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BONE

JOINT
SOFT TISSUE
Modeling/RE-modeling
CELLS of BONE
OSTEOPROGENITOR (STEM)(TGF)
OSTEOBLASTS (surface of spicule), under
control of calcitonin to take blood calcium and
put it into bone.
OSTEOCYTES (are osteoblasts which are
now completely surrounded by bone)

OSTEOCLASTS (macrophage lineage),


under control of PTH to chew up the calcium of
bone and put it into blood
Proteins (organic) of BONE
Type 1 (TYPE [B]ONE) collagen (90%)
Cell adhesion proteins, i.e. CAMs: Osteopontin,
fibronectin, thrombospondin
Calcium-binding proteins: Osteonectin, sialoprotein
Proteins involved in mineralization: Osteocalcin
Enzymes: Collagenase, Alk. Phos.
Growth factors
IGF-1, TGF-, PDGF
Cytokines
Prostaglandins, IL-1, IL-6, RANKL
Proteins Concentrated from Serum
2 microglobulin Albumin
IGF, insulin-like growth factor
TGF, transforming growth factor
PDGF, platelet-derived growth factor
IL, interleukin
RANKL, RANK ligand
Minerals (IN-organic) of BONE
HYDROXY-APATITE
Ca5(PO4)3(OH)
Ca10(PO4)6(OH)2
ADJECTIVES of BONE
Compact
Dense
Cortical

Spongy
Cancellous
Membranous
Endosteal
Spicular
Woven vs. Lamellar
-BLASTS/-CLASTS

Ca++ PTH

Ca++ Calcitonin

BONE DISEASES
1) MALFORMATIONS AND DISEASES CAUSED BY DEFECTS IN NUCLEAR PROTEINS
AND TRANSCRIPTION FACTORS, polydactyly, syndactyly, absence of a bone
2) DISEASES CAUSED BY DEFECTS IN HORMONES AND SIGNAL TRANSDUCTION
MECHANISMS, achondroplasia, thanatophoria
3) DISEASES ASSOCIATED WITH DEFECTS IN EXTRACELLULAR STRUCTURAL
PROTEINS
Type 1 Collagen Diseases (Osteogenesis Imperfecta)
Types 2, 10, and 11 Collagen Diseases
4) DISEASES ASSOCIATED WITH DEFECTS IN FOLDING AND DEGRADATION OF
MACROMOLECULES
Mucopolysaccharidoses
5) DISEASES ASSOCIATED WITH DEFECTS IN METABOLIC PATHWAYS (ENZYMES,
ION CHANNELS, AND TRANSPORTERS)
Osteopetrosis
6) DISEASES ASSOCIATED WITH DECREASED BONE MASS
Osteoporosis
7) DISEASES CAUSED BY OSTEOCLAST DYSFUNCTION
Paget Disease (Osteitis Deformans)
8) DISEASES ASSOCIATED WITH ABNORMAL MINERAL (Ca++) HOMEOSTASIS
Ricketts and Osteomalacia
Hyperparathyroidism
Renal Osteodystrophy
1) MALFORMATIONS AND
DISEASES CAUSED BY DEFECTS
IN NUCLEAR PROTEINS AND
TRANSCRIPTION FACTORS
proteinDNAmRNA
Congenital absence of a, usually single,
bone: phalanx, rib, clavicle
Supernumerary digit (polydactyly)
Syndactyly
CRANIORACHISCHISIS
2) DISEASES CAUSED BY
DEFECTS IN HORMONES AND
SIGNAL TRANSDUCTION
MECHANISMS
Achondroplasia, dwarf (non-lethal)
Thanatophoria, dwarf (lethal, FGF-3
mutations)
a point mutation (usually Arg for Gly375) in the gene that
codes for FGF receptor 3 (FGFR3), which is located on
the short arm of chromosome 4. In the normal growth
plate, activation of FGFR3 inhibits cartilage proliferation,
hence the term achondroplastic;
A MUTATION causes FGFR3 to be constantly activated.
Achondroplastic dwarf Thanatophoric dwarf, often lethal

Short arms and extra folds of skin


3) DISEASES ASSOCIATED WITH
DEFECTS IN EXTRACELLULAR
STRUCTURAL PROTEINS
OSTEOGENESIS IMPERFECTA TYPES
(Brittle bone disease, too LITTLE bone),
BLUE sclerae
Mutations in genes which code for the alpha-
1 and alpha-2 chains of COLLAGEN 1
Mutations of COLLAGEN 2,10, 11 manifest
themselves as CARTILAGE diseases,
ranging from joint cartilage destruction to
fatal sequelae
Osteogenesis Imperfecta

BLUE SCLERA
4) DISEASES ASSOCIATED WITH
DEFECTS IN FOLDING AND
DEGRADATION OF MACROMOLECULES
(glycosaminoglycans)
MUCOPOLYSACCHARIDOSIS (one of MANY lysosome
storage diseases)
DECREASES in ENZYMES which degrade:
DERMATAN

HEPARAN
KERATAN

Chiefly CARTILAGE disorders: short, chest wall,


malformed bones
MUCOPOLYSACCHARIDOSES
5) DISEASES ASSOCIATED WITH
DEFECTS IN METABOLIC
PATHWAYS (ENZYMES, ION
CHANNELS, AND
TRANSPORTERS)
OSTEOPETROSIS, 4 types
One common one has a CARBONIC
ANHYDRASE deficiency, i.e., acid
DECREASED osteoclast resorption
MARBLE bone, increased bone, brittle,
sclerotic bone
OSTEOPETROSIS
6) DISEASES ASSOCIATED WITH
DECREASED BONE MASS
OSTEOPOROSIS
PEAK bone mass is early adulthood
Normal decline, slow
Osteoporosis is accelerated bone loss
Factors:
AGE
Physical activity
Estrogen withdrawal (menopause)
Nutrition (Ca++)
Genetics
Categories of Generalized Osteoporosis
Primary
Postmenopausal Idiopathic
Senile
Secondary
Endocrine disorders Rheumatologic disease
Hyperparathyroidism Drugs
Hypo-hyperthyroidism Anticoagulants
Hypogonadism Chemotherapy
Pituitary tumors Corticosteroids
Diabetes, type 1 Anticonvulsants
Addison disease Alcohol
Neoplasia Miscellaneous
Multiple myeloma Osteogenesis imperfecta
Carcinomatosis Immobilization
Gastrointestinal Pulmonary disease
Malnutrition, Malbs., Hepatic Insuf., Vit Homocystinuria
C,D
Anemia
OSTEOPOROSIS
7) DISEASES CAUSED BY
OSTEOCLAST DYSFUNCTION
Paget Disease (Osteitis
Deformans)
Matrix madness, Osteoblasts/-cytes gone wild
THREE PHASES:
1) Increased osteoclast resorption
2) Increased hectic bone formation (osteoblasts)
3) Osteosclerosis

ELEVATED ALKALINE-PHOSPHATASE
ELEVATED urine HYDROXYPROLINE
PAGETs DISEASE (of BONE)
85% MONOSTOTIC, WHOLE BONE
15% POLY-OSTOTIC (skull, pelvis)
JIGSAW, NOT LAMINAR, BONE

CLINICAL: PAIN!!!
(MICROFRACTURES)
PAGETs DISEASE

NON-Lamellar bone
8) DISEASES ASSOCIATED WITH
ABNORMAL MINERAL
HOMEOSTASIS
Ricketts and Osteomalacia
VITAMIN D deficiency/dysfunction
Hyperparathyroidism, PRIMARY (PTH ADENOMA)
ENTIRE SKELETON
OSTEITIS FIBROSIS CYSTICA (von Recklinghausens disease
(of bone)
BROWN* TUMOR
Hyperparathyroidism, SECONDARY (RENAL) (NOT AS
SEVERE AS 1)
Renal Osteodystrophy = ANY bone disorder due to
chronic renal disease
PRIMARY
HYPERPARATHYROIDISM

OSTEITIS FIBROSA BROWN TUMOR


CYSTICA
RENAL OSTEODYSTROPHY
PHOSPHATE RETENTION
HYPOPHOSPHATEMIA
HYPOCALCEMIA
INCREASED PTH
INCREASED OSTEOCLASTS
METABOLIC ACIDOSIS release of
HYDROXYAPATITES from matrix
FRACTURES
FRACTURES,
adjectives
Complete, incomplete
Closed, open (communicating)
Communited (splintered, greenstick)
Displaced (NON-aligned)
PATHOGENIC, (non-traumatic, 2 to other
disease, often metastases)
STRESS fracture
FRACTURES
THREE PHASES
HEMATOMA, minutes days PDGF, TGF-, FGF
SOFT CALLUS (PRO-CALLUS), ~1 week
HARD CALLUS (BONY CALLUS), several weeks

COMPLICATIONS
PSEUDARTHROSIS (non-union)
INFECTION (especially OPEN [communicating]
fractures)
FRACTURES
OSTEONECROSIS
Also called AVASCULAR necrosis
Also called ASEPTIC necrosis

CAUSE: ISCHEMIA
Trauma
Steroids
Thrombus/Embolism
Vessel injury, e.g., radiation
INCREASED intra-osseous pressurevascular
compression
Venous hypertension too
OSTEONECROSIS
Disorders Associated with Osteonecrosis
Idiopathic Pregnancy

Trauma Gaucher disease

Corticosteroid Sickle cell and other


anemias
administration
Infection Alcohol abuse
Dysbarism Chronic pancreatitis
Radiation therapy Tumors
Connective tissue Epiphyseal disorders
disorders
OSTEONECROSIS
OSTEONECROSIS
OSTEOMYELITIS
Pyogenic: Staph, E. coli, Pseudom, Kleb,
Salmonella
Hematogenous
Contiguous, e.g., from a nearby joint
Direct implantation
TB
Syphilis
OSTEOMYELITIS
DX: X-ray, Bone scan
OSTEOMYELITIS
DX: Histology
OSTEOMYELITIS
COMPLICATIONS
Subperiosteal abscess
Draining sinus
Joint involvement

SEQUESTRUM (dead bone)


vs.
INVOLUCRUM (new bone)
OSTEOMYELITIS
Tuberculous
Usually blood borne
TB of spine is known as POTTS
disease

Syphilis
CONGENITAL
TERTIARY, SABRE shins
POTTs DISEASE
SABER SHINS
Classification of Primary Tumors Involving Bones
Histologic Type Benign Malignant
Hematopoietic (40%) Myeloma

Malignant lymphoma
Chondrogenic (22%) Osteochondroma Chondrosarcoma

Chondroma Dedifferentiated chondrosarcoma

Chondroblastoma Mesenchymal chondrosarcoma

Chondromyxoid fibroma

Osteogenic (19%) Osteoid osteoma Osteosarcoma

Osteoblastoma
Unknown origin (10%) Giant cell tumor tumor

Giant cell tumor


Adamantinoma
Histiocytic origin Fibrous histiocytoma Malignant fibrous histiocytoma

Fibrogenic Metaphyseal fibrous defect (fibroma) Desmoplastic fibroma

Fibrosarcoma
Notochordal Chordoma
Vascular Hemangioma Hemangioendothelioma

Hemangiopericytoma
Lipogenic Lipoma Liposarcoma
Neurogenic Neurilemmoma
BONE TUMORS
BONE
CARTILAGE
FIBROUS
MISC.
Ewings sarcoma
Giant Cell Tumor
METASTASES
BONE- BONE TUMORS
OSTEOMA
OSTEOID OSTEOMA (nidus)
OSTEOBLASTOMA
OSTEOSARCOMA (OSTEOGENIC
SARCOMA)
OSTEOMA
SOLITARY
MIDDLE AGE
FROM SUBPERIOSTEAL or ENDOSTEAL
surfaces
SKULL, FACE, most common
Totally BENIGN
To be distinguished from REACTIVE BONE,
(can be difficult)
FRONTAL SINUS

Why am I not showing you HISTOLOGY?


OSTEOID OSTEOMA
At least 2 cm in diameter
Teens, twenties, APPENDICULAR
skeleton
M>>F
PAINFUL

Has a NIDUS
Responds to aspirin
Induces a MARKED bony reaction
NIDUS
OSTEOBLASTOMA
AXIAL SKELETON, i.e., SPINE
NO nidus
NO bony reaction
NOT relieved by aspirin
OSTEOSARCOMA
(OSTEOGENIC SARCOMA)

LATE TEENS
KNEES
METAPHYSES
PAINFUL!!!
TYPES of OSTEOSARCOMAS
The anatomic portion of the bone from which they
arise (intramedullary, intracortical, or surface)
Degree of differentiation
Multicentricity (synchronous, metachronous[NOT
synchronous])
Primary (pre-existing bone is unremarkable) or
secondary (e.g., osteosarcoma associated with pre-
existing disorders such as benign tumors, Paget
disease, bone infarcts, previous irradiation)
Histologic variants (osteoblastic, chondroblastic,
fibroblastic, telangiectatic, small cell, and giant cell)
The most common subtype is osteosarcoma that arises in the
metaphysis of long bones; is primary, solitary, intramedullary, and
poorly differentiated; and produces a predominantly bony matrix
BONE- CARTILAGE TUMORS
OSTEOCHONDROMA
(EXOSTOSIS)
CHONDROMA
CHONDROBLASTOMA
CHONDROMYXOID FIBROMA
CHONDROSARCOMA
OSTEOCHONDROMA
(EXOSTOSIS)
Common, Cartilage AND Bone present
Often MULTIPLE as a hereditary
syndrome
M>>>F
PELVIS, SCAPULAE, RIBS
CHONDROMA
Chondroma vs. EN-chondroma
PURE Hyaline Cartilage
MULTIPLE enchondromas = Olliers dis.
Maffucci Synd. if hemangiomas present
CHONDROBLASTOMA
RARE, in teenagers
M>>F
KNEES, usually
Epiphyses
MUCH LESS matrix than a chondroma
CHONDROMYXOID FIBROMA
RAREST of all
TEENS, MALES
MYXOID concept
ATYPIA
CHONDROSARCOMA
ANATOMY
INTRAMEDULLARY
JUXTACORTICAL
HISTOLOGY
CONVENTIONAL
HYALINE
MYXOID
CLEAR
DE-DIFFERENTIATED
MESENCHYMAL
CHONDROSARCOMA
BONE- FIBROUS TUMORS
FIBROUS CORTICAL DEFECT/NON-
OSSIFYING FIBROMA
FIBROUS DYSPLASIA
FIBROSARCOMA/MALIGNANT
FIBROUS HISTIOCYTOMA
FIBROUS CORTICAL DEFECT
COMMON, usually LESS
THAN 1 CM
CHILDREN >2
IF MORE THAN 5-6 CM,
they are then called NON-
OSSIFYING FIBROMA
FIBROUS DYSPLASIA
BENIGN TUMOR
THREE TYPES
SINGLE BONE (70%)
POLY-OSTOTIC (27%)
POLY-OSTOTIC (3%) with caf-au-lait
and endocrine disorders, especially
precocious puberty
1) CURVED thin spicules
2) LACK of osteoblastic rimming
FIBROSARCOMA/MFH
METAPHYSES of LONG BONES
PELVIC FLAT BONES
LYTIC
FRACTURES
OF COURSE, SARCOMATOUS
METASTASIS
FIBROSARCOMA/MFH
MISC. TUMORS of BONE
EWING sarcoma/PNET
(Primitive NeuroEctodermal
Tumor)
GIANT CELL TUMOR
METASTASES
EWING/PNET
SAME TUMOR
SMALL ROUND BLUE CELL TUMOR
NEUROENDOCRINE CELL ORIGIN
CHROMOSOME TRANSLOCATION 11&22
SECOND most COMMON bone
malignancy in CHILDREN
ARISE IN MEDULLARY CAVITY of BONE
LOOK LIKE LYMPHOMA
GCT (Giant Cell Tumor), BONE
METASTASES
MALE: PROSTATE
FEMALE: BREAST
RENAL, THYROID also
seek bone early also

LYTIC?
BLASTIC?
SYNOVIAL JOINTS
TWO KINDS of cells
form the synovial intima
1) fibroblasts
Hyaluronin
Lubricin
2) macrophages
The SUB-intima is loose CT or fat
JOINT DISEASES
ARTHRITIS
DEGENERATIVE (OSTEOARTHRITIS)
RHEUMATOID
JUVENILE RHEUMATOID
NON-INFECTIOUS: Ankylosing Spond.,
Reactive, Psoriasis, IBD
INFECTIOUS: Supp., TB, Lyme, Viral
GOUT (URATE)
PSEUDOGOUT (PYROPHOSPHATE)
Tumors (all are of synovium)
Ganglion (Synovial Cyst), non-neoplastic
Giant Cell Tumor (Pigmented VilloNodular Synovitis[PVNS]), benign
Synovial Sarcoma, malignant
DEGENERATIVE ARTHRITIS
aka, OSTEOARTHRITIS
Etiology/Risk Factors: Age, Trauma,
Genes
Pathogenesis: Progressive EROSION
of articular cartilage
Morphology: X-Ray, eburnation,
joint mice, osteophytes
Clinical Expression: PAIN, Limitation
of motion
HEBERDENS NODES
DIP, NOT MP or PIP
RHEUMATOID ARTHRITIS
Rheumatoid arthritis (RA) is a
chronic systemic inflammatory
disorder that may affect many tissues
and organsskin, blood vessels,
heart, lungs, and musclesbut
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.
TWO KINDS of cells
form the synovial intima
1) fibroblasts
Hyaluronin
Lubricin
2) macrophages
The SUB-intima is loose CT or fat
RHEUMATOID ARTHRITIS
Etiology/Risk Factors: Autoimmune
Pathogenesis: Progressive SYNOVITIS
Morphology: Synovial lymphocytes,
macrophages, plasma cells, neutrophils,
osteoclasts, pannus, hyperemia,
rheumatoid nodules, vasculitis
Clinical Expression: PAIN, Limitation of
motion, malaise, fatigue, rheumatoid
factor IgMIgG-Fc,
HANDSWRISTELBOWS

The rheumatoid nodule shows palisading


fibroblasts
DIAGNOSIS
CLINICAL FEATURES (1% of population F>>M)
MORNING STIFFNESS, MEAN AGE 45 YRS
ARTHRITIS in MORE THAN 3 JOINT AREAS
TYPICAL hand findings, MP ULNAR deviation
SYMMETRIC ARTHRITIS
SERUM RHEUMATOID FACTOR
TYPICAL X-RAY findings
JUVENILE Rheumatoid Arthritis

Begins BEFORE age 16, by


definition
Generally LARGER joints than RA
Often POSITIVE ANA
SERONEGATIVE ARTHRITIDES
ANKYLOSING SPONDYLITIS (aka,
rheumatoid spondylitis, or Marie-
Strumpell Disease [HLA-B27] (M>>F)
REACTIVE ARTHRITIS (FOLLOWS
GU or GI INFECTIONS)
REITER SYDROME (urethral &
conjunctival inflammation too) [HLA-B27]
Arthritis associated with IBD
PSORIATIC ARTHRITIS [HLA-B27]
Ankylosing Spondylitis
INFECTIOUS ARTHRITIS
From OSTEOMYELITIS
USUALLY SUPPURATIVE
GC, staph, strep, H. flu, E. coli,
(Salmonella in sicklers)
4 cardinal signs, fever,
leukocytosis, ESR
INFECTIOUS ARTHRITIS
TB
LYME Disease, i.e., Borrelia
burgdorferi, from Ixodes ticks
VIRAL
Parvovirus B19
Rubella
Hepatitis C
GOUT
Endpoint of HYPERURICEMIA from
ANY cause resulting in JOINT
deposition of monosodium urate
crystals (TOPHI)
ACUTE
CHRONIC
10% of population has
hyperuricemia (>7 mg/dl), but only
1/20 of these has gout
Classification of Gout
Clinical Category Metabolic Defect
Primary Gout (90% of cases)
Enzyme defects unknown (85%90% Overproduction of uric acid
of primary gout)
Normal excretion (majority)
Increased excretion (minority)
Underexcretion of uric acid with
normal production
Known enzyme defectse.g., partial Overproduction of uric acid
HGPRT deficiency (rare)
Secondary Gout (10% of cases)
Associated with increased nucleic Overproduction of uric acid with
acid turnovere.g., leukemias increased urinary excretion
Chronic renal disease Reduced excretion of uric acid with
normal production
Inborn errors of metabolisme.g., Overproduction of uric acid with
complete HGPRT deficiency (Lesch- increased urinary excretion
Nyhan syndrome)
HGPRT, hypoxanthine guanine phosphoribosyl transferase.
HYPERURICEMIA GOUT
Age of the individual and duration of the
hyperuricemia are factors. Gout rarely appears before
20 to 30 years of hyperuricemia. M>>F
Genetic predisposition is another factor. In
addition to the well-defined X-linked abnormalities of
HGPRT, primary gout follows multifactorial inheritance
and runs in families.
Heavy alcohol consumption predisposes to attacks
of gouty arthritis.
Obesity increases the risk of asymptomatic gout.
Certain drugs (e.g., thiazides) predispose to the
development of gout.
Lead toxicity increases the tendency to develop
gout
FEATURES
TOPHACEOUS ARTHRITIS
GOUTY NEPHROPATHY
GOUTY NEPHROPATHY
GOUT
Associated with ATHEROSCLEROSIS
Associated with HYPERTENSION
Pseudo-GOUT
Gout: Monosodium Urate
Pseudo-GOUT: Calcium Pyrophosphate

PSEUDOGOUT is also called


CHONDROCALCINOSIS, or CPPD (Calcium
Phosphate Deposition Disease)

IDIOPATHIC, HEREDITARY, SECONDARY


Secondary joint damage,
hyperparathyroidism, hemochromatosis,
hypomagnesemia, hypothyroidism, ochronosis, and
diabetes
GOUT vs. PSEUDOGOUT
JOINT TUMORS
BENIGN
GANGLION (SYNOVIAL CYST)
GIANT CELL TUMOR of TENDON SHEATH,
aka PVNS, Pigmented VilloNodular
Synovitis
MALIGNANT
SYNOVIAL SARCOMA
GANGLION
PVNS/GCT
Synovial Sarcoma
SOFT TISSUE TUMORS
FAT
FIBROUS TISSUE
FIBROHISTIOCYTIC
SKELETAL MUSCLE
SMOOTH MUSCLE
VASCULAR
PERIPHERAL NERVE
UNCERTAIN: SYNOVIAL SARCOMA, ALVEOLAR
SOFT PART SARCOMA, EPITHELIOD SARCOMA
CAUSES
MOSTLY UNKNOWN
RADIATION association
CHEMICAL BURN association
THERMAL BURN association
TRAUMA association
VIRUS association (HHV8 for Kaposi)
GENETICS
Parts of many SYNDROMES
MANY TRANSLOCATIONS
Chromosomal and Genetic Abnormalities in Soft Tissue Sarcomas
Tumor Cytogenetic Abnormality Genetic Abnormality
Extraosseous Ewing sarcoma and t(11:22)(q24;q12) FLI-1-EWS fusion gene
primitive neuroectodermal tumor
t(21:22)(q22;q12) ERG-EWS fusion gene
t(7;22)(q22;q12) ETV1-EWS fusion gene
Liposarcomamyxoid and round cell t(12:16)(q13;p11) CHOP/TLS fusion gene
type
Synovial sarcoma t(x;18)(p11;q11) SYT-SSX fusion gene
Rhabdomyosarcomaalveolar type t(2;13)(q35;q14) PAX3-FKHR fusion gene
t(1;13)(p36;q14) PAX7-FKHR fusion gene
Extraskeletal myxoid chondrosarcoma t(9;22)(q22;q12) CHN-EWS fusion gene
Desmoplastic small round cell tumor t(11;22)(p13;q12) EWS-WT1 fusion gene

Clear cell sarcoma t(12;22)(q13;q12) EWS-ATF1 fusion gene


Dermatofibrosarcoma protuberans t(17:22)(q22;q15) COLA1-PDGFB fusion
gene
Alveolar soft part sarcoma t(X;17)(p11.2;q25) TFE3-ASPL fusion gene
Congenital fibrosarcoma t(12;15)(p13;q23) ETV6-NTRK3 fusion
gene
SOFT TISSUE TUMORS
ALL SPINDLY
Deep (desmoid) vs. Superficial (skin)
Importance of counting MITOSES
Importance of STAGING
Importance of IMMUNOPEROXIDASE
Importance of CONSULTATION
FAT
LIPOMA
LIPOSARCOMA

NORMAL FAT LIPOMA, LIPOSARCOMA,


encapsulated often retroperitoneal
FIBROUS TISSUE
NODULAR FASCIITIS
(pseudosarcomatous)
FIBROMATOSES
(plantar, palmar, penile)
FIBROSARCOMA
MYOSITIS OSSIFICANS
BENIGN FIBROUS TISSUE
PROLIFERATION PLUS
OSSEOUS METAPLASIA
FIBROHISTIOCYTIC
FIBROUS HISTIOCYTOMA
DERMATOFIBROSARCOMA
PROTUBERANS
MALIGNANT FIBROUS HISTIOCYTOMA
SKELETAL MUSCLE
RHABDOMYOMA
RHABDOMYOSARCOMA
SMOOTH MUSCLE
LEIOMYOMA
LEIOMYOSARCOMA
VASCULAR
HEMANGIOMA
LYMPHANGIOMA
HEMANGIOENDOTHELIOMA
HEMANGIOPERICYTOMA
ANGIOSARCOMA
PERIPHERAL NERVE
NEUROFIBROMA
SCHWANNOMA
GRANULAR CELL TUMOR
MALIGNANT (SCHWANNOMA)
UNCERTAIN
SYNOVIAL SARCOMA
ALVEOLAR SOFT PART SARCOMA
EPITHELIOD SARCOMA