Downloaded 27 times
![FRACTURES
• THREE PHASES
– HEMATOMA, minutes days PGDF, TGF-β,
FGF
– SOFT CALLUS (“PRO”-CALLUS), ~1 week
– HARD CALLUS (BONY CALLUS), several
weeks
• COMPLICATIONS
– PSEUDARTHROSIS
– INFECTION (especially OPEN [communicating]
fractures)](https://image.slidesharecdn.com/27-ortho-140902155754-phpapp01/85/27-ortho-33-320.jpg)
![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
– Ganglion (Synovial Cyst)
– Giant Cell Tumor (Pigmented VilloNodular Synovitis[PVNS])
– Synovial Sarcoma](https://image.slidesharecdn.com/27-ortho-140902155754-phpapp01/85/27-ortho-84-320.jpg)
![“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](https://image.slidesharecdn.com/27-ortho-140902155754-phpapp01/85/27-ortho-95-320.jpg)
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27 ortho
This document discusses bone structure and diseases. It describes the cells that make up and remodel bone, including osteoprogenitors, osteoblasts, osteoclasts, and osteocytes. It also discusses the proteins and minerals that compose bone tissue. A variety of bone diseases are outlined including malformations, diseases of bone cells and proteins, metabolic diseases, diseases of decreased or abnormal bone mass, tumors, fractures, osteonecrosis, osteomyelitis, and other conditions. Specific bone tumors are also described such as osteochondroma, chondroma, chondroblastoma, and osteosarcoma.
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27 ortho
- 1. BONE JOINT SOFTTISSUE
- 3.
- 4. CELLS of BONE • OSTEOPROGENITOR (“STEM”)(TGFβ) • OSTEOBLASTS (surface of spicule) • OSTEOCYTES (completely within spicule) • OSTEOCLASTS (macrophage lineage)
- 5. Proteins (organic) ofBONE • Type 1 collagen (90%) • Cell adhesion proteins • Calcium-binding proteins • Proteins involved in mineralization • Enzymes • Growth factors – GF-1, TGF-β, PDGF • Cytokines – Prostaglandins, IL-1, IL-6, RANKL • Proteins Concentrated from Serum – β2 –microglobulinAlbumin – IGF, insulin-like growth factor – TGF, transforming growth factor – PDGF, platelet-derived growth factor – IL, interleukin – RANKL, RANK ligand
- 6. Minerals (INorganic) ofBONE HYDROXY-APATITE Ca5(PO4)3(OH) Ca10(PO4)6(OH)2
- 7. ADJECTIVES of BONE •Compact •Spongy • Cancellous • Membranous • Dense • Cortical • Endosteal • Woven • Lamellar • Spicular
- 8.
- 10.
- 11. 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 HOMEOSTASIS – Ricketts and Osteomalacia – Hyperparathyroidism – Renal Osteodystrophy
- 12. 1) MALFORMATIONS AND DISEASES CAUSED BY DEFECTS IN NUCLEAR PROTEINS AND TRANSCRIPTION FACTORS • Congenital absence of a, usually single, bone: phalanx, rib, clavicle • Supernumerary digit (polydactyly) • Syndactyly • CRANIORACHISCHISIS
- 14. 2) DISEASES CAUSEDBY DEFECTS IN HORMONES AND SIGNAL TRANSDUCTION MECHANISMS • Achondroplasia, dwarf (non-lethal) • Thanatophoria, dwarf (lethal) • 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; • A MUTATION causes FGFR3 to be constantly activated.
- 16. 3) DISEASES ASSOCIATEDWITH DEFECTS IN EXTRACELLULAR STRUCTURAL PROTEINS • OSTEOGENESS 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
- 17.
- 18. 4) DISEASES ASSOCIATEDWITH DEFECTS IN FOLDING AND DEGRADATION OF MACROMOLECULES • MUCOPOLYSACCHARIDOSIS (one of MANY lysosome storage diseases) • DECREASES in ENZYMES which degrade: – DERMATAN – HEPARAN – KERATAN • Chiefly CARTILAGE disorders: short, chest wall, malformed bones
- 19.
- 20. 5) DISEASES ASSOCIATEDWITH DEFECTS IN METABOLIC PATHWAYS (ENZYMES, ION CHANNELS, AND TRANSPORTERS) • OSTEOPETROSIS, 4 types • One common one has a CARBONIC ANHYDRASE deficiency • DECREASED osteoclast resorption • “MARBLE” bone, brittle, sclerosis
- 21.
- 22. 6) DISEASES ASSOCIATEDWITH DECREASED BONE MASS •OSTEOPOROSIS • “PEAK” bone mass is early adulthood • Normal decline, slow • Osteoporosis is accelerated bone loss • Factors: – AGE – Physical activity – Estrogen – Nutrition (Ca++) – Genetics
- 23. Categories of GeneralizedOsteoporosis 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 C,D Homocystinuria Anemia
- 24.
- 25. 7) DISEASES CAUSEDBY 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
- 26. PAGET’s DISEASE (ofBONE) 85% MONOSTOTIC, WHOLE BONE 15% POLY-OSTOTIC (skull, pelvis) “JIGSAW”, NOT LAMINAR, BONE CLINICAL: PAIN!!! (MICROFRACTURES)
- 27.
- 28. 8) DISEASES ASSOCIATEDWITH ABNORMAL MINERAL HOMEOSTASIS – Ricketts and Osteomalacia • VITAMIN D deficiency/dysfunction – Hyperparathyroidism, PRIMARY (PTH ADENOMA) • ENTIRE SKELETON • OSTEITIS FIBROSIS CYSTICA (von Recklinghausen’s disease (of bone) • “BROWN” TUMOR – Hyperparathyroidism, SECONDARY (RENAL) (NOT AS SEVERE AS 1º) – Renal Osteodystrophy = ANY bone disorder due to chronic renal disease
- 29. PRIMARY HYPERPARATHYROIDISM OSTEITISFIBROSA CYSTICA “BROWN” “TUMOR”
- 30. RENAL OSTEODYSTROPHY •PHOSPHATE RETENTION • HYPOPHOSPHATEMIA • HYPOCALCEMIA • INCREASED PTH • INCREASED OSTEOCLASTS • METABOLIC ACIDOSIS release of HYDROXYAPATITES from matrix
- 31.
- 32. FRACTURES, adjectives •Complete, incomplete • Closed, open (communicating) • Communited (splintered) • Displaced (NON-aligned) • PATHOGENIC, (non-traumatic, 2º to other disease, often metastases) • “STRESS” fracture
- 33. FRACTURES • THREEPHASES – HEMATOMA, minutes days PGDF, TGF-β, FGF – SOFT CALLUS (“PRO”-CALLUS), ~1 week – HARD CALLUS (BONY CALLUS), several weeks • COMPLICATIONS – PSEUDARTHROSIS – INFECTION (especially OPEN [communicating] fractures)
- 34.
- 35. OSTEONECROSIS • Alsocalled 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
- 36. OSTEONECROSIS Disorders Associatedwith Osteonecrosis Idiopathic Pregnancy Trauma Gaucher disease Corticosteroid administration Sickle cell and other anemias Infection Alcohol abuse Dysbarism Chronic pancreatitis Radiation therapy Tumors Connective tissue disorders Epiphyseal disorders
- 37.
- 38.
- 39. OSTEOMYELITIS • Pyogenic:Staph, E. coli, Pseudom, Kleb –Hematogenous –Contiguous – Direct implantation • TB • Syphilis
- 40. OSTEOMYELITIS • DX:X-ray, Bone scan
- 41. OSTEOMYELITIS • DX:Histology
- 42. OSTEOMYELITIS • COMPLICATIONS –Subperiosteal abscess – Draining sinus – Joint involvement • SEQUESTRUM vs. INVOLUCRUM
- 44. OSTEOMYELITIS • Tuberculous –Usually blood borne –TB of spine is known as POTTS disease • Syphilis –CONGENITAL –TERTIARY, “SABRE” shins
- 45.
- 46.
- 47. Classification of PrimaryTumors 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
- 48. BONE TUMORS •BONE • CARTILAGE • FIBROUS • MISC. –Ewing’s “sarcoma” –Giant Cell Tumor –METASTASES
- 50. BONE- BONE TUMORS • OSTEOMA • OSTEOID OSTEOMA • OSTEOBLASTOMA • OSTEOSARCOMA (OSTEOGENIC SARCOMA)
- 51. OSTEOMA • SOLITARY • MIDDLE AGE • FROM SUBPERIOSTEAL or ENDOSTEAL surfaces • SKULL, FACE, most common • Totally BENIGN • To be distinguished from REACTIVE BONE
- 52. FRONTAL SINUS Whyam I not showing you HISTOLOGY?
- 53. 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
- 54.
- 55. OSTEOBLASTOMA • AXIALSKELETON, i.e., SPINE • NO Nidus • NO bony reaction • NOT relieved by aspirin
- 56. OSTEOSARCOMA (OSTEOGENIC SARCOMA) LATE TEENS KNEES METAPHYSES PAINFUL!!!
- 57. TYPES of OSTEOSARCOMAS • • The anatomic portion of the bone from which they arise (intramedullary, intracortical, or surface) • • Degree of differentiation • • Multicentricity (synchronous, metachronous) • • Primary (underlying 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)
- 58. The most commonsubtype is osteosarcoma that arises in the metaphysis of long bones; is primary, solitary, intramedullary, and poorly differentiated; and produces a predominantly bony matrix
- 59. BONE- CARTILAGE TUMORS • OSTEOCHONDROMA (EXOSTOSIS) • CHONDROMA • CHONDROBLASTOMA • CHONDROMYXOID FIBROMA • CHONDROSARCOMA
- 60. OSTEOCHONDROMA (EXOSTOSIS) •Common, Cartilage AND Bone present • Often MULTIPLE as a hereditary syndrome • M>>>F • PELVIS, SCAPULAE, RIBS
- 62. CHONDROMA • Chondromavs. EN-chondroma • PURE Hyaline Cartilage • MULTIPLE enchondromas = Ollier’s dis. • Maffucci synd. if hemangiomas present
- 63. CHONDROBLASTOMA • RARE,in teenagers • M>>F • KNEES, usually • Epiphyses • MUCH LESS matrix than a chondroma
- 64. CHONDROMYXOID FIBROMA •RAREST of all • TEENS, MALES • “MYXOID” concept • “ATYPIA”
- 65. CHONDROSARCOMA • ANATOMY – INTRAMEDULLARY – JUXTACORTICAL • HISTOLOGY – CONVENTIONAL • HYALINE • MYXOID – CLEAR – DE-DIFFERENTIATED – MESENCHYMAL
- 66.
- 68. BONE- FIBROUS TUMORS • FIBROUS CORTICAL DEFECT/NON-OSSIFYING FIBROMA • FIBROUS DYSPLASIA • FIBROSARCOMA/MALIGNANT FIBROUS HISTIOCYTOMA
- 69. FIBROUS CORTICAL DEFECT • COMMON, usually LESS THAN 1 CM • CHILDREN >2 • IF MORE THAN 5-6 CM, they are then called NON-OSSIFYING FIBROMA
- 70. FIBROUS DYSPLASIA •BENIGN TUMOR • THREE TYPES –SINGLE BONE (70%) –POLY-OSTOTIC (27%) –POLY-OSTOTIC (3%) with café-au-lait and endocrine disorders, especially precocious puberty
- 71. 1) CURVED spicules 2) LACK of osteoblastic rimming
- 72. FIBROSARCOMA/MFH • METAPHYSESof LONG BONES • PELVIC FLAT BONES • LYTIC • FRACTURES • OF COURSE, SARCOMATOUS METASTASIS
- 73.
- 74. MISC. TUMORS ofBONE • EWING sarcoma/PNET (Primitive NeuroEctodermal Tumor) • GIANT CELL TUMOR • METASTASES
- 75. EWING/PNET • SAMETUMOR • SMALL ROUND • NEUROENDOCRINE • IDENTICAL CHROMOSOME TRANSLOCATION • SECOND most COMMON bone malignancy in CHILDREN • ARISE IN MEDULLARY CAVITY of BONE • LOOK LIKE LYMPHOMA
- 77. GCT (Giant CellTumor), BONE
- 78. METASTASES MALE: PROSTATE FEMALE: BREAST RENAL, THYROID also seek bone early also LYTIC? BLASTIC?
- 83.
- 84. 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 – Ganglion (Synovial Cyst) – Giant Cell Tumor (Pigmented VilloNodular Synovitis[PVNS]) – Synovial Sarcoma
- 85. DEGENERATIVE ARTHRITIS •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
- 88. HEBERDEN’S NODES DIP,NOT MP or PIP
- 89. RHEUMATOID ARTHRITIS Rheumatoidarthritis (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.
- 90. 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 IgM-IgGFc,
- 91. HANDSWRISTELBOWS The rheumatoid“nodule” shows “palisading” fibroblasts
- 92. DIAGNOSIS • CLINICALFEATURES (1% of population F>>M) – MORNING STIFFNESS – ARTHRITIS in MORE THAN 3 JOINT AREAS – “TYPICAL” hand findings – SYMMETRIC ARTHRITIS – SERUM RHEUMATOID FACTOR – “TYPICAL” X-RAY findings
- 94. “JUVENILE” Rheumatoid Arthritis • Begins BEFORE age 16, by definition • Generally LARGER joints than RA • Often POSITIVE ANA
- 95. “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
- 96.
- 97. INFECTIOUS ARTHRITIS •From OSTEOMYELITIS • USUALLY SUPPURATIVE • GC, staph, strep, H. flu, E. coli, (Salmonella in sicklers) • 4 cardinal signs, fever, leukocytosis, ESR
- 98. INFECTIOUS ARTHRITIS •TB • LYME Disease, i.e., Borrelia burgdorferi • VIRAL –Parvovirus B19 –Rubella –Hepatitis C
- 99. GOUT • Endpointof HYPERURICEMIA from ANY cause resulting in JOINT deposition of Monosodium crystals (TOPHI) –ACUTE –CHRONIC • 10% of population has hyperuricemia (>7 mg/dl), but only 1/20 of these has gout
- 100. Classification of Gout Clinical Category Metabolic Defect Primary Gout (90% of cases) Enzyme defects unknown (85%–90% of primary gout) ■ Overproduction of uric acid Normal excretion (majority) Increased excretion (minority) Underexcretion of uric acid with normal production Known enzyme defects—e.g., partial HGPRT deficiency (rare) ■ Overproduction of uric acid Secondary Gout (10% of cases) Associated with increased nucleic acid turnover—e.g., leukemias ■ Overproduction of uric acid with increased urinary excretion Chronic renal disease ■ Reduced excretion of uric acid with normal production Inborn errors of metabolism—e.g., complete HGPRT deficiency (Lesch- Nyhan syndrome) ■ Overproduction of uric acid with increased urinary excretion HGPRT, hypoxanthine guanine phosphoribosyl transferase.
- 101. HYPERURICEMIA GOUT •Age of the individual and duration of the hyperuricemia are factors. Gout rarely appears before 20 to 30 years of hyperuricemia. • 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 saturnine gout
- 102. FEATURES • TOPHACEOUSARTHRITIS • GOUTY NEPHROPATHY
- 106.
- 107. GOUT • Associatedwith ATHEROSCLEROSIS • Associated with HYPERTENSION
- 108. 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
- 109.
- 110. JOINT TUMORS •BENIGN – GANGLION (SYNOVIAL CYST) – GIANT CELL TUMOR of TENDON SHEATH, aka PVNS, Pigmented VilloNodular Synovitis • MALIGNANT – SYNOVIAL SARCOMA
- 111.
- 112.
- 113. “SOFT TISSUE” TUMORS • FAT • FIBROUS TISSUE • FIBROHISTIOCYTIC • SKELETAL MUSCLE • SMOOTH MUSCLE • VASCULAR • PERIPHERAL NERVE • UNCERTAIN: SYNOVIAL SARCOMA, ALVEOLAR SOFT PART SARCOMA, EPITHELIOD SARCOMA
- 114. CAUSES • MOSTLYUNKNOWN • RADIATION association • CHEMICAL BURN association • THERMAL BURN association • TRAUMA association • VIRUS association (HHV8 for Kaposi) • GENETICS • Parts of many SYNDROMES • MANY TRANSLOCATIONS
- 115. Chromosomal and GeneticAbnormalities 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 Liposarcoma—myxoid and round cell type t(12:16)(q13;p11) CHOP/TLS fusion gene Synovial sarcoma t(x;18)(p11;q11) SYT-SSX fusion gene Rhabdomyosarcoma—alveolar 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
- 116. SOFT TISSUE TUMORS • ALL “SPINDLY” • Deep (desmoid) vs. Superficial • Importance of MITOSES • Importance of STAGING • Importance of IMMUNOPEROXIDASE • Importance of CONSULTATION
- 117. FAT • LIPOMA • LIPOSARCOMA NORMAL FAT LIPOMA, encapsulated LIPOSARCOMA, often retroperitoneal
- 118. FIBROUS TISSUE •NODULAR FASCIITIS (pseudosarcomatous) • FIBROMATOSES (plantar, palmar, penile) • FIBROSARCOMA
- 119. MYOSITIS OSSIFICANS •BENIGN FIBROUS TISSUE PROLIFERATION PLUS OSSEOUS METAPLASIA
- 120. FIBROHISTIOCYTIC • FIBROUSHISTIOCYTOMA • DERMATOFIBROSARCOMA PROTUBERANS • MALIGNANT FIBROUS HISTIOCYTOMA
- 121. SKELETAL MUSCLE •RHABDOMYOMA • RHABDOMYOSARCOMA
- 122. SMOOTH MUSCLE •LEIOMYOMA • LEIOMYOSARCOMA
- 125. VASCULAR • HEMANGIOMA • LYMPHANGIOMA • HEMANGIOENDOTHELIOMA • HEMANGIOPERICYTOMA • ANGIOSARCOMA
- 126. PERIPHERAL NERVE •NEUROFIBROMA • SCHWANNOMA • GRANULAR CELL TUMOR • MALIGNANT (SCHWANNOMA)
- 127. UNCERTAIN • SYNOVIALSARCOMA • ALVEOLAR “SOFT PART” SARCOMA • EPITHELIOD SARCOMA
Editor's Notes
- #4 Intramembranous and Endochondral ossification, note: 1, Reserve zone. 2, Zone of proliferation. 3, Zone of hypertrophy. 4, Zone of mineralization. 5, Primary spongiosa.
- #16 Achondroplastic and thanatophoric dwarfs
- #22 Diffusely DENSE bone with Erlenmeyer Flask deformity of distal humerus
- #58 Primary = YOUNGER patients, Secondary = OLDER patients
- #62 Osteochondroma
- #68 Conventional hyaline, mesenchymal, clear, conventional myxoid
- #78 GCT occurs in patients, 20s-40-s, and GCT has a MACROPHAGE lineage
- #110 Biurate has the OPPOSITE polarization pattern of pyrophosphate. In GOUT, as seen here, the yellow needles are vertical and the blue needles are horizontal, under polarization. IN PSEUDOGOUT, the OPPOSITE is seen.
- #113 These diseases are related, but PVN appears as shaggy or “villous” projections of synovium, and GCT is a solid tumor. BOTH are regarded as BENIGN proliferations of synovium and reactive cells.
- #119 What is a herring bone pattern?
- #125 The MAIN difference between leiomyomas and leiomyosarcomas is the number of mitoses per high power field! How many do you see here?