PATOLOGI TULANG DAN

SENDI
 INTRODUCTION
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.
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 MATRIKS TULANG

OSTEOBLAST
ORGANIK MINERAL
OSTEOSIT
-CALSIUM
OSTEOCLAST COLLAGEN TYPE 1 - CARBONAT
- MAGNESIUM
NON COLLAGEN - SODIUM
- MANGAN
MATRIKS :
- ZINC
- PROTEOGLYCANS
- FLUORIDE
- GLYCOSAMINOGLYCAN
- PROTEIN
- LEMAK
- AIR

- 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)
AKTOR-FAKTOR YANG DAPAT MENGAKIVASI OSTEOBLAST DAN
ENGEKSPRESIKAN RANK LIGAND (OSTEOCLAST DIFERENSIAL FAKTOR /ODF)

HORMON PARATHYROID (PTH)

INTERLEUKIN 1 DAN 11
1,25 DEHYDROXYVITAMIN D3
PROSTAGLANDIN E2 (PGE2)
GLUCOCORTIKOID
TUMOR NEKROSIS FAKTOR ALFA

KTIVITAS ABSORBSI OLEH OSTEOCLAST DIHAMBAT OLEH

STEOPROTEGRIN (ODF BLOCKERS) YANG DIHASILKAN OLEH OSTEOBLAST
AN SEL STROMA SERTA OLEH HORMON CALCITONIN
 PERTUMBUHAN TULANG (OSIFIKASI)
 Dipengaruhi :
 1. hormon hipofisis,thyroid,kortex
 adrenal,parathyroid,estrogen dan androgen.
 2. vitamin A --- mempengaruhi kegiatan Osteoklas.
 vitamin B komplek --- pembentukan callus
 vitamin C --- merangsang osteoblas
 vitamin D ---- pengendapan mineral Pada tulang
 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 kalsium
Dalam diet
Rangsangan Aktivasi Reabsorbsi
Sekresi PTH Osteoklas Kalsium tulang

Berkurannya
Absorbsi kalsium
Meningkatnya
sensitivitas Osteok
terhadap PTH
Menurunnya sintesis vit. D
Yang 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 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.
Bovis Mandibula Osteomyelitis & periostitis

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
 B

A
 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.
 Renal Osteodystrophy

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
■ 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
 Fractures
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 intact
compound, when the fracture site communicates with the skin surface
Pathologic 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.
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

Immediate - first week

- 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.
4- 6 weeks

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 enchondral
Ossification

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
In the early stages of callus formation, an excess of fibrous
tissue, 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

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 to
be an intrinsic disease of articular cartilage in which biochemical
and metabolic alterations result in its breakdown.
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, Residual
articular 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

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.

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 = Arthritis

Gejala 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;Mycoplasma
1. bertambahnya cairan sendi (synovial) , keruh, fibrin
→sendi tampak bengkak
2. permukaan sendi tebal
3. Cairan fibrin bisa berubah jadi jaringan ikat
 GOUT
Gout:
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