patologi tulang dan sendi

PATOLOGI TULANG DAN SENDI

The skeletal system is as vital to life as any organ system because of its essential roles in mechanical support and mineral homeostasis.

Skeleton also houses the hematopoietic elements, protects viscera, and determines body size and shape.

The skeletal system is composed of bones that vary in size and shape (tubular, flat, cuboid).

The bones are interconnected by a variety of joints that allow for a wide range of movement while maintaining structural stability.

Bone is a type of connective tissue, and it is unique because it is one of the few tissues that normally undergo mineralization.

INTRODUCTION

Biochemically, composed of admixture of inorganic elements (65%) and organic matrix (35%).

The inorganic component, calcium hydroxyapatite 110Ca:6(PO,):(OH),], is the mineral that gives bone strength and hardness, and is the storehouse for 99% of the body's calcium, 85% of the body's phosphorus, and 65% of the body's sodium and magnesium.

The formation of hydroxyapatite crystal in bone is a phase transformation from liquid to solid analogous to the conversion of water to ice.

The process involves the initiation and induction of mineralization by the organic matrix and it is tightly regulated by numerous factors.'

The rate of mineralization can vary, but normally there is a 12- to 15-day lag time between the formation of the matrix and its mineralization. Bone that is

unmineralized is known as osteoid.

The organic component includes the cells of bone and the proteins of the matrix.

The bone-forming cells include the osteoprogenitor cells, osteoblasts, and osteocytes.

The generation and stimulation of these cells are regulated by cytokines and growth factors such as bone morphogenic proteins (BMPs), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), insulin-like growth factor, and transforming growth factor-13

SEL-SEL DAN MATRIKS TULANG

SEL- SEL TULANG

OSTEOBLAST

OSTEOSIT

OSTEOCLAST

MATRIKS TULANG

ORGANIK

COLLAGEN TYPE 1

NON COLLAGENMATRIKS : - PROTEOGLYCANS- GLYCOSAMINOGLYCAN- PROTEIN- LEMAK- AIR

MINERAL

-CALSIUM- CARBONAT- MAGNESIUM- SODIUM- MANGAN- ZINC- FLUORIDE

- 65% BERAT TLG - MENGERASKAN TLG

STRUKTUR TULANG NORMAL

OSTEOBLAST

- BERASAL DARI SEL MESENKIM

- AKITIF OSTEOBLAST ; SITOPLASMA MEMBESAR DAN BASOFILIK

- INAKTIF OSTEOBLAST : SITOPLASMA MENGECIL DAN PUCAT

- TERLETAK PADA PERMUKAAN SEMUA JENIS TULANG

(PERIOSTEUM, ENDOSTEUM, TRABEKULAR DAN INTRAKORTIKAL)

- FUNGSI :

1. MEMBENTUK MATRIK TULANG (OSTEOID/ORGANIK)

2. MERANGSANG TERJADINYA MINERALISASI TULANG

3. MERANGSANG AKTIVITAS OSTEOCLAST

4. MENJAGA HOMEOSTASIS CALSIUM MELALUI INTERAKSINYA

DENGAN OSTEOSIT

5. DETEKTOR KERUSAKAN MIKRO PADA TULANG

- GANGUAN FUNGSI OSETOBLAST DAPAT DIKETAHUI DENGAN CARA

MENGUKUR KADAR ENZIM ALKALINE FOSFATASE DAN OSTEOCALSIN

PLASMA DARAH

OSTEOSIT

- MERUPAKAN OSTEOBLAST YANG TERPENDAM PADA MATRIK TULANG

YANG TELAH MENGALAMI MINERALISASI

- TERLETAK PADA RUANG SEMPIT DALAM MATRIKS TULANG (LAKUNA)

- BERINTERAKSI DENGAN OSTEOSIT DAN SEL TULANG LAINNYA MELALUI

CANALICULI

- PADA HIPOCALSEMIA OSTEOSIT DPT MERESORBSI PERILACUNAR MATRIKS

HINGGA MENGAKIBATKAN PELEBARAN LAKUNA (OsTeOCYTIC OSTEOLYSIS)

OSTEOCLAST

- MERUPAKAN SEL BERINTI BANYAK (MULTINUCLEATED CELL)- BERASAL DARI HEMATOPOETIC STEM SEL DARI SERI GRANULOSITIK ATAU MONOSITIK - SITOPLASMANYA BERSIFAT EOSINOFILIK DAN MEMILIKI BRUSHBORDER- TERLETAK PADA LAKUNA HOWSHIP`S- FUNGSI 1. MEREBSORBSI TULANG MELALUI AKTIVITAS YG MELIBATKAN SEL TULANG LAINNYA (OSTEOBLAST-OSTEOSIT DAN SEL STROMA) 2. PROLIFERASI OSTEOPROGENITOR (MELALUI GROWTH FACTOR)

- RESORBSI DAPAT TERJADI BILA :

- TERDAPAT AKSES PADA PERMUKAAN TLG (NORMAL TERTUTUP OLEH

OSTEOBLAST DAN UNMINERALIZED BONE MATRIKS)

- OSTESOBLAST DAN STROMAL CELL TERAKTIVASI DAN

MENGEKSPRESIKAN RANK LIGAND

- OSTEOCLAST TERAKTIVASI OLEH MEDIATOR INFLAMASI DAN

NEKROSIS ( IL-1 DAN TNF ALFA)

FAKTOR-FAKTOR YANG DAPAT MENGAKIVASI OSTEOBLAST DAN

MENGEKSPRESIKAN RANK LIGAND (OSTEOCLAST DIFERENSIAL FAKTOR /ODF)

1. HORMON PARATHYROID (PTH)

2. INTERLEUKIN 1 DAN 11

3. 1,25 DEHYDROXYVITAMIN D3

4. PROSTAGLANDIN E2 (PGE2)

5. GLUCOCORTIKOID

6. TUMOR NEKROSIS FAKTOR ALFA

AKTIVITAS ABSORBSI OLEH OSTEOCLAST DIHAMBAT OLEH

OSTEOPROTEGRIN (ODF BLOCKERS) YANG DIHASILKAN OLEH OSTEOBLAST

DAN SEL STROMA SERTA OLEH HORMON CALCITONIN

PERTUMBUHAN TULANG (OSIFIKASI)

Dipengaruhi :Dipengaruhi : 1. hormon hipofisis,thyroid,kortex 1. hormon hipofisis,thyroid,kortex adrenal,parathyroid,estrogen dan androgen.adrenal,parathyroid,estrogen dan androgen. 2. vitamin A --- mempengaruhi kegiatan Osteoklas.2. vitamin A --- mempengaruhi kegiatan Osteoklas. vitamin B komplek --- pembentukan callusvitamin B komplek --- pembentukan callus vitamin C --- merangsang osteoblasvitamin C --- merangsang osteoblas vitamin D ---- pengendapan mineral Pada tulangvitamin D ---- pengendapan mineral Pada tulang 3. Kalsium dan phospor.3. Kalsium dan phospor.

PROSES OSIFIKASI

1. OSIFIKASI INTRAMEMBRANOUS :

- JARINGAN MESENKIM → TULANG

- SEL MESENKIM → OSTEOBLAST

- CONTOH : PEMBENTULKAN TULANG-TULANG PIPIH

2. OSIFIKASI ENDOCHONDRAL

- JAR. TULANG RAWAN HYALIN SBG MODEL → TULANG

- SEL MESENKIM → SEL CHONDROSIT → OSTEOBLAST

- CONTOH PEMBENTUKAN TULANG PANJANG

TAHAP-TAHAP OSIFIKASI

ENDOCHONDRAL :

1. RESTING ZONE

2. PROLIFERATION ZONE

3. HYPERTROPHIC ZONE

A. MATURATION

B. DEGENERATION

C. CALSIFICATION

PENYAKIT-PENYAKIT TULANG

1. GANGGUAN PERTUMBUHAN DAN PERKEMBANGAN TULANG

A. OSTEOPETROSIS - MERUPAKAN PENYAKIT OSTEOSKLEROTIK

(PENINGKATAN KEPADATAN TULANG PER UNIT AREA)

- CAUSA : KEGAGALAN OSTEOCLAST DALAM MERESORPSI

TULANG SELAMA PROSES OSIFIKASI

- HEWAN PENDERITA : ANJING, DOMBA, KUDA, SAPI DAN

BEBERAPA STRAIN MENCIT

- HISTOPATOLOGI :

- GROWTH PLATE : NORMAL

- TULANG TRABECULAR : TERDAPAT TULANG RAWAN

- TULANG KOMPAKTA : NORMAL

B. OSTEOGENESIS INPERFEKTA - MERUPAKAN BENTUK OSTEOPENI ( KURANGNYA MASA TULANG)

- KELAINAN INI DAPAT TERJADI PADA : TULANG, DENTIN,

TENDON DAN SKLERA

- DAPAK KLINIK PADA HEWAN TERSERANG : MULTIPLE FRAKTURE

PERSENDIAN KENDOR, GANGGUAN PERTUMBUHAN DENTIN

- CAUSA : KEGAGALAN OSTEOBLAST/ODONTOBLAST DALAM

SINTESIS COLLAGEN TIPE 1 DAN PROTEIN

NONCOLLAGEN TERTENTU

- HEWAN PENDERITA : DOMBA, SAPI DAN ANAK ANJING

- HISTOPATOLOGI :

- GROWTH PLATE : NORMAL

- TULANG TRABECULAR : LEBIH DOMINAN DR TLG. NORMAL

- TULANG KOMPAKTA : PERTUMBUHAN LAMBAT

- GIGI : BERWARNA PINK KRN PULPA DENTIS TERLIHAT

AKIBAT TIPISNYA MAHKOTA GIGI

C. CRANIOMANDIBULAR OSTEOPATHY (LION JAW)

- MERUPAKAN GANGGUAN OSIFIKASI TERUTAMA PADA TULANG

PIPIH AKIBAT FAKTOR GENETIK

- DITEMUKAN PADA ANJING TERRIER

- BENTUK KELAINAN :

- PENEBALAN DAN DEFORMITAS PADA TLG

MANDIBULA ; OCCIPTAL DAN TEMPORAL

- HISTOPATOLOGI :

- GROWTH PLATE : TIDAK TERLIBAT

- TULANG TRABECULAR : DENSITAS MENINGKAT AKIBAT

PROLIFERASI DAN PENINGKATAN AKTIVITAS OSTEOBLAST

PADA ENDOOSTEUM

- TULANG KOMPAKTA : MENEBAL AKIBAT PENINGKATAN

AKIVITAS OSTEOBLAST PADA PERIOSTEUM SERTA

GANGGUAN PROSES MODELING DAN REMODELING

2. PENYAKIT TULANG METABOLIK

A. OSTEOPOROSIS - MERUPAKAN PENYAKIT PENYAKIT TULANG SISTEMIK AKIBAT GANGGUAN NUTRISI, HORMONAL, ATAU TOKSIN

- ABNORMALITAS DAPAT DITEMUI BAIK PADA TULANG YANG SEDANG TUMBUH ATAU TULANG DEWASA (SELAMA PROSES MODELLING DAN REMODELLING)

- SECARA KLINIS DITANDAI DENGAN SAKIT PADA TULANG DAN FRAKTUR SEKUNDER SEHINGGA DENSITAS TULANG MENURUN

- BERKURANGNYA DENSITAS TULANG TANPA DISERTAI RASA SAKIT SERING DISEBUT OSTEOPENIA

- PADA HEWAN YANG SEDANG TUMBUH OSTEOPOROSIS BERSIFAT REVERSIBLE

- PADA HEWAN DEWASA SECARA FISIOLOGIS REPLACEMENT/PENGGANTIAN TULANG TERJADI SANGAT LAMBAT

- CAUSA : DEFISIENSI KALSIUM

- CAUSA : - DEFISIENSI KALSIUM

- KELAPARAN

- KURANGNYA AKTIVITAS FISIK

- AKIBAT PEMAKAIAN GLUKOKORTIKOID JANGKA

PANJANG

- BERKURANGNYA ESTROGEN (POST MENOPAUSAL

OSTEOPOROSIS)

GAMBARAN HISTOPATOLOGI :

- GROWTH PLATE : MENIPIS

- TULANG TRABEKULAR : MENIPIS, JUMLAH BERKURANG

- TULANG KOMPAKTA : MENIPIS KARENA MENINGKATNYA AKTIVITAS

ABSORBSI OSTEOKLAS; BERPORI

Berkurangnya kalsiumDalam diet Rangsangan Aktivasi Reabsorbsi

Sekresi PTH Osteoklas Kalsium tulang

BerkurannyaAbsorbsi kalsium Meningkatnya

sensitivitas Osteok terhadap PTH

Menurunnya sintesis vit. DYang aktif oleh ginjal

Kadar estrogen Rendah

Vit. D aktif : terbentuk dalam ginjal ( di tubulus proksimalis )

B. RICKETSIA DAN OSTEOMALACIA

- KEDUANYA MERUPAKAN BENTUK PENYAKIT TULANG YANG

DIAKIBATKAN OLEH KEGAGALAN DALAM PROSES MINERALISASI

TULANG YANG DIIKUTI DENGAN DEFORMITAS DAN FKAKTUR

- RICKETSIA TERJADI PADA TULANG YANG SEDANG TUMBUH

(TERUTAMA PADA OSIFIKASI ENDOKONDRAL)

- OSTEOMALACIA TERJADI PADA TULANG DEWASA

- GEJALA KLINIS : NYERI TULANG, FRAKTUR, DEFORMITAS

(SCOLIOSIS; KIPHOSIS)

- CAUSA :

- DEFISIENSI VIT.D ATAU FOSFOR

- PENYAKIT GINJAL KRONIS

- HISTOPATOLOGI :

- GROWTH PLATE : MENEBAL; TERBENTUK NODUL; JUMLAH

KONDROSIT PADA ZONA PROLIFERASI MENINGKAT

- TULANG TRABEKULER : OSTEOID (MATRIK YANG TIDAK

BERMINERAL) MENINGKAT

- TULANG KOMPAKTA : RELATIF LUNAK PADA KEADAAN PARAH,

TULANG DAPAT DIIRIS DENGAN PISAU; MUDAH BENGKOK

Pelvis osteomalaciaPelvis osteomalacia

2. PERADANGAN INFEKSIUS PADA TULANG

- PERADANGAN PADA TLG DISEBUT OSTEOITIS

- PERIOSTITIS BILA PERADANGAN MELIBATKAN PERIOSTEUM

OSTEOMEYLITIS PERADANGAN PADA TULANG DAN RUANG SUMSUM

- CAUSA :

- BAKTERI (80- 90% OLEH STAPHYLOCOCCUS AUREUS) ;

ARCANOBAKTERIUM PYOGENES (PADA SAPI) DAN E. COLI

- VIRUS (HOG CHOLERA; CANINE HEPATITIS; FELINE LEUKIMIA )

- JAMUR (BLASTOMYCES DERMATITIDIS (SERING

MENGAKIBATKAN PYOGRANULOMATOUS)

Pathogenesis :

Organisms may reach the bone by (1) hematogenous spread, (2) extension from a contiguous site, and (3) direct implantation (non hematogenous) on fracture

Most cases of osteomyelitis are hematogenous in origin and develop in the long bones or vertebral bodies.

The initiating bacteremia may follow occult injury to the intestinal mucosa during defecation, vigorous chewing of hard foods, or minor infections of the skin.

Etiologi : Blastomyces Actinomyces

Patogenesis : Luka pada mucosa mulut (erupsi gigi) portal entry bakteri

masuk os mandibula radang kronik pyogranulomatous

Nekrosis menyebabkan hilangnya jaringan tulang Infeksi berlanjut

ke periostal pembentukan tulang baru dan jaringan ikat.

Ciri Khas : fistula yang kering, mandibula membesar, gigi mudah lepas

Bovis Mandibula Osteomyelitis & periostitis

A

B

OSTEONECROSIS (AVASCULAR NECROSIS)/BONE INFARCTION

- Occur in the medullary cavity of the metaphysic or diaphysis and the

Subchondral region of the epiphysis.

- All forms of bone necrosis result from ischemia.

- The mechanisms that produce ischemia include

(1) mechanical vascular interruption (fracture),

(2) corticosteroids

(3) thrombosis and embolism (nitrogen bubbles in dysbarism)

(4) vessel injury (secondary to vasculitis, radiation therapy),

(5) increased intraosseous pressure with vascular compression

(6) venous hypertension

“ Although the disease states associated with bone infarcts are diverse in many cases the cause of necrosis is uncertain”.

A B

Femoral head with a subchondral, wedge-shaped pale yellow area of osteonecrosis. The space between the overlying articular cartilage and bone is caused by trabecular compression fractures without repair.

The term renal osteodystrophy is used to describe collectively all of the skeletal changes of chronic renal disease, including :

(1) increased osteoclastic bone resorption mimicking osteitis fibrosa

cystica,

(2) delayed matrix mineralization (osteomalacia)

(3) osteosclerosis

(4) growth retardation

(5) Osteoporosis

Renal Osteodystrophy

■ Chronic renal failure results in phosphate retention and hyperphosphatemia

■ Hyperphosphatemia, in turn, induces secondary hyperparathyroidism because phosphate regulates PTH secretion.

■ high levels of phosphorus reduced the conversion of 25-(OH)D, to the more active metabolite 1,25-(OH)D; and reduced intestinal absorption of calcium because of low levels of 1,25-(OH),D

■ PTH secretion markedly increases at all levels of serum calcium. 1,25- (OH),D, suppresses PTH gene expression and secretion; in renal failure, there is a decrease in the binding of 1,25-(OH),D, to parathyroid cells; and there is decreased degradation and excretion of PTH because of compromised renal function.

The resultant secondary hyperparathyroidism produces increased osteoclast activity.

■ Metabolic acidosis associated with renal failure stimulates bone resorption and the release of calcium hydroxyapatite from the matrix.

■ Other factors that are important in the genesis of renal osteodystrophy are iron accumulation in bone and aluminum deposition at the site of mineralization. Aluminum deposition, in particular, has received a great deal of attention because of its iatrogenic origin. The sources of the aluminum include dialysis solutions prepared from water with a high aluminum content and oral aluminumcontaining phosphate binders. Aluminum interferes with the deposition of calcium hydroxyapatite and hence promotes osteomalacia. Aluminum is not only toxic to bone but also has been implicated as the cause of dialysis encephalopathy and microcytic anemia in patients with chronic renal failure.

■ Another complication seen in association with renal osteodystrophy is the deposition of masses of amyloid in bone and periarticular structures. The amyloid is formed from f3,-microglobulin, which is increased in the serum of patients who undergo long-term hemodialysis

Traumatic and nontraumatic fractures are some of the most common pathologic conditions affecting bone.

Fractures are classified as complete or incomplete; closed (simple), when the overlying tissue is intactcompound, when the fracture site communicates with the skin surfacePathologic fracture. If the break occurs in bone already altered by a disease process, it is described as a A stress fracture is a slowly developing fracture that follows a period of increased physical activity in which the bone is subjected to new repetitive loads—as in sports training or marching in military boot camp.

Bone is unique in its ability to repair itself; it can completely reactivating processes that normally occur during embryogenesis. zone.

Fractures

Bone repair is a highly regulated process that can be accomplished by a

series of interactions and communications among the various cells and

proteins located in the healing

BONE HEALING

- Immediately after fracture, rupture of blood vessels results in a hematoma. The clotted blood provides a fibrin mesh, which helps seal off the fracture site - Simultaneously, degranulated platelets and migrating inflammatory cells release PDGF, TGF-13, FGF, and other cytokines, which activate the osteoprogenitor cells tissues and stimulate the production of osteoclastic and osteoblastic activity.

- The hematoma is organizing, this fusiform and predominantly uncalcified tissue—called soft tissue callus or procallus—provides some anchorage between the ends of the fractured bones but offers no structural rigidity for weight bearing.

Immediate - first week

The activated osteoprogenitor cells deposit subperiosteal trabeculae of woven bone that are oriented perpendicular to the cortical axis and within the medullary cavity.

In some cases the activated mesenchymal cells in the soft tissues and bone surrounding the fracture line also differentiate into chondroblasts that make fibrocartilage and hyaline cartilage.

In an uncomplicated fracture, the repair tissue reaches its maximal girth at the end of the second or third week, which helps stabilize the fracture site, but it is not yet strong enough for weight bearing.

The newly formed cartilage along the fracture line undergoes enchondralOssification

In this fashion, the fractured ends are bridged by a bony callus, and as it mineralizes, the stiffness and strength of the callus increase to the point that controlled weight bearing can be tolerated

4- 6 weeks

In the early stages of callus formation, an excess of fibroustissue, cartilage, and bone is produced.

If the bones are not perfectly aligned, the volume of callus is greatest in the concave portion of the fracture site.

As the callus matures and transmits weight-bearing forces, the portions that are not physically stressed are resorbed, and in this manner the callus is reduced in size until the shape and outline of the fractured bone has been reestablished.

The medullary cavity is also restored, and after this has been completed it may be impossible to demonstrate the site of previous injury.

Callus

Osteoarthritis, also called degenerative joint disease, is the most common type of joint disease

It is characterized by the progressive erosion of articular cartilage.

The term osteoarthritis implies an inflammatory disease. However, although inflammatory cells may be present, osteoarthritis is considered tobe an intrinsic disease of articular cartilage in which biochemicaland metabolic alterations result in its breakdown.

OSTEOARTHRITIS

Pathogenesis

Articular cartilage is the major target of degenerative changes in osteoarthritis.

Normal articular cartilage is strategically located at the ends of bones to perform two functions: (1) bathed in synovial fluid, it ensures virtually friction-free movements within the joint (2) in weight-bearing joints, it spreads the load across the joint surface in a

manner that allows the underlying bones to absorb shock and weight without being crushed.

Two major components of the cartilage: a special type of collagen (type II) and proteoglycans, both secreted by chondrocytes.

Articular cartilage is not static; it undergoes turnover in which "worn out" matrix components are degraded and replaced. This balance is maintained by chondrocytes, which not only synthesize the matrix but also secrete matrix-degrading enzymes.

Severe osteoarthritis with small islands of residual articular cartilage next to exposed subchondral bone. 1, Eburnated articular surface. 2, Subchondral cyst. 3, Residualarticular cartilage.

Severe osteoarthritis of the hip. The joint space is narrowed, and there is subchondral sclerosis with scattered oval radiolucent cysts and peripheral osteophyte lipping (arrows).

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder that may affect many tissues and organs—skin, blood vessels, heart, lungs, and muscles—but principally attacks the joints, producing a nonsuppurative proliferative and inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints.

Although the cause of RA remains unknown, autoinununity plays a pivotal role in its chronicity and progression.

RHEUMATOID ARTHRITIS

About 1% of the world's population is afflicted by RA, women two to three times more often than men. It is most common in those age 40 to 70, but no age is immune.

Patologi sendi

Radang Sendi = ArthritisGejala klinis :

• pincang , malas jalan• tidak bisa jalan• tak bisa berdiri.

Penyebab :* Arthritis non-infektiosa :

• pecahan-pecahan tulang, duri dsb. Rasa nyeri• traumatic secara sekunder → infectious.

* Arthritis infectiosa : berasal radang dari organ lain mis : radang ginjal Hematogenous → arthritis.* Arthritis : trauma.------- infectious. Sifat eksudat : fibrinous s/d purulent → endapan fibrin → kasar pada permukaan sendi.

Fibrinous synovitis :(rdg sendi berfibrin)Kausa E.colli; streptococus;Haemophilus;Mycoplasma1. bertambahnya cairan sendi (synovial) , keruh, fibrin

→sendi tampak bengkak2. permukaan sendi tebal3. Cairan fibrin bisa berubah jadi jaringan ikat

GOUTGout: terjadi pada spesies yang tidak mempunyai Enzim Urease (manusia,burung,reptil)

Penyebabnya : Ada kaitannya dengan Hiperurisemia (asam urat serum tinggi)

Gout primer : merupakan akibat langsung asam urat serum tinggi. Akibat penurunan ekskresi asam urat.Gout sekunder : pembentukan asam urat yg berlebih. Ekskresi asam urat kurang akibat penyakit lain

Faktor yang berperan : 1. Diet tinggi purin, karena asam urat dibentuk dari purin ,adenine dan guanine. 2. Puasa yang lama karena terjadi peningkatan kadar asam keton yang mengganggu ekskresi asam urat.oleh ginjal 3. Kadar laktat yang tinggi dalam darah mengganggu ekskresi asam urat oleh Ginjal. Gejala kilinis : bengkak ,radang lokal ,terjadi pengendapan kristala sam urat dalam sendi merangsang respon pagositosis oleh leukosit terjadi : keradangan

Gambaran makroskopis : jaringan tulang diganti jaringan trabekulae. Bagian kortex tulang menipis .rongga medulla melebar