ANATOMI SISTEM MUSKULOSKELETAL

I. Pertumbuhan dan Perkembangan Tulang

Jaringan tulang terdiri dari :

1. Komponen cortical
- Sistem Haversian : saluran yang terdiri dari pembuluh darah
- Pembuluh darah sistem havers mengangkut zat fosfor dan kalsium menuju matriks
sehingga matriks tulang menjadi keras
2. Komponen cancellous
- Trabekula yang dibatasi oleh jaringan lemak / hematopoietic marrow

Pembentukan tulang :
1. Ossifikasi endochondral (enchondral)  perkembangan spongiosa
Proses pembentukan tulang ini terbagi menjadi beberapa tahap:
1. Perkembangan model kartilago
2. Pertumbuhan model kartilago
3. Perkembangan pusat osifikasi primer
4. Perkembangan pusat osifikasi sekunder
5. Perubahan kartilago articular dan lempeng epifisis
 tulang panjang
2. Ossifikasi intramembranous (membranous) = penulangan primer
Terdapat beberapa langkah dalam proses pembentukan tulang ini yaitu:
1. Perkembangan pusat pembentukan tulang. 
2. Kalsifikasi
3. Pembentukan Trabecula
4.Perkembangan periosteum
 perkembangan cortex  proses mengubah kartilago menjadi tulang
 tulang pipih & tulang tubular, vertebra, basis cranii, ethmoid, medial dan lateral ends
clavicula
 Embrio 7 minggu  jaringan mesenkim  sel kartilago (chondroblast & chondrocytes) 
kartilago hyaline
 TRAUMA

1. Fraktur dan Dislokasi

- Fraktur : terputusnya kontinuitas tulang. Fraktur terbagi 2 yaitu komplit dan inkomplit
- Dislokasi : Terlepasnya kompresi jaringan tulang dari kesatuan sendi; permukaan artikular
tidak intak
- Subluksasi : Terlepasnya sebagian jaringan tulang dari sendi dimana sebagian permukaan
artikular masih intak

Evaluasi Radiologik :

1. Diagnosis dan evaluasi tipe fraktur atau dislokasi

2. Monitor penanganan dan komplikasi

Evaluasi Radiologik Fraktur :

1. Lokasi anatomi dan luas fraktur

2. Tipe fraktur
3. Alignment fragmen fraktur (displacement, angulasi, rotasi, foreshortening, distraction)
4. Arah garis fraktur terhadap axis longitudinal tulang
5. Adanya gambaran khas seperti impaksi, depresi, atau kompresi
6. Adanya abnormalitas yang berhubungan dengan fraktur seperti dislokasi / diastasis
7. Tipe fraktur yang khas akibat stress atau sekunder dari proses patlogik pada tulang
Fraktur pada anak :
- Greenstick fracture
- Torus fracture → buckling of the cortex
- Battered child fracture → metaphyseal corner fracture of distal femur & proximal tibia
- Child abuse fractures
1. Corner fracture → fraktur avulsi pada ujung metafisis
2. Bucket handle fracture → avulsi metafisis tulang menyerupai disc / bucket handle → >>> tibia,
distal femur, proximal humeri → bilateral
3. Lateral & posterior rib fracture
4. Skull fractures → multiple ‘eggshell’ fracture, occipital impression fracture, fracture crossing
sutures
Corner fracture Bucket handle fracture

Tanda tidak langsung pada fraktur :

1. Soft tissue swelling
2. Obliterasi atau displacement fat stripes
 Subtle fracture  distal radius, carpal scaphoid, trapezium, basis metacarpal I
 Posisi lateral  pronator quadratus fat stripe (lemak antara pronator quadratus
(quadratironator) & tendon flexor digitorum profundus)  displaced anterior / blurred /
obliterasi (MacEwan sign)

 Scaphoid fat stripe (garis radiolusen yang paralel permukaan lateral os scaphoid antara
ligamentum kolateral radial dan synovial sheat abductor pollicis longus & extensor pollicis
brevis)  obliterasi/displaced (fraktur carpal scaphoid, radial styloid, trapezium, basis
metacarpal I)

3. Periosteal & endosteal reaction  tanda radiologik awal fraktur

4. Joint effusion
 Fat-pad sign  distensi kapsula artikular oleh cairan sinovial / hemoragik  elbow
trauma

5. Intracapsular fat-fluid level / fat-blood interface (FBI sign)

 Fraktur melibatkan permukaan artikular tulang  darah & lemak sumsum tulang
sendi (lipohemaarthrosis)  FBI sign

6. Double cortical line  fraktur depresi / impaksi

7. Buckling of the cortex (Torus fracture)  posisi lateral  tulang tubular pada anak
8. Irregular metaphyseal corners  fraktur avulsi metafisis  infant / anak (battered child
syndrome)
Evaluasi Trauma Setelah Penanganan
Penyembuhan fraktur terdiri dari 3 fase :
- Fase inflammatory (reactive)  2-7 hari (vasodilatasi, eksudasi serum, infiltrasi sel inflamasi)
- Fase reparative  1 bulan  pembentukan callus periosteal & endosteal o/ osteoblast periosteal
& bone marrow
- Fase remodelling  3 bulan – 1 tahun  callus periosteal & endosteal removed, woven
immature bone diganti dengan secondary lammelar (cortical /trabecular) bone

Penyembuhan fraktur tergantung pada beberapa faktor :

- Usia
- Lokasi & tipe fraktur
- Posisi fragmen fraktur
- Aliran darah
- Kualitas immobilisasi / fiksasi
- Adanya infeksi / osteonekrosis

Komplikasi fraktur :
- Delayed union → fraktur yang tidak union setelah 16-24 minggu
- Nonunion → pseudoarthrosis (pembentukan cavitas menyerupai celah sendi pada daerah fraktur)
→ biasanya dipakai untuk istilah fraktur yang tidak union dalam 9 bulan
1. Reactive (Hypertrophic & oligotrophic) (1) → exuberant bone reaction → flaring & sclerosis
bone → well-vascularized new bones → R/ intramedullary nailing / compression platting
2. Nonreactive (atrophic) (2) → bone reaction (-), blood supply <<< → R/ decortication & bone
grafting
3. Infected nonunion (3) → osteomyelitis
 R/ inactive osteomyelitis → decortication & bone grafting + compression platting
 R/ active osteomyelitis → antibiotik, sequestrectomy + bone grafting + intramedullary nail
- Malunion
- Disuse osteoporosis
- Reflex sympathetic dystrophy syndrome / Sudeck atrophy → diffuse osteoporosis, soft tissue
swelling, nyeri, joint stiffness, vasomotor instability, dystrophic skin changes
X-Ray : soft tissue swelling, osteoporosis berat
Bone scan Tc : blood flow ↑, blood pool, ↑ uptake periarticular
1. Fase akut (inflamasi) (1-7 minggu)→nyeri regional difus, inflamasi, edema, hipo/hipertermia
2. Fase dystrophic (3-24 bulan) → nyeri saat aktivitas, sensitivitas kulit terhadap
tekanan/perubahan temperatur ↑, atrofi otot & kulit
3. Fase atrofi / lanjut → irreversible scleroderma-like skin changes & aponeurotic & tendinous
retraction
- Volkmann ischemic contracture → iskemik otot diikuti fibrosis → fraktur supracondylar humerus
‘Five Ps’ syndrome → pulselessness, pain, pallor, paresthesia, paralysis
X-Ray : Kontraktur fleksi pada wrist dan interphalangeal joint of the finger, hiperekstensi MCP
akibat soft tissue atrofi

Sudeck atrophy Volkmann ischemic contracture

- Posttraumatic myositis ossificans → zonal phenomenon (area radiolusen pada bagian tengah lesi
(immature bone) dikelilingi oleh area radioopak (mature ossification)
T1WI : isointens, sedikit hiperintens dibandingkan otot, + C : peripheral rim enhancement, T2WI :
hiperintens, kalau mature → hipointens pada bagian perifernya, hiperintens T1WI, T2WI (lemak)
- Osteonecrosis (ischemic / avascular necrosis) →o/k intraluminal vascular obstruction, vascular
compression, disruption blood vessel →>> caput femoris, os scaphoid, caput humeri
- Injury to major blood vessels → pendarahan, hematoma, AVF, pseudoaneurysma
- Growth disturbance → tethering epifisis & metafisis tulang
- Posttraumatic arthritis

Fraktur Supracondyler Humerus

Extra-articular Epicondylar Fraktur dari epicondylus medial
atau lateral
Supracondylar Garis fraktur terdapat diatas
epicondylus
Intra-articular Transcondylar Bidang fraktur terdapat didalam
kapsul sendi dan terjadi fraktur dari
condylus medialis dan lateralis
Bicondylar Fraktur interarticuler yang
memisahkan condylus medialis dan
lateralis

OSTEOCHONDROSIS
- Pertumbuhan tulang progresif akibat necrosis tulang →dekade I → L>P → biasanya single &
unilateral
- Gejala klinis : nyeri, pergerakan terbatas, riwayat trauma (+)
1. Legg-Calve-Perthes : caput femoris
2. Kienbock’s disease : os lunatum
3. Preiser’s disease : os scaphoid
4. Panner’s disease : capitulum humeri
5. Freiberg’s disease : distal metatarsal digiti II
6. Kohler disease : os naviculare
7. Osgood Schlatter : ligamentum patellar pada tuberositas tibiae
8. Sinding-Larsen-Johansonn : proximal patellar tendon → jumper’s knee (fragmentasis inferior
portion of the patella)
9. Sever disease : os calcaneus apophysis
10.Thiemann’s disease : digiti II dan V → physeal closure + shortened middle phalanges
11.Scheuermann’s disease : kifosis lower thoracic, pembentukan cartilaginous node, irregular
vertebral outlines, + mild scoliosis, intervertebral disc space
narrowing
 Scheuermann’s disease

Legg-Calve-Perthes. A. Soft tissue distortion (arrowheads), sclerotic femoral ossification center that is laterally displaced
and contains radiolucent fissures, and metaphyseal irregularity. B. Metaphyseal “cysts”. Observe the large cystic lesion of
the medial metaphysis of the femur (arrow), which is associated with a fragmented, sclerotic, and laterally placed ossific
nucleus. C. The broad and short femoral neck containing multiple radiolucent lesions. Most of the epiphyseal ossification
center is destroyed
I II III IV
GRADES OF FEMORAL INVOLVEMENT IN
LEGG-CALVE-PERTHES DISEASE
Site of epiphyseal anterior anterior almost whole (CATTERALL CLASSIFICATION)
involvement part part whole epiphysis
epiphysis

Sequestrum No Yes Yes Yes

Crescent sign No anterior anterior and anterior and

extends posteriorly
posteriorly

Collapse No Yes Yes Yes

Metaphyseal No Localized Diffuse Diffuse

abnormalities

Freiberg’s disease. Initial radiograph reveals minimal increased

radiodensity of the head of the 3rd metatarsal bone (arrow). Two
weeks later, the depression of the articular surface of the
metatarsal head and the sclerosis are more apparent (arrow

Kohler disease

Panner’s disease
 Sever disease
12.Blount’s disease / tibia vara : gangguan pertumbuhan pada aspek medial epifisis tibia
proksimal
2 tipe :
- Tipe infantile : dekade I → X-ray : bowing, alignment proximal tibia tidak sejajar dengan
femur, posisi tibia varus dengan angulasi metafisis, tibial shaft is adducted without intrinsic
curvature, depressed medial tibial metaphysis + osseus excrescence / spur

I (2-3 thn) deformitas varus os tibia progresif + growth plate irreguler + aspek
medial metafisis protrusi membentuk ‘medial & distal beak’
II (2½ - 4 thn) depresi lateromedial pada garis ossifikasi dari aspek medial
metafisis dengan wedge-shaped ujung medial epifisis
III (4-6 thn) The cartilage-filled depression in the metaphyseal beak deepens.
The medial part of the bone epiphysis remains wedge-shaped and is less
distinct. Small calcific foci may be evident beneath the medial border
IV (5 to 10 years). With increasing bone maturation, the cartilaginous growth
plate is reduced to a narrow plate, and the bone epiphysis occupies an
increasing part of the end of the bone.
The medial margin of the epiphysis shows definite irregularity
V (9 to 11 years) The bone epiphysis and the corresponding articular surface
are greatly deformed.
The epiphysis is separated in two portions by a clear band, extending
medially from the lateral portion of the growth plate to the articular
cartilage
VI (10 to 13 years) The branches of the medially located double growth plate
ossify, whereas growth continues in the normal lateral part.
Stages V and VI represent phases of irreparable structural damage

- Tipe adolescent (8-15 tahun) → unilateral (90%), leg shortening, mild to moderate varus
deformity (10-200), medial wedging epifisis tibia proksimal, tibial growth plate medial (-)
jika berdiri

Stadium osteonecrosis (Heinberg modified Ficat & Arlet stage)

- Stadium 0 : normal
- Stadium I : normal radiograph, abnormal bone scan/MRI
- Stadium II : mottled sclerosis on radiograph
- Stadium III : subchondral collapse (crescent sign) without flattening of the articular surface
- Stadium IV : flattening / lose of bone contour without joint space narrowing
- Stadium V : joint space loss or other manifestation of joint degeneration (subchondral cyst)
- Stadium VI : Advanced degenerative change
MRI :
T1WI : Hypointense ischemic area
 Linear serpentine area of decreased signal intensity
Loss of high-signal intensity subchondral fat
T2WI : periarticular edema → high signal intensity double line sign → linear area of decreased
signal (necrosis) parallel an adjacent linear area of edema / hemorrhage (hyperintense)

Bone infarct → osteonecrosis pada metafisis / diafisis

Imaging :
X-Ray : - medullary lesion → sheet like central lucency
- serpiginous border → shell like sclerosis
- discrete calcification
- periostitis
MRI : T1WI → hipointens perifer dengan peripheral rim enhancement post contrast
Central signal usually that of marrow
T2WI → ill defined non spesific area of high signal → infarct akut
Double line sign → hiperintense inner ring (granulation tissue), hipointense outer ring
Sclerosis
Central signal usually that of marrow
 LANGERHANS CELL HISTIOCYTOSIS (LCH)

- Kumpulan penyakit idiopatik ditandai dengan proliferasi histiosit, bisa localized / systemic
- Tipe LCH :
1. Unifocal LCH (eosinophilic granuloma of bone)
 Usia : 5-15 tahun
 Gejala : asimptomatik atau nyeri
 X-Ray : - Lesi litik punched-out dengan ujung bersiku pada kepala
- Vertebral plana →flattened vertebral bodies
- Lesi litik tulang multiple → vertebra, costa, mandibula, femur, ilium, scapula

Vertebral plana
- Etiologi : trauma, osteoporosis, LCH (single level), osteogenesis imperfecta,
leukemia, vertebral metastases, multiple myeloma, lymphoma (multiple level),
osteomyelitis, vertebral hemangioma
- Entire skeleton → platyspondyly

 DD / Epidermoid inclusion cyst

o Benign, slow-growing tumor of the skull
o Usia : 20-40 tahun, prevalensi usia dermoid sedikit lebih muda dibandingkan
epidermoid
o Painless subcutaneous swelling. Kalau besar, dapat menyebabkan kompresi n. Cranialis
o Imaging :
 Intradiploic
 Lesi litik berbatas tegas yang melibatkan tabula interna dan externa dengan batas
sclerotik → CT (hipodens tidak menyangat post kontras), MRI (T1WI hipointens,
T2WI hiperintense)
 Sering pada os parietal, os frontal, os occipital dan orbita
 Dermoid cyst biasanya di midline pada frontotemporal & os parietal. Paling sering
pada garis sutura didekat fontanella anterior
o Komplikasi : berhubungan dengan sinus/dural sinus, infeksi
2. Acute disseminated LCH (Lettered-Siwe disease)
 Aggresive systemic disorder → acute, diffuse, often fatal
 Usia < 2 tahun
 Gejala : demam, anemia, thrombocytopenia, pulmonary infiltrate, skin lesions,
pembesaran KGB, hepatosplenomegaly
 D/ rash, adenopathy, hepatosplenomegaly, diffuse lung involvement
 R/ Intensive chemotherapy → 5 year survival 50%
3. Multifocal LCH (Hand-Schuller-Christian disease)
 Usia : 2-10 tahun
 D/ demam, erupsi difus (scalp, canalis acusticus), otitis media, mastoiditis, URI, bone lesion,
mild lymhadenopathy, hepatomegaly, splenomegaly, diabetes insipidus (posterior stalk of
hypothalamus)
 Triad : Diabetes insipidus, calvaria bone defects , exophtalmus
 TUMOR TULANG

 Matriks osteoid : Densely mineralized, cloudlike or cottonlike in

morphology
 Matriks chondroid : Calcifications in bizzare shapes resembling ring and archs
 Matriks fibrous : No mineralization; classically referred to as groud glass in
appereance

Important terms in making diagnosis of bone tumors :

 Age
 Aggressiveness of the lesion
o Pattern of bone destruction
o Zone of transition
o Periosteal reaction
o Presence or absence of the soft tissue involvement
o Presence of tumor matrix
o Site in skeleton
o Location in bone
o Patient’s age
 Location of the lesion

Tumor osteogenik Tumor chondroid Tumor fibrous

Osteoid osteoma Enchondroma Nonossifying fibroma
Osteoblastoma Osteochondroma Fibrous dysplasia
Osteoma Chondroblastoma Malignant fibrous
histiocytoma
Enostosis (bone island) Chondromyxoid fibroma Fibrosarcoma
Osteosarcoma Chondrosarcoma Adamantinoma

Bone marrow Epiphyseal tumor Metaphyseal Diaphyseal tumor

tumor tumor
Giant cell tumor Chondroblastoma Osteoblastoma Enchondroma
Eosinophilic Giant cell tumor Osteochondroma Fibrous dysplasia
granuloma
Lymphangioma Aneurysmal bone Nonossifying Ewing’s sarcoma
cyst fibroma
Multiple myeloma Eosinophilic Osteoid osteoma Chondrosarcoma
granuloma
Ewing’s sarcoma Clear cell Chondromyxoid Fibrosarcoma
chondrosarcoma fibroma
Lymphoma Metastasis Giant cell tumor Metastasis
Leukemia Osteosarcoma
Metastasis
Osteopenia : densitas tulang menurun akibat produksi tulang ↓ / resorpsi tulang ↑
- Terdiri atas :
1. Osteoporosis (quantitas tulang ↓)
2. Osteomalacia (mineralisasi tulang ↓)
- DD/
1. Osteogenesis imperfecta
2. Scurvy
3. Leukemia
4. Steroid therapy
5. Juvenile osteoporosis

Rickets
- Osteomalacia pada anak akibat defisiensi vitamin D
- Etiologi : gangguan / kelainan gastric/biliary/enteric/renal osteodistrofi → absorpsi intestinal ↓↓
1. Osteoporosis (quantitas tulang ↓)
2. Osteomalacia (mineralisasi tulang ↓)
- 2 tipe :
1. Infantile rickets (6-18 bulan)
2. Vitamin D-resistant rickets (> 30 bulan)
- Imaging
1. Diffuse osteoporosis → trabekula tulang kasar → bowing deformities
2. Pelebaran growth plate
3. Metafisis cupping dan flaring → fraying
4. Rachitis rosary