast melalui sitokin seperti IL-7. Hal lain yang ditemukan adalah bahwa defisiensi estrogen menyebabkan tulang menjadi sensitif terhadap efek hormon paratiroid.

 

Estrogen Dan Osteoporosis

 

Gambaran Efek Estrogen Terhadap Biomolekuler Homeostasis Tulang

Fraktur osteoporotik merepresentasikan kepentingan klinis dari gangguan di dalam tulang ini.Kejadian ini dapat diakibatkan trauma minor, seperti jatuh dari posisi duduk atau berdiri, dan dari trauma mayor, seperti seorang pejalan kaki yang ditabrak dalam sebuah kecelakaan lalu lintas.Fraktur patologis, yang terjadi sekunder terhadap trauma minor, adalah karakteristik osteoporosis.

Fraktur Akibat Osteoporosis

Etiologi

Osteoporosis diklasifikasi menurut etiologi dan lokalisasi pada kerangka. Osteoporosis pada awalnya dibagi dalam kategori lokal dan generalisata. Kedua kategori utama ini diklasifikasikan lebih jauh menjadi osteoporosis primer dan sekunder. Osteoporosis postmenopausal terutama disebabkan defisiensi estrogen; osteoporosis senilis terutama akibat penuaan tulang dan defisiensi kalsium.

Osteoporosis primer terjadi pada pasien dimana penyebab sekunder osteoporosis tidak dapat ditemukan, termasuk osteoporosis juvenil dan idiopatik. Osteoporosis idiopatik dapat dibagi  menjadi postmenopausal (tipe I) dan senilis(tipe II), sebagai berikut:

a)       Osteoporosis juvenil biasanya terjadi pada anak-anak atau dewasa muda jenis kelamin manapun. Pasien-pasien ini memiliki fungsi gonad yang normal. Usia onset biasanya 8 – 14 tahun. Karakteristik khusus osteoporosis juvenil adalah nyeri tulang mendadak dan/atau fraktur setelah trauma.

b)      Osteoporosis tipe I (osteoporosis postmenopausal) terjadi pada wanita usia 50-65 tahun. Osteoporosis tipe ini dikenal dari terdapatnya fase akselerasi dari hilangnya tulang. Kerapuhan tulang ini terjadi terutama pada tulang trabekular. Pada fase ini, fraktur pergelangan tangan distal dan badan vertebral sering terjadi.

c)       Osteoporosis tipe II (senilis) terjadi pada wanita dan pria lebih dari 70 tahun. Bentuk osteoporosis ini mencerminkan kehilangan tulang yang berhubungan dengan umur. Fraktur terjadi di tulang kortikal dan trabekular. Selain daripada fraktur pergelangan tangan dan vertebral, fraktur panggul juga sering ditemukan pada pasien-pasien dengan osteoporosis tipe II.

d)      Osteoporosis sekunder terjadi ketika ada penyakit, defisiensi, atau obat yang menyebabkan terjadinya osteoporosis. Sebanyak sepertiga wanita postmenopausal, juga banyak pria dan wanita premenopausal, memiliki penyebab rapuhnya tulang yang berdampingan.

Penyebab genetik (kongenital) dari osteoporosis termasuk hal-hal berikut:

  • Cystic fibrosis
  • Ehlers-Danlos syndrome
  • Glycogen storage disease
  • Gaucher disease
  • Hemochromatosis
  • Homocystinuria
  • Hypophosphatasia
  • Idiopathic hypercalciuria
  • Marfan syndrome
  • Menkes steely hair syndrome
  • Osteogenesis imperfecta
  • Porphyria
  • Riley-Day syndrome
  • Hypogonadal states

 

Keadaan hipogonad yang dapat menyebabkan osteoporosis termasuk:

  1. A.       Androgen insensitivity
  2. B.       Anorexia nervosa/bulimia nervosa
  3. C.       Female athlete triad
  4. D.       Hyperprolactinemia
  5. E.       Panhypopituitarism
  6. F.       Premature menopause
  7. G.       Turner syndrome
  8. H.       Klinefelter syndrome

 

Kelainan endokrin yang dapat menyebabkan osteoporosis termasuk berikut:

  • Acromegaly
  • Adrenal insufficiency
  • Cushing syndrome
  • Estrogen deficiency
  • Diabetes mellitus
  • Hyperparathyroidism
  • Hyperthyroidism
  • Hypogonadism
  • Pregnancy
  • Prolactinoma

 

 

Keadaan defisiensi yang dapat menyebabkan osteoporosis termasuk berikut ini:

  1. Calcium deficiency
  2. Magnesium deficiency
  3. Protein deficiency
  4. Vitamin D deficiency
  5. Operasi Geriatrik
  6. Celiac disease
  7. Gastrectomy
  8. Malabsorption
  9. Malnutrition
  10. Parenteral nutrition
  11. Primary biliary cirrhosis

 

Penyakit peradangan yang dapat menyebabkan osteoporosis termasuk:

  • Inflammatory bowel disease
  • Ankylosing spondylitis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus

 

Kelainan hematologis dan neoplastik yang dapat menyebabkan osteoporosis termasuk:

  • Hemochromatosis
  • Hemophilia
  • Leukemia
  • Lymphoma
  • Multiple myeloma
  • Sickle cell anemia
  • Systemic mastocytosis
  • Thalassemia
  • Penyakit metastasis

 

Pengobatan yang diketahui menyebabkan atau mempercepat rusaknya tulang termasuk hal berikut”

  • Anticonvulsants - Phenytoin, barbiturates, carbamazepine (agen-agen ini diasosiasikan dengan defisiensi vitamin D yang diinduksi pengobatan)
  • Antipsychotic drugs
  • Antiretroviral drugs
  • Aromatase inhibitors - Exemestane, anastrozole
  • Chemotherapeutic/transplant drugs - Cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, methotrexate
  • Furosemide
  • Glucocorticoids and corticotropin- Prednisone (≥5 mg/d for ≥3 mo)
  • Heparin (jangka panjang)
  • Hormonal/endocrine therapies - Gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormone-releasing hormone (LHRH) analogs, depomedroxyprogesterone, excessive thyroid supplementation
  • Lithium
  • Methotrexate
  • Selective serotonin reuptake inhibitors
  • Thyroxine (excessive)

 

Penyebab lainosteoporosis adalah:

  • Alcoholism
  • Amyloidosis
  • Chronic metabolic acidosis
  • Congestive heart failure
  • Depression
  • Emphysema
  • Chronic atau end-stage renal disease
  • Chronic liver disease
  • HIV disease/AIDS
  • Idiopathic calciuria
  • Idiopathic scoliosis
  • Immobility
  • Multiple sclerosis
  • Ochronosis
  • Transplantasi organ
  • Pregnancy/lactation
  • Sarcoidosis
  • Weightlessness

 

Faktor-faktor risiko untuk osteoporosis seperti usia lanjut dan berkurangnya bone mineral density (BMD), telah ditetapkan  menurut relasi langsung dan kuat terhadap insiden fraktur; namun, banyak faktor lain yang dianggap faktor risiko berdasarkan hubungannya dengan BMD sebagai indikator lain osteoporosis. Faktor-faktor risiko osteoporosis termasuk berikut ini:

a)       Usia lanjut (lebih dari 49 tahun)

b)      Jenis kelamin wanita

c)       Etnis Putih atau Asia

d)      Faktor-faktor genetik seperti riwayat keluarga osteoporosis

e)       Postur kurus atau kecil

f)        Amenorhea

g)      Menarche yang terlambat

h)      Menopause dini

i)        Kondisi Postmenopausal

j)        Kurang aktivitas fisik atau imobilisasi

k)       Penggunaan obat-obatan – Antikonvulsan, steroid sistemik, suplemen tiroid, heparin, agen-agen kemoterapi, insulin

l)        Penggunaan alkohol dan tembakau

m)    Defisiensi Androgen atau Estrogen

n)      Defisiensi Kalsium

 

 

Mengukur BMD

 

Studi oleh Cummings et al menemukan hubungan indirek diantara jumlah faktor risiko dan angka kepadatan tulang. Studi juga  mengidentifikasi faktor-faktor yang tidak meningkatkan risiko fraktur, termasuk warna rambut, jumlah anak yang diberi ASI, riwayat merokok sebelumnya, atau menggunakan benzodiazepin jangka pendek.

Faktor nutrisi berpengaruh terhadap risiko terjadinya osteoporosis. Faktor risiko osteoporosis dalam bidang nutrisi antara lain:

a)       Kurangnya kalsium, terutama dalam jangka panjang

b)      Kurangnya vitamin D, terutama bila tidak cukup terpapar sinar matahari

c)       Kurangnya protein

d)      Konsumsi alkohol berlebihan

e)       Konsumsi natrium berlebihan

f)        Konsumsi kafein berlebihan, jika konsumsi kalsium rendah

g)      Kurangnya zat mikronutrien lain (Vitamin A, folat, vitamin B12, Vitamin K)

Defisiensi kalsium merupakan suatu keadaan dimana konsentrasi kalsium total dalam serum kurang dari 8,5 mg/dL (2,2 mmol/L) atau kadar kalsium ion kurang dari 1,0 mmol/L (Rujianto, 2001). Defisiensi kalsium besar terjadi selama periode pertumbuhan cepat tulang (modeling) sampai puncak massa tulang dan ini sangat berpengaruh terhadap kerapuhan tulang seseorang (Rosenberg, 2005).

Leptin bekerja di SSP menurunkan asupanmakanan dan meningkatkan energi. Pada jaringan perifer leptin mencegahdeposisi lemak di jaringan non adipose. Leptin bisa menjadi mediator antaralemak tubuh dan tulang oleh karena sirkulasi leptin berkorelasi positif denganmassa lemak pada orang sehat. Leptin dapat menunjukkan ekspresi pada osteoblastmanusia selama proses mineralisasi dan akan meningkatkan aktifitas osteogenik pada sumsum tulang manusia. Pada fetal leptin membantu pertumbuhan tulang.Leptin berpotensial efek anabolik pada tulang, namun leptin dengan densitasmassa tulang belum bisa dijelaskan secara rinci (Blain, 2002).

Efek jangka panjang hormon tiroid pada tulang adalah meningkatkanproduksi somatomedin IGF-1 di sel hati, merangsang resorpsi tulang lewatosteoclast-activating factor. Pada wanita pre dan post menopause yangmenggunakan hormon tiroid menyebabkan penurunan densitas mineral tulang(Djokomoeljanto, 2003).

Hiperparatiroidisme adalah aktifitas berlebih kelenjar paratiroidmemproduksi hormon paratiroid. Hormon paratiroid (Parathyroid Hormone) atauPTH mengatur regulasi dan mempertahankan keseimbangan kadar kalsium danfosfat. Aktifitas satu atau lebih kelenjar paratiroid menyebabkan hiperkalsemiadan rendahnya kadar fosfat dalam darah. Fungsi utama PTH adalah untuk menormalkan kadar konsentrasi Ca2+yang menurun dalam darah, fungsi PTHyang lain adalah (Fauci, 2008) :

1. PTH mengaktifasi osteoclast melalui stimulasi RANKL, sehinggamenghasilkan resorpsi tulang dan mengeluarkan Ca2+dan fosfat dari tulang,

2. PTH mengakselerasi sintesis kalsitriol tahap akhir di ginjal, sehingga akandihasilkan peningkatan reabsorbsi Ca2+ pada usus,

3. Dalam ginjal, PTH meningkatkan sintesis kalsitriol dan reabsorbsi Ca2+,dimana hal ini menjadi penting karena berhubungan dengan peningkatancadangan Ca2+akibat proses 1 dan 2 diatas.

PTH juga menginhibisireabsorbsi fosfat di ginjal menghasilkan hipofosfatemia. Yang akanmenstimulasi pelepasan Ca2+dari tulang atau mencegah presipitasi kalsium-fosfat pada jaringan (Despopoulos, 2003).Klasifikasi dan etiologi hiperparatiroidisme: (Fauci, 2008)

  1. Hiperparatiroidisme primer. Disebabkan hiperfungsi kelenjar paratiroid itu sendiri. Terjadi sekresiberlebih PTH, karena : adenoma, hiperplasia, karsinoma kelenjar paratiroid
  2. Hiperparatiroidisme sekunder. Disebabkan suatu reaksi kelenjar paratiroid terhadap hipokalsemiadisebabkan bukan hanya patologis kelenjar paratiroid, seperti pada gagalginjal kronik.
  3. Hiperparatiroidisme tersier. Disebabkan oleh karena hiperplasia kelenjar paratiroid dan kehilangan responterhadap kalsium. Kelainan ini banyak terjadi pada pasien dengan gagal ginjal kronik yangberlangsung lama.

Keganasan baik itu tumor padat atau keganasan hematologi dapatmemberikan efek pada tulang melalui sitokin proinflamasi IL-1 dan IL-6 yangmerangsang prekursor mitogenik osteoclast dalam meningkatkan resorpsi tulang,diperkuat oleh IL-6 yang akan mengaktifkan NK- RANKL dan TNF-sehingga kecepatan remodeling tulang terganggu dan prosesbone turnover menjadi lebih lama, dan terjadi kematian sel alamiah yaitu apoptosis (DispenziariA, 2004; Rosenberg, 2007).

Adapun obat-obatan yang dapat mempengaruhi risiko terjadinyaosteoporosis adalah obat steroid, obat anti-konvulsan, heparin, antasida aluminium,metotreksat dan terapi pengganti tiroksin (Lane, 2001).Hiperprolaktinemia berbeda dengan menopause, dimana dapat terjadi olehkarena hormone producing tumor, pemberian obat anti-dopaminergik, gagal ginjaldan liver (oleh karenalack of dopamine), hipotiroidisme meningkatkan pelepasanprolaktin melalui peningkatan sekresi TRH. Akibat hiperprolaktinemia adalahgalaktorea (aliran produksi ASI menurun), tendensi terjadi hiperglikemia,penghambatan pelepasan hormone gonadotropin disertai hipogonadisme,amenorea, kehilangan libido dan impotensi pada laki-laki. Hiperprolaktinemiadiperiksa kadar prolaktin sedangkan menopause diperiksa kadar FSH ataufolliclestimulating hormone.

Satu penemuan yang sangat menarik dari studi adalah masukan diet dari kalsium tidak berkorelasi terhadap risiko fraktur panggul. Studi kohort longitudinal dan prospektif, mengevaluasi efek kalsium diet pada insiden fraktur dan osteoporosis.Hasilnya menemukan bahwa masukan vitamin D yang rendah diasosiasikan dengan lebih tingginya angka kejadian fraktur pada kwartal pertama.Risiko fraktur tipe manapun, atau dari osteoporosis, tidak berkurang lebih jauh pada kwartal konsumsi kalsium tertinggi, namun berhubungan dengan fraktur panggul yang lebih tinggi.Studi menyimpulkan bahwa peningkatan gradual pada diet kalsium tidak mengurangi risiko fraktur atau osteoporosispada wanita.

Satu studi berusaha menemukan apakah nilai BMD dari femoral neck  dan skor World Health Organization Fracture Risk Algorithm (FRAX) berhubungan dengan risiko fraktur panggul  dan nonvertebral pada dewasa yang lebih tua dengan diabetes mellitus tipe 2. Menggunakan data dari 3 studi prospektif observasional, statistik dari fraktur yang dilaporkan sendiri, dianalisis 9449 wanita dan 7436 pria di Amerika. Hasilnya menemukan bahwa peserta dengan DM tipe 2 memiliki risiko fraktur yang lebih tinggi  dan skor T daripada mereka tanpa DM tipe 2, menyimpulkan bahwa skor BMD T dan skor FRAX dari collum femur berhubungan dengan risiko fraktur panggul dan fraktur non-vertebra yang lebih pada pasien-pasien berusia tua dengan DM tipe 2.

Karakteristik Umum dan Klinis Dari Populasi Studi, Menurut BMD

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