Uploaded byasdgja
PPTX, PDF25 views

umy-benignbonetumors-140824003220-phpapp01.pptx

Benign bone tumors are diverse in morphology and biological potential. Most bone tumors are benign lesions seen in patients under 30 years old. Radiology is important for determining the exact location, extent of growth, and aggressiveness of bone tumors. The best test for diagnosis is a biopsy, as it confirms if a tumor is malignant or benign and determines the bone cancer type and stage. There are several classification systems for bone tumors, including the Enneking and Campanacci staging systems, which help determine prognosis and appropriate treatment.

Embed presentation

Download to read offline
1 / 104
2 / 104
3 / 104
4 / 104
5 / 104
6 / 104
7 / 104
8 / 104
9 / 104
10 / 104
11 / 104
12 / 104
13 / 104
14 / 104
15 / 104
16 / 104
17 / 104
18 / 104
19 / 104
20 / 104
21 / 104
22 / 104
23 / 104
24 / 104
25 / 104
26 / 104
27 / 104
28 / 104
29 / 104
30 / 104
31 / 104
32 / 104
33 / 104
34 / 104
35 / 104
36 / 104
37 / 104
38 / 104
39 / 104
40 / 104
41 / 104
42 / 104
43 / 104
44 / 104
45 / 104
46 / 104
47 / 104
48 / 104
49 / 104
50 / 104
51 / 104
52 / 104
53 / 104
54 / 104
55 / 104
56 / 104
57 / 104
58 / 104
59 / 104
60 / 104
61 / 104
62 / 104
63 / 104
64 / 104
65 / 104
66 / 104
67 / 104
68 / 104
69 / 104
70 / 104
71 / 104
72 / 104
73 / 104
74 / 104
75 / 104
76 / 104
77 / 104
78 / 104
79 / 104
80 / 104
81 / 104
82 / 104
83 / 104
84 / 104
85 / 104
86 / 104
87 / 104
88 / 104
89 / 104
90 / 104
91 / 104
92 / 104
93 / 104
94 / 104
95 / 104
96 / 104
97 / 104
98 / 104
99 / 104
100 / 104
101 / 104
102 / 104
103 / 104
104 / 104
BONE TUMORS BENIGN BONE TUMORS PRESENTOR- UMESH YADAV JR-ORTHO,PGIMS ,ROHTAK UMY
OVERVIEW UMY • Bone tumors are very diverse in morphology and biological potential (can be no big deal or rapidly fatal) • MOST bone tumors are benign lesions • Most benign lesions are seen <30 years of age • A new bone tumor in the elderly is more likely to be malignant • No bone is safe (though most primaries are in long bones) • Location in the bone gives important Dx info • More common benign lesions typically present as incidental findings (non-painful, stable size) • Be cautious with painful lesions and those that grow relatively fast (over weeks or months) • Pathological fracture can be the first sign of tumor
• Bone neoplasms are very difficult to diagnose specifically on radiologic testing alone • So why is radiology important? – Exact location of lesion – Extent of growth/metastasis – Aggressiveness • Best test for Dx= X-ray • Best test for staging= CT or MRI • Quick shout out to the pathologists– histologic grade is the most important prognostic feature of bone sarcomas and essential for staging most of the bone tumor types. UMY
Primary Bone Tumor Tumor from Bone Tissue benign Osteochondroma, Giant cell tumor, Osteoma, Chondroma, Chondroblastoma malignant Osteosarcoma, Chondrosarcoma, Fibrosarcoma Tumor from Bone Affiliated Tissue benign Osteoangioma, Odontogenic tumor (exp. Adamantinoma) malignant Ewing's sarcoma, Reticulum cell sarcoma of bone, Notochordoma, Myeloma Metastatic Tumor Carcinoma, Sarcoma, Neuroblastoma Carcinoma, Sarcoma, Neuroblastoma Classification of Bone Tumor UMY Tumor-like lesion Bone cyst, Fibrous dysplasia
UMY
Benign tumors UMY Bone-forming • Osteoid Osteoma • Bone island Cartilage Lesions • Chondroma • Osteochondroma Fibrous lesions • Non ossifying fibroma • Cortical desmoid • Benign fibrous histocytoma • Fibrous displasia • Osteofibrous dysplasia • Desmoplastic fibroma Cystic Lesions Unicameral bone cyst Aneurismal bone cyst Intraosseous ganglion cyst Epideromoid cyst Fatty tumors Lipoma Vascular tumors Hemangioma
INVESTIGATIONS • X-RAY CT SCAN MRI • TECHNETIUM 99 BONE SCAN- (scintigraphic) study that makes use of Technetium99m (Tc99m-methylene diphosphonate (MDP)) as active agent. • 3 stages which follow IV injection of the tracer. • 1) Flow phase • 2 to 5-sec images are obtained for 60 seconds after injection • demonstrates perfusion and characterises the blood flow to a particular area • 2) Blood pool phase • the blood-pool image is obtained 5 min after injection • demonstrated the blood pool, not the blood flow • inflammation causes capillary dilatation and increased blood flow • If the study is going to be a triphasic bone scan, a third phase is added. • 3) Delayed phase • the bone image is obtained 2 - 4 hours later • urinary excretion has decreased the amount of the radionuclide in soft tissue UMY
FDG-PET • FDG-PET- Flourine 18-fluorodeoxyglucose labelled- Positron Emission Tomography uses radioactive glucose to locate cancer. This glucose contains a radioactive atom that is absorbed by the cancerous cells and then detected by a special camera • Radiolabelled biocompound such as 2-fluoro-2-deoxy-D- glucose (FDG) is injected intravenously. • Uptake of this compound followed by further breakdown occurs in the cells. Tumor cells have a high metabolic rate hence this compound is also metabolised by tumor cells. • FDG is metabolised to FDG-6-phosphate which cannot be further metabolised by tumor cells hence it accumulates and concentrates in tumor cells. This accumulation is detected aU n Md Y quantified.
BIOPSY UMY • Most conclusive test because it confirms if the tumor is malignant or benign, the bone cancer type (primary or secondary bone cancer), and stage. • TYPES- • 1. Needle biopsy: During this procedure, a small hole is made in the affected bone and a tissue sample from the tumor is removed. two types - • Fine needle aspiration: During this procedure, the tissue sample is removed with a thin needle attached to a syringe. • Core needle aspiration: During this procedure, the surgeon removes a small cylinder of tissue sample from the tumor with a rotating knife like device. • 2. Incisional biopsy: During this procedure, the surgeon cuts into the tumor and removes a tissue sample.
UMY
ENNEKING STAGING UMY Enneking described the most widely used staging system for benign bone tumors . The stages are denoted by the Arabic numerals 1, 2, and 3, whereas malignant bone tumors are classified by Roman numerals (I, II, III). Stage 1-LATENT- low biological activity, well marginated , often incidental ,may resolve spontaneously. -NOF Stage 2-ACTIVE-Symptomatic,limited bone destruction, may present with pathological fracture- ABC Stage 3-AGGRESSIVE- Bone destruction/Soft tissue extension, require complete work-up and a removal with wide margins to avoid possible local recurrence. -GCT
• For Malignant tumors ,adopted by the Musculoskeletal Tumor Society, and originally developed by Enneking UMY Stage Grade Local Extent Metastasis 1A low intracompartmental - 1B low extracompartmental - 2A high intracompartmental - 2B high extracompartmental - 3 Any Any + Grade is determined by histological parameters. Low-grade tumors generally have few mitotic figures, little if any cellular atypia, and have a relatively non-infiltrative growth pattern. High-grade tumors tend to have marked cellular atypia, hyperchromatism, and nuclear pleomorphism. They often demonstrate an infiltrative growth pattern
CAMPANACCI STAGING UMY • Radiological grading system – Better for prognosticating aggressiveness then histology • Used for Giant Cell Tumours • GRADE 1--Intramedullary lesion confined to bone • GRADE 2--Thinned, expanded cortex • GRADE 3--Cortical breakout.
SURGERY PRINCIPLES • Surgical margin is described by one of four terms— intralesional, marginal, wide, or radical. • Intralesional Resection--Plane of surgical dissection is within the tumor. • Often described as “debulking” because it leaves behind gross residual tumor. • Marginal resection--achieved when the closest plane of dissection passes through the pseudocapsule.( surrounding reactive tissue around tumor ) • For most benign lesions and some low-grade malignancies UMY
… UMY
Wide Resection UMY • Is achieved when the plane of dissection is in normal tissue • If the plane of dissection touches the pseudocapsule at any point, the margin should be defined as being marginal and not wide. • for high-grade malignancies. Radical resection • All the compartments that contain tumor are removed en bloc. • Involves removing the entire bone and the compartments of any involved muscles. • Rarely used now a days
Curettage UMY • Simple Curettage- -cortical window over the lesion -bulk of the tumor is scooped out -cavity is enlarged back to normal host bone in each direction with a power burr. -copiously irrigated to remove any debris and tumor cells. • Extended curettage- »use of adjuvants, such as liquid nitrogen, phenol, polymethyl methacrylate, or thermal cautery
CARTILAGE LESIONS UMY - Osteochondroma - Chondroma Enchondroma-arising in medullary canal Periosteal chondroma/juxtacortical chondromas-arise on bone surface
Osteochondroma UMY • Developmental anomalies rather than tumors. • They are usually sporadic, but can be part of: Hereditary multiple exostoses (HME) - also known as diaphyseal aclasis Trevor disease- Osteochondroma on epiphyseal side of growth plate. An osteochondroma can be either sessile or pedunculated, and is seen in the metaphyseal region typically projecting away from the epiphysis.
• They most commonly arise from appendicular skeleton, especially around the knee . • Lower limb - 50% of all cases femur (especially distal) - most common : 30% • Tibia (especially proximal) - 15- 20% • Less common locations - feet, scapula • upper limb • humerus - 10-20% • hands, pelvis • spine - the posterior elements of spine are an uncommon, but not rare, site for these tumours UMY
• Pathologically Osteochondromas are essentially a part of the growth plate. • Separates and continues growing independently, without an associated epiphysis • The medullary cavity is continuous with the parent bone, and they are capped by hyaline cartilage UMY
Osteochondroma • Clinically, osteochondromas present as slow-growing masses, which can be painful if they impinge on a nerve or if the stalk is fractured. In many cases, they are detected as an incidental finding. Osteochondroma. On this lateral view of the ankle, a benign osteochondroma is seen projecting posteriorly on a stalk. The end (arrows) is often covered with a cartilaginous cap. These lesions always occur near a UM jo Yint but point away from it.
• • • • MRI MRI is best at assessing cartilage thickness (and thus assessing for malignant transformation), presence of oedema in bone or adjacent soft tissues and visualising neurovascular structures in the vicinity. The cartilage cap of osteochondromas appears the same as cartilage elsewhere, with intermediate to low signal on T1 and high signal on T2 and STIR weighted images. A cartilage cap of over 1.5cm in thickness is suspicious for malignant degeneration. UMY
T1 T2 STIR (FAT SUPPRESSION) UMY
UMY
S/S UMY • M C symptom of an osteochondroma is a painless mass near the joints. The knee and shoulder are more commonly involved. • If the stalk of a pedunculated osteochondroma breaks, pain and swelling may start immediately. • If located under a tendon-- Snapping of the tissue over the tumor may cause activity-related pain. • If located near a nerve or blood vessel, such as behind the knee causing numbness and tingling in that extremity, periodic changes in blood flow, loss of pulse or changes in color of the limb.
RISK OF MALIGNAT TRANSFORMATION- 1%- SOLITARY OSTEOCHONDROMA 5%- MULTIPLE HEREDITARY EXOSTOSIS UMY
TREATMENT UMY Nonsurgical Treatment Most of the time, solitary osteochondroma is not removed surgically. Observe it & take regular X-rays to keep track of any changes. Surgical Treatment When surgery is recommended, it is best to wait until growth complete (a mature skeleton by X-ray evaluation) before removing a solitary osteochondroma. This decreases the chance of the tumor growing back. Surgery may be considered if the osteochondroma: Is causing pain with activity Puts pressure on a nerve or blood vessel Has a large cap of cartilage The osteochondroma is removed at the level of the normal bone. Some of the inside of the bone may also be removed.
Hereditary multiple exostosis UMY - autosomal dominant - 2 Genes-EXT1-Ch8 , EXT2- Ch 11 -< 10 yrs Clinical features : - knobby appearance - short stature or even dwarf ( limbs short in relation to trunk ) - Deformity of forearm - in 40 – 60 % ulna short , radius bowed , loss of pronation n supination , tibiofibular synostosis , genu valgum , coxa valga
DD : multiple enchondromatosis , achondroplasia UMY Treatment : excision of symptomatic exostosis correction of deformity & limb length discrepancy
UMY
UMY
Enchondroma UMY • Common benign medullary cartilaginous neoplasm • Usually found in children or young adults which can lead to pathological fractures or undergo malignant degeneration. • 3-10 % of all bone tumours and 12-24 % of benign bone tumours • Enchondromas are most frequently diagnosed in childhood to early adulthood with a peak incidence of 10-30 years. • Complicated by a pathological fracture or malignant transformation into a low grade chondrosarcoma • (clinically if an enchondroma is painful in the absence of a fracture, it should be considered malignant
ENCHONDROMA • Enchondromas arise from rests of growth plate cartilage/chondrocytes that subsequently proliferate and slowly enlarge and are composed of mature hyaline cartilage. • they are seen in any bone formed from cartilage. • Two syndromes are associated with multiple enchondromas: Ollier disease Maffucci syndrome. • small tubular bones of the hands and feet : 50% • large tubular bones e.g. femur, tibia, humerus UMY
ENCHONDROMA UMY • Rarely an enchondroma may extend through the cortex and demonstrate a exophytic growth pattern. This is known as an enchondroma protuberans, and may either be seen sporadically or as part of Ollier disease. • Almost all enchondromas are located in the medullary cavity of tubular bones. D/ds: • bone infarct , chondrosarcoma, intraosseous ganglion • other benign lytic bone lesions, • metastases • granulomatous disease : sarcoidosis, tuberculosis
IMAGING • X-ray & CT Typically enchondromas are small 1 - 2cm lytic lesions with non-aggressive features. narrow zone of transition sharply defined scalloped margins : may have mild endosteal scalloping expansion of the overlying cortex may be present but there should not be cortical breakthrough unless fractured Chondroid calcifications may be present : rings and arcs calcification-STIPPLED/PUNCTATE/POPCORN no periosteal rxn. • The majority of enchondromas more frequently arise in the metaphyseal region,. A cartilaginous lesion in an epiphysis is more likely to be a chondrosarcoma . UMY
UMY
IMAGES UMY
IMAGING UMY • MRI • MRI is useful in evaluating for soft tissue extension and for confirming the diagnosis. • Enchondromas appear as well circumscribed somewhat lobulated masses replacing marrow. • T1 Intermediate to low signal • T1 C+ (Gd) enhancement is variable, and may be seen both peripherally or of translesional septae. Similar pattern of enhancement may be seen in chondrosarcomas. • T2 Typically of background intense high signal
MRI STIR • T1 • Hypointense T2 Hyperintense UMY
OLLIER”S DISEASE • Ollier disease also known as enchondromatosis, is a non- hereditary, sporadic, skeletal disorder characterised by multiple enchondromas that are principally located in the metaphyseal regions. • Plain films show multiple enchondromas. Larger lesions can show cartilage calcification in a typical rings and arcs pattern. • Imaging characterestics are of same as ENCHONDROMAS UMY
MAFUCCI’S SYNDROME UMY • Maffucci syndrome is a congenital non hereditary mesodermal dysplasia characterised by multiple enchondromas with soft-tissue cavernous haemangiomas. • Imaging findings are multiple enchondromas seen associated with soft tissue swelling and phleboliths. • Enchondromas degenerate into chondrosarcomas in 15-51% of cases and soft- tissue haemangiomas to vascular sarcomas in 3-5%.
OLLIER’S DISEASE  MAFFUCI’S DISEASE  UMY
Chondroblastoma UMY • Rare benign cartilaginous neoplasms( CODMAN TUMOR ) • Less than 1% of all primary bone tumours, occurring predominantly in young patients (< 20 years of age). There is a male predilection. • Pathologically composed of chondroblasts, chondroid matrix, cartilage with occasional giant multi-nucleated cells.* with surrounding chondroblasts. • Aneurysmal bone cysts can be seen secondarily to underlying chondroblastoma. • Patient may present as synovitis of knee.
SITE • Epiphysis of a long bone (70% occurring in the humerus (most frequent), femur and tibia, ~ 10% are found in the hands and feet) UMY
IMAGING • X-rays • epiphyseal • well defined lytic lesions; either smooth or lobulated margins with a thin sclerotic rim • Internal calcifications can be seen in up to 40-60% of cases • They range in size from 1-10cm, with most being 3-4cm at diagnosis • CT • better delineation of the relationship to the growth plate and articular surface • Solid periosteal reaction (seen in up to 50% of cases) and internal calcification (calcified matrix seen in ~ 1/2 of cases) and cortical breach are also more easily appreciated. • Endosteal scalloping may be UMs Y een
image UMY
UMY
IMAGING UMY • MRI • Ideal for the evaluation of transphyseal or transcortical extension. • Demonstrating associated surrounding bone marrow oedema. •These lesions have signal typical of cartilage: T1 - lesion itself is of low to intermediate signal T2 / STIR - lesion is of intermediate to high signal • Fluid-fluid levels may occasionally be seen .
image • T1 T2 STIR UMY
MICROSCOPY UMY • Sheets of chondroblasts with background of chondroid matrix. • Polygonal cells with distinct cytoplasm. • Dystrophic calcification surrounding individual cells – “CHICKEN WIRE “ appearance. • Abundant Giant cells • Secondary ABC in 20 % cases.
TREATMENT • The goal for treatment of chondroblastoma is to remove the tumor and prevent damage to the end of the affected bone. • Treatment may include: Surgical removal of the tumor - Biopsy and curettage with possible use of adjuvant liquid nitrogen or phenol, or a mechanical burr. It may be necessary to reconstruct articular surfaces due to subchondral erosion. Bone grafting /bone cement used Any joint invasion is usually secondary to previous instrumentation. UMY
BONE FORMING TUMORS UMY Osteoid osteoma Osteoblastoma Bone island
OSTEOID OSTEOMA UMY - Osteoblastic mass called nidus surrounded by zone of reactive sclerosis - 2nd decade - M > F - Site : proximal femur ( mc ) , tibia , spine ( posterior elements ) Not seen in bones of membranous origin C/F : Dull pain , worse at night , relieved with NSAID s , not related to position or function , often aggravated by alcohol
- Pain is elicited by local pr. - O.O is suspected in spine when a pt < 30 yrs complains of constant back pain , when spine is stiff and scoliotic & SLRT is positive with no signs of nerve root compression. Radiological findings : Radiolucent nidus ( 1.5 cm) with reactive sclerosis in cortex , DD : Osteoblastoma , Non-suppurative osteomyelitis of garre , Brodies abscess, Stress # , Diagnosis : Tc99 bone scan – Inc uptake “Headlight in fog “ & “Double – density sign “ CT – BULLS EYE appearance UMY
UMY
UMY
Pathology : Nidus – osteoblasts & nonmyelinated axons Stroma – osteoblasts , osteoclasts , fibroblasts & blood filled capillaries - Transform into osteoblastoma but no malignant transformation. Treatment : Self limiting lesions – conservative treatment with NSAIDs – not well tolerated - Surgery : to eradicate pain producing nidus ( accurate localization is hence crucial ) methods : - en bloc resection or burr down tech. Latest is percutaneous radiofrequency ablation UMY
OSTEOBLASTOMA UMY - Histologically similar to O.O but differing in progressive growth & absence of reactive perifocal bone formation. - Potentially malignant - Mc site : vertebral column ( post. Elements) - C.F : pain of varying intensity pathological # neurological problems Radiographic features : nothing particularly distinctive well circumscribed lesion , CT – COTTON WOOLappearance due to irregular opacities
- Radiopacity expression of quantity & degree of maturation of osteoid substance. Bone scan – localizing smaller lesions esp in spine Pathology : very vascular DD : Osteoid osteoma Osteosarcoma ( increase in sr.ALP). Treatment : curettage & bone grafting UMY
UMY
UMY
FIBROUS LESIONS UMY Nonossifying fibroma Cortical desmoid Benign fibrous histiocytoma Fibrous dysplasia Osteofibrous dysplasia
NON OSSIFYING FIBROMA UMY - Also called Fibrous cortical defect or Metaphyseal cortical defect or Fibrous xanthomas - Mc musculoskeletal tumor - Occurs in 30 % of children - 1st two decades - Site : femur , tibia , humerus ( 8 % - multiple lesions) - Asymptomatic - X ray : well defined , eccentric , radiolucent lesion in metaphysis ,multilocular app or rim of sclerosis , doesn’t expand the cortex & no periosteal reaction. - Treatment : observation
UMY
FIBROUS DYSPLASIA UMY -intrinsic defect of endochondral bone maturation  immature ossification pattern -Characterized by replacement of normal bone & marrow by fibrous tissue & small woven spicules of bone  weakbone . - Solitary or multifocal - ALBRIGHT ‘ S SYN : polyostotic F.D + café au lait spots + endocrinopathies . - MAZABRAUD SYN- Polyostotic FD+ Intramuscular myxomas - Site : rib , femur , humerus , tibia , maxilla - C.F : monostotic – asymptomatic bone pain , skeletal deformities .
RADIOGRAPHIC APPEARENCE Radiographic features : - Epiphysis or metaphysis or diaphysis - Well defined geographic lytic lesions - Ground glass matrix : intramedullary radiolucencies - Cortical thinning - Secondary deformities esp. in wt , bearing bones - Shepherd’s crook deformity ( microfractures – on tension side of bone ) - Poorly defined areas of osteolysis - Cortical destruction - Soft tissue involvement suspect malignant transformation UMY
UMY
Shepherd's crook deformity UMY • Coxa varus angulation of the proximal femur, classically seen in femoral involvement by fibrous dysplasia, although may be seen in other disorders such as Paget disese of bone and osteogenesis imperfecta. • The shape of the proximal femur resembles that of the staff carried by herders (shepherds), which is known as a crook.
Shepherd's crook deformity UMY
TREATMENT UMY - Monostotic lesions  asymp  no Rx Indications : severe deformity persistent pain pathological # - Curettage & grafting ( cortical allograft prfrd. d/t slower absorption) - Internal fixation +/- osteotomy - Bisphosphonates : beneficial
CYSTIC LESIONS UMY Unicameral bone cyst Aneurysmal bone cyst Intraosseous ganglion cyst
UNICAMERAL BONE CYST UMY - Developmental anamoly of physis - Transient failure of ossification of physeal cartilage & cyst formation - < 20 yrs age , M > F - Spontaneously resolve in late adolescence , rarely persist into adulthood - Site : proximal humerus , proximal femur , calcaneum . Active cysts are juxtaposed to physis (within 1 cm) C.F : usually asymptomatic , pathological #
- Cysts progress from active to quiescent to involutional UMY - stage . cysts usually shrink as patient approaches skeletal maturity. - Radiographic features : metaphysis of immature skeleton , DIGNOSTIC- well marginated , centrally located ,purely lytic lesion. radiolucent that expand and thin the cortex . FALLEN FRAGMENT SIGN - # fragment in the cyst DD :ABC & fibrous dysplasia
UMY
FALLEN FRAGMENT SIGN UMY
Bone cyst of humerus Pathologic fracture “Falling Fragment Sign” UMY
MRI MR signal characteristics for an uncomplicated lesion include T1 - low signal T2 - high signal Usually there no fluid-fluid levels unless there has been a complication with haemorrhage. CT and MRI add little to the diagnosis, but are however helpful in eliminating other entities that can potentially mimic a simple bone cyst UMY
T1 T2 UMY
TREATMENT Small asymp lesions in upper extremities- observation & follow up Larger lesions need Rx Symptomatic lesions Lesions in lower extremities Various options are Curettage +/ - bone grafting +/- int. fixation Aspiration & inj of steroids or bone products UMY
Aneurysmal bone cyst (ABC) • Benign , Expansile • Primarily seen in children and adolescents (80% l <20yrs of age) • Blood-filled spaces of variable size separated by connective tissue (trabeculae of bone or osteoid tissue) and osteoclast giant cells •Not lined by endothelium. Types • Primary • Secondary (e.g chondroblastoma, fibrous dysplasia, giant cell tumour (GCT), osteosarcoma UM )Y
• Location Long bones – tibia & fibula (24%), femur (13%), Spine 20-30% (posterior elements). sacrum • A variant of ABCs is the giant cell reparative granuloma.( SOLID ABC) • seen in the tubular bones – hand , feet craniofacial skeleton. UMY
Radiographic features • X ray sharply defined, expansile osteolytic lesions, with thin sclerotic margins. Eccentricity is typical. But very often missed out due to cortical thinning due to ballooning. CT Demonstrates these findings to a greater degree, and is also better at assessing cortical breach and extension into soft tissues. Fluid fluid levels (better than MRI) UMY
UMY
UMY
MRI UMY • MRI Demonstrate Fluid Fluid level in lesion. To distinguish between Primary and secondary (if solid component Is present.) The cysts are of variable signal, with surrounding rim of low T1 and T2 signal. Focal areas of high T1 and T2 signal are also seen presumably representing areas of blood of variable age. SBC vs ABC on MRI- Presence of double density fluid level & intralesional septations- ABC
BONE SCAN • Doughnut sign - increased uptake peripherally with a photopenic centre. UMY
TREATMENT UMY Excision – cortical based or surface tumors Extended intralesional curettage & grafting – central lesions Embolisation – vertebral & pelvicABC Low dose radiation – effective method but not used d/t malignant transformation.
ANJALI ,20F,ABC Rx-Curettage+ G Bone grafting PRE OP IMMEDIATE POST OP FOLLOW UP UMY
DHRUV 8/M ABC Rx-curettage+ Chron os grafting UMY
DEFINITION: Distinct neoplasm arising from non-bone forming supportive connective tissue of marrow with network of stromal cells regularly interspersed with giant cells. ( Jaffe & Liechtenstein ) -75-80% OF PATIENTS 20-50 YRS Male:Female- 1:1.3 (Benign) -3:1 (Malignant) UMY
Site • 55% AROUND THE KNEE • 10% in the distal radius • 6% in the proximal humerus • SPINE rarely involved (commoner in the sacrum) • In the head and neck region the maxilla and mandible are more commonly involved. • SIGNS&SYMPTOMS 1. PAIN 2. SWELLING 3. JOINT RESTRICTION 4. MUSCLE WASTING 5. NEUROLOGICALSIGNS 6. PATHOLOGICAL# 7. PULMONARYMETS- 3 % UMY
Pathology GROSS-  End of bone is expanded.  Eccentric lesion at the epiphyseo-metaphyseal region.  Thin periosteum.  Fleshy dark brown, soft, friable mass.  Cystic spaces seen. UMY
Pathology Microscopy-  Vascularized network of round,oval or spindle shaped stromal cells and multinucleated giant cells( 40-60 nuclei /cell) with numerous centrally placed nuclei UMY
GRADING SYSTEM Jaffe,Lichenstein and Portis(1940) GRADE 1- o Conventional GCT GRADE 2- o Boderline tumours GRADE 3- o Sarcomatous type of stroma Modified grading Sannerkin et al(1980) • Malignant GCT- with frank sarcomatous changes and full metastatic potential • Borderline GCT- without sarcomatous changes but with abnormal mitoses or vascular permeation or both • Conventional GCT- without features of any of the above two types No correlation exists between histological grading and clinical behavior of the tumour. Hence grading not widely accepted. UMY
RADIOLOGY Type of Osteolysis • Geographic destruction (I) • Moth-eaten (II) Permeative(III) Lodwick 1A 1B 1C UMY
RADIOLOGY • Expansile UMY
RADIOLOGY • TRABACULATION PURE LYTIC (60%) FINE TRABACULTION(40%) UMY
SCINTI GRAPHY Less useful Inconsistent uptake “Doughnut sign” M.R.I. Soft tissue spread Joint breach Locate N.V. bundle T1-Dark,T2-Bright ABC-20% C.T Intraossous content Intra articular spread Cortical breach Site of window ANGIO GRAPHY Locate vessels type of feeders For embolisation INVESTIGATIONS UMY
SURGICAL TREATMENT Stage1& Stage2 --- Intralesional or Marginal Excision Stage3 --- Wide resection with Reconstruction Radiation, Embolaisation UMY
Curettage & Bone Grafting INDICATION STAGE-1&2 ADEQUATE WINDOW MOTORISED BURR ( 20,000 rpm ) BISPHOSPHONATES- Locally or systemically prevent recurrence. IV ZOLENDRONIC ACID USE FOR PRIMARY GCT UNDER STUDY UMY
DEPENDING ON SITE UMY • AROUND KNEE-Hemicondylar osteoarticular allograft reconstruction / rotation hinge endoprosthesis. • AGGRESSIVE LESION OF DISTAL RADIUS- Primary resection & reconstruction with proximal fibular autograft( arthroplasty or arthrodesis) • EXPENDABLE BONES( DISTAL ULNA/PROX. FIBULA)- Priamry resection without reconstruction. • Spine /pelvis- Irradiation/embolization/both • PULMONARY METS- Resection
‘E’ OF GCT UMY • EPIPHYSEAL • ECCENTRIC • EXPANSILE • EXTENDED CURETTAGE • EXCISION –IF EXTENDED CURETTAGE FAILS
UMY

More Related Content

PPT
Bone Tumors Benign Ppt
byPramod Mahender
 
PPTX
Bone Tumors (2).pptx
byAhmadShamy1
 
PPTX
Bone tumors introduction and general principles
byBarun Patel
 
PPTX
approch to bone tumors .pptx
bySparshSingh25
 
PPT
BONE TUMORS.ppt
byHOME
 
PPTX
LEC 1; INTRODUCTION TO BONE TUMOURS.pptx
byKeyaArere
 
PPTX
most frequent carcinomas malignant epithelial tumorsbonetumors--gate015555555...
byzoh64mohabat
 
PPTX
benign tumors of bone 1.pptx
byasdgja
 
Bone Tumors Benign Ppt
byPramod Mahender
 
Bone Tumors (2).pptx
byAhmadShamy1
 
Bone tumors introduction and general principles
byBarun Patel
 
approch to bone tumors .pptx
bySparshSingh25
 
BONE TUMORS.ppt
byHOME
 
LEC 1; INTRODUCTION TO BONE TUMOURS.pptx
byKeyaArere
 
most frequent carcinomas malignant epithelial tumorsbonetumors--gate015555555...
byzoh64mohabat
 
benign tumors of bone 1.pptx
byasdgja
 

Similar to umy-benignbonetumors-140824003220-phpapp01.pptx

PPT
Bone tumours
bySidharth Yadav
 
PPTX
Bone tumors
byMohammad Ihmeidan
 
PPTX
approach to bone tumors.pptx
byhariramhalder
 
PPTX
Musculoskeletal tumor by Eugene Kanyemera.pptx
byeugenekanyemera007
 
PPTX
Musculoskeletal tumor by Eugene Kanyemera.pptx
byeugenekanyemera007
 
PPTX
Musculoskeletal tumors
byAhmed Youssef
 
PPTX
Tumors around knee
byDrzameer
 
PPTX
ApproachToOrthopedic Oncologyggggggggggggggggg.pptx
bysefidsiyah2020
 
PPTX
LONG BONE TUMOURS ORTHOPAEDICS ,PPTX....
byBipulBorthakur
 
PPT
Amal bont tumours
byAmal Jose
 
PPTX
Bone tumors.pptx
byAll India Institute of Medical Sciences, Bhopal
 
PPTX
Bone tumors
byNaveen Kumar
 
PPTX
Bone tumors and their diagnosis and management
byBewketuDagnachew1
 
PPTX
BONE TUMOUR.pptx
bymohammadabdulnaveed
 
PPTX
Bone tumours (1).pptx for ug and pg students
byAbishekMeganathan
 
PPTX
Bone tumour
byDrSiddique H. Ranna
 
PPTX
Tumours of bone classification general description
bysaadraza303
 
PPTX
Bone tumors.pptx
byydnxq7zfcz
 
PPTX
Tumors Musculoskeletal.. VAPMS college of physiotherapy, vskp.
byRajani Cartor
 
PPTX
Bone tumours
byPrashanth Kumar
 
Bone tumours
bySidharth Yadav
 
Bone tumors
byMohammad Ihmeidan
 
approach to bone tumors.pptx
byhariramhalder
 
Musculoskeletal tumor by Eugene Kanyemera.pptx
byeugenekanyemera007
 
Musculoskeletal tumor by Eugene Kanyemera.pptx
byeugenekanyemera007
 
Musculoskeletal tumors
byAhmed Youssef
 
Tumors around knee
byDrzameer
 
ApproachToOrthopedic Oncologyggggggggggggggggg.pptx
bysefidsiyah2020
 
LONG BONE TUMOURS ORTHOPAEDICS ,PPTX....
byBipulBorthakur
 
Amal bont tumours
byAmal Jose
 
Bone tumors.pptx
byAll India Institute of Medical Sciences, Bhopal
 
Bone tumors
byNaveen Kumar
 
Bone tumors and their diagnosis and management
byBewketuDagnachew1
 
BONE TUMOUR.pptx
bymohammadabdulnaveed
 
Bone tumours (1).pptx for ug and pg students
byAbishekMeganathan
 
Bone tumour
byDrSiddique H. Ranna
 
Tumours of bone classification general description
bysaadraza303
 
Bone tumors.pptx
byydnxq7zfcz
 
Tumors Musculoskeletal.. VAPMS college of physiotherapy, vskp.
byRajani Cartor
 
Bone tumours
byPrashanth Kumar
 

More from asdgja

PPTX
malignantbonetumor-190228134628.pptx
byasdgja
 
PPTX
malignantbonetumours-170608150210.pptx
byasdgja
 
PPTX
genetic disorders of bone 1.pptx
byasdgja
 
PPTX
anandbenignbonetumors-150803083037-lva1-app6892.pptx
byasdgja
 
PPTX
benignbonetumors-140418025726-phpapp01.pptx
byasdgja
 
PPTX
bcfinalextracredit-161220220220.pptx
byasdgja
 
PPTX
marfansyndrome-220129064039.pptx
byasdgja
 
PPTX
67740e9c-b09b-41ae-b013-49542858c4c0-150528193201-lva1-app6892.pptx
byasdgja
 
PPTX
gaucherdisease-170222084210.pptx
byasdgja
 
PPTX
mucopolysachridosis-150903060000-lva1-app6892 (1).pptx
byasdgja
 
PPTX
motor neuron disease.pptx
byasdgja
 
malignantbonetumor-190228134628.pptx
byasdgja
 
malignantbonetumours-170608150210.pptx
byasdgja
 
genetic disorders of bone 1.pptx
byasdgja
 
anandbenignbonetumors-150803083037-lva1-app6892.pptx
byasdgja
 
benignbonetumors-140418025726-phpapp01.pptx
byasdgja
 
bcfinalextracredit-161220220220.pptx
byasdgja
 
marfansyndrome-220129064039.pptx
byasdgja
 
67740e9c-b09b-41ae-b013-49542858c4c0-150528193201-lva1-app6892.pptx
byasdgja
 
gaucherdisease-170222084210.pptx
byasdgja
 
mucopolysachridosis-150903060000-lva1-app6892 (1).pptx
byasdgja
 
motor neuron disease.pptx
byasdgja
 

Recently uploaded

PDF
Artículo Biomol Interaction between ZMIZ2 and AR promotes prostate cancer pro...
bySebastianCastrillon10
 
PPTX
SAPIENT3.0 Medi-trivia Quiz (FINALS) | F.A.Q. 2025
byDr. Anindya
 
PPT
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
PPTX
Anatomy of temporal & infratemporal fossa.pptx
byClevin Aswani
 
PDF
Seminario biología molecula - EBV-miR-BART5-3p
bysalvarez1862004
 
PPTX
Sympathetic Nervous System in Pain Medicine | Anatomy, CRPS & Sympathetic Blo...
byDaradia: The Pain Clinic
 
PPTX
BENIGN BREAST DISEASES BBD/ Fibroadenoma, Fibrocystic Diseases/ ANDI.pptx
byDr Sushil Gyawali
 
PPTX
The Autonomic Nervous System and Visceral Reflexes
bycotomato21
 
PPTX
TRIGEMINAL NERVE trigeminal nuclei .pptx
byTanushKumar13
 
PPTX
Cardiovascular Disease ppt. S.Y D-Pharm.
byAkshata Jain
 
PPTX
ANTIMICROBIAL STEWARDSHIP PROGRAME Vijay.pptx
byVIJAYARengan1
 
PPTX
Tonsillitis tonsillitis tonsillitis tonsillitis tonsillitis tonsillitis
byssusera62a06
 
PDF
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
PPT
Treating With Precision in CRSwNP: Defining the Role of Targeted Biologic The...
byPVI, PeerView Institute for Medical Education
 
PPTX
Sample Acceptance-Rejection-Criteria in lab
byKISMAT ALI
 
PDF
ARCHES OF FOOT -Prof.Dr.N.Mugunthan. KMMC Medical College & Hospitals.pdf
byKanyakumari Medical Mission Research Center, Muttom
 
PPTX
OXFORD TECHNIQUE ,Zinovieff OXFORD TECHNIQUE
byDrTabassumAzmi1
 
PPTX
Preformulation Studies for new Pharmaceutical substances
byMenaka V
 
PPTX
ACTINOMYCETES- Introduction,Pathogenesis,clinical manifestations,Epidemiology...
byAmeenKhan59
 
PPTX
Acute kidney injury and its management.pptx
byrozhnuraddin
 
Artículo Biomol Interaction between ZMIZ2 and AR promotes prostate cancer pro...
bySebastianCastrillon10
 
SAPIENT3.0 Medi-trivia Quiz (FINALS) | F.A.Q. 2025
byDr. Anindya
 
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
Anatomy of temporal & infratemporal fossa.pptx
byClevin Aswani
 
Seminario biología molecula - EBV-miR-BART5-3p
bysalvarez1862004
 
Sympathetic Nervous System in Pain Medicine | Anatomy, CRPS & Sympathetic Blo...
byDaradia: The Pain Clinic
 
BENIGN BREAST DISEASES BBD/ Fibroadenoma, Fibrocystic Diseases/ ANDI.pptx
byDr Sushil Gyawali
 
The Autonomic Nervous System and Visceral Reflexes
bycotomato21
 
TRIGEMINAL NERVE trigeminal nuclei .pptx
byTanushKumar13
 
Cardiovascular Disease ppt. S.Y D-Pharm.
byAkshata Jain
 
ANTIMICROBIAL STEWARDSHIP PROGRAME Vijay.pptx
byVIJAYARengan1
 
Tonsillitis tonsillitis tonsillitis tonsillitis tonsillitis tonsillitis
byssusera62a06
 
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
Treating With Precision in CRSwNP: Defining the Role of Targeted Biologic The...
byPVI, PeerView Institute for Medical Education
 
Sample Acceptance-Rejection-Criteria in lab
byKISMAT ALI
 
ARCHES OF FOOT -Prof.Dr.N.Mugunthan. KMMC Medical College & Hospitals.pdf
byKanyakumari Medical Mission Research Center, Muttom
 
OXFORD TECHNIQUE ,Zinovieff OXFORD TECHNIQUE
byDrTabassumAzmi1
 
Preformulation Studies for new Pharmaceutical substances
byMenaka V
 
ACTINOMYCETES- Introduction,Pathogenesis,clinical manifestations,Epidemiology...
byAmeenKhan59
 
Acute kidney injury and its management.pptx
byrozhnuraddin
 

umy-benignbonetumors-140824003220-phpapp01.pptx

  • 1.
    BONE TUMORS BENIGN BONETUMORS PRESENTOR- UMESH YADAV JR-ORTHO,PGIMS ,ROHTAK UMY
  • 2.
    OVERVIEW UMY • Bone tumorsare very diverse in morphology and biological potential (can be no big deal or rapidly fatal) • MOST bone tumors are benign lesions • Most benign lesions are seen <30 years of age • A new bone tumor in the elderly is more likely to be malignant • No bone is safe (though most primaries are in long bones) • Location in the bone gives important Dx info • More common benign lesions typically present as incidental findings (non-painful, stable size) • Be cautious with painful lesions and those that grow relatively fast (over weeks or months) • Pathological fracture can be the first sign of tumor
  • 3.
    • Bone neoplasmsare very difficult to diagnose specifically on radiologic testing alone • So why is radiology important? – Exact location of lesion – Extent of growth/metastasis – Aggressiveness • Best test for Dx= X-ray • Best test for staging= CT or MRI • Quick shout out to the pathologists– histologic grade is the most important prognostic feature of bone sarcomas and essential for staging most of the bone tumor types. UMY
  • 4.
    Primary Bone Tumor Tumor from Bone Tissue benign Osteochondroma,Giant cell tumor, Osteoma, Chondroma, Chondroblastoma malignant Osteosarcoma, Chondrosarcoma, Fibrosarcoma Tumor from Bone Affiliated Tissue benign Osteoangioma, Odontogenic tumor (exp. Adamantinoma) malignant Ewing's sarcoma, Reticulum cell sarcoma of bone, Notochordoma, Myeloma Metastatic Tumor Carcinoma, Sarcoma, Neuroblastoma Carcinoma, Sarcoma, Neuroblastoma Classification of Bone Tumor UMY Tumor-like lesion Bone cyst, Fibrous dysplasia
  • 5.
  • 6.
    Benign tumors UMY Bone-forming • OsteoidOsteoma • Bone island Cartilage Lesions • Chondroma • Osteochondroma Fibrous lesions • Non ossifying fibroma • Cortical desmoid • Benign fibrous histocytoma • Fibrous displasia • Osteofibrous dysplasia • Desmoplastic fibroma Cystic Lesions Unicameral bone cyst Aneurismal bone cyst Intraosseous ganglion cyst Epideromoid cyst Fatty tumors Lipoma Vascular tumors Hemangioma
  • 7.
    INVESTIGATIONS • X-RAY CTSCAN MRI • TECHNETIUM 99 BONE SCAN- (scintigraphic) study that makes use of Technetium99m (Tc99m-methylene diphosphonate (MDP)) as active agent. • 3 stages which follow IV injection of the tracer. • 1) Flow phase • 2 to 5-sec images are obtained for 60 seconds after injection • demonstrates perfusion and characterises the blood flow to a particular area • 2) Blood pool phase • the blood-pool image is obtained 5 min after injection • demonstrated the blood pool, not the blood flow • inflammation causes capillary dilatation and increased blood flow • If the study is going to be a triphasic bone scan, a third phase is added. • 3) Delayed phase • the bone image is obtained 2 - 4 hours later • urinary excretion has decreased the amount of the radionuclide in soft tissue UMY
  • 8.
    FDG-PET • FDG-PET- Flourine18-fluorodeoxyglucose labelled- Positron Emission Tomography uses radioactive glucose to locate cancer. This glucose contains a radioactive atom that is absorbed by the cancerous cells and then detected by a special camera • Radiolabelled biocompound such as 2-fluoro-2-deoxy-D- glucose (FDG) is injected intravenously. • Uptake of this compound followed by further breakdown occurs in the cells. Tumor cells have a high metabolic rate hence this compound is also metabolised by tumor cells. • FDG is metabolised to FDG-6-phosphate which cannot be further metabolised by tumor cells hence it accumulates and concentrates in tumor cells. This accumulation is detected aU n Md Y quantified.
  • 9.
    BIOPSY UMY • Most conclusivetest because it confirms if the tumor is malignant or benign, the bone cancer type (primary or secondary bone cancer), and stage. • TYPES- • 1. Needle biopsy: During this procedure, a small hole is made in the affected bone and a tissue sample from the tumor is removed. two types - • Fine needle aspiration: During this procedure, the tissue sample is removed with a thin needle attached to a syringe. • Core needle aspiration: During this procedure, the surgeon removes a small cylinder of tissue sample from the tumor with a rotating knife like device. • 2. Incisional biopsy: During this procedure, the surgeon cuts into the tumor and removes a tissue sample.
  • 10.
  • 11.
    ENNEKING STAGING UMY Enneking describedthe most widely used staging system for benign bone tumors . The stages are denoted by the Arabic numerals 1, 2, and 3, whereas malignant bone tumors are classified by Roman numerals (I, II, III). Stage 1-LATENT- low biological activity, well marginated , often incidental ,may resolve spontaneously. -NOF Stage 2-ACTIVE-Symptomatic,limited bone destruction, may present with pathological fracture- ABC Stage 3-AGGRESSIVE- Bone destruction/Soft tissue extension, require complete work-up and a removal with wide margins to avoid possible local recurrence. -GCT
  • 12.
    • For Malignanttumors ,adopted by the Musculoskeletal Tumor Society, and originally developed by Enneking UMY Stage Grade Local Extent Metastasis 1A low intracompartmental - 1B low extracompartmental - 2A high intracompartmental - 2B high extracompartmental - 3 Any Any + Grade is determined by histological parameters. Low-grade tumors generally have few mitotic figures, little if any cellular atypia, and have a relatively non-infiltrative growth pattern. High-grade tumors tend to have marked cellular atypia, hyperchromatism, and nuclear pleomorphism. They often demonstrate an infiltrative growth pattern
  • 13.
    CAMPANACCI STAGING UMY • Radiologicalgrading system – Better for prognosticating aggressiveness then histology • Used for Giant Cell Tumours • GRADE 1--Intramedullary lesion confined to bone • GRADE 2--Thinned, expanded cortex • GRADE 3--Cortical breakout.
  • 14.
    SURGERY PRINCIPLES • Surgicalmargin is described by one of four terms— intralesional, marginal, wide, or radical. • Intralesional Resection--Plane of surgical dissection is within the tumor. • Often described as “debulking” because it leaves behind gross residual tumor. • Marginal resection--achieved when the closest plane of dissection passes through the pseudocapsule.( surrounding reactive tissue around tumor ) • For most benign lesions and some low-grade malignancies UMY
  • 15.
  • 16.
    Wide Resection UMY • Isachieved when the plane of dissection is in normal tissue • If the plane of dissection touches the pseudocapsule at any point, the margin should be defined as being marginal and not wide. • for high-grade malignancies. Radical resection • All the compartments that contain tumor are removed en bloc. • Involves removing the entire bone and the compartments of any involved muscles. • Rarely used now a days
  • 17.
    Curettage UMY • Simple Curettage- -corticalwindow over the lesion -bulk of the tumor is scooped out -cavity is enlarged back to normal host bone in each direction with a power burr. -copiously irrigated to remove any debris and tumor cells. • Extended curettage- »use of adjuvants, such as liquid nitrogen, phenol, polymethyl methacrylate, or thermal cautery
  • 18.
    CARTILAGE LESIONS UMY - Osteochondroma -Chondroma Enchondroma-arising in medullary canal Periosteal chondroma/juxtacortical chondromas-arise on bone surface
  • 19.
    Osteochondroma UMY • Developmental anomaliesrather than tumors. • They are usually sporadic, but can be part of: Hereditary multiple exostoses (HME) - also known as diaphyseal aclasis Trevor disease- Osteochondroma on epiphyseal side of growth plate. An osteochondroma can be either sessile or pedunculated, and is seen in the metaphyseal region typically projecting away from the epiphysis.
  • 20.
    • They mostcommonly arise from appendicular skeleton, especially around the knee . • Lower limb - 50% of all cases femur (especially distal) - most common : 30% • Tibia (especially proximal) - 15- 20% • Less common locations - feet, scapula • upper limb • humerus - 10-20% • hands, pelvis • spine - the posterior elements of spine are an uncommon, but not rare, site for these tumours UMY
  • 21.
    • Pathologically Osteochondromas are essentiallya part of the growth plate. • Separates and continues growing independently, without an associated epiphysis • The medullary cavity is continuous with the parent bone, and they are capped by hyaline cartilage UMY
  • 22.
    Osteochondroma • Clinically, osteochondromas present asslow-growing masses, which can be painful if they impinge on a nerve or if the stalk is fractured. In many cases, they are detected as an incidental finding. Osteochondroma. On this lateral view of the ankle, a benign osteochondroma is seen projecting posteriorly on a stalk. The end (arrows) is often covered with a cartilaginous cap. These lesions always occur near a UM jo Yint but point away from it.
  • 23.
    • • • • MRI MRI is bestat assessing cartilage thickness (and thus assessing for malignant transformation), presence of oedema in bone or adjacent soft tissues and visualising neurovascular structures in the vicinity. The cartilage cap of osteochondromas appears the same as cartilage elsewhere, with intermediate to low signal on T1 and high signal on T2 and STIR weighted images. A cartilage cap of over 1.5cm in thickness is suspicious for malignant degeneration. UMY
  • 24.
    T1 T2 STIR (FATSUPPRESSION) UMY
  • 25.
  • 26.
    S/S UMY • M Csymptom of an osteochondroma is a painless mass near the joints. The knee and shoulder are more commonly involved. • If the stalk of a pedunculated osteochondroma breaks, pain and swelling may start immediately. • If located under a tendon-- Snapping of the tissue over the tumor may cause activity-related pain. • If located near a nerve or blood vessel, such as behind the knee causing numbness and tingling in that extremity, periodic changes in blood flow, loss of pulse or changes in color of the limb.
  • 27.
    RISK OF MALIGNAT TRANSFORMATION- 1%-SOLITARY OSTEOCHONDROMA 5%- MULTIPLE HEREDITARY EXOSTOSIS UMY
  • 28.
    TREATMENT UMY Nonsurgical Treatment Most ofthe time, solitary osteochondroma is not removed surgically. Observe it & take regular X-rays to keep track of any changes. Surgical Treatment When surgery is recommended, it is best to wait until growth complete (a mature skeleton by X-ray evaluation) before removing a solitary osteochondroma. This decreases the chance of the tumor growing back. Surgery may be considered if the osteochondroma: Is causing pain with activity Puts pressure on a nerve or blood vessel Has a large cap of cartilage The osteochondroma is removed at the level of the normal bone. Some of the inside of the bone may also be removed.
  • 29.
    Hereditary multiple exostosis UMY -autosomal dominant - 2 Genes-EXT1-Ch8 , EXT2- Ch 11 -< 10 yrs Clinical features : - knobby appearance - short stature or even dwarf ( limbs short in relation to trunk ) - Deformity of forearm - in 40 – 60 % ulna short , radius bowed , loss of pronation n supination , tibiofibular synostosis , genu valgum , coxa valga
  • 30.
    DD : multipleenchondromatosis , achondroplasia UMY Treatment : excision of symptomatic exostosis correction of deformity & limb length discrepancy
  • 31.
  • 32.
  • 33.
    Enchondroma UMY • Common benignmedullary cartilaginous neoplasm • Usually found in children or young adults which can lead to pathological fractures or undergo malignant degeneration. • 3-10 % of all bone tumours and 12-24 % of benign bone tumours • Enchondromas are most frequently diagnosed in childhood to early adulthood with a peak incidence of 10-30 years. • Complicated by a pathological fracture or malignant transformation into a low grade chondrosarcoma • (clinically if an enchondroma is painful in the absence of a fracture, it should be considered malignant
  • 34.
    ENCHONDROMA • Enchondromas arisefrom rests of growth plate cartilage/chondrocytes that subsequently proliferate and slowly enlarge and are composed of mature hyaline cartilage. • they are seen in any bone formed from cartilage. • Two syndromes are associated with multiple enchondromas: Ollier disease Maffucci syndrome. • small tubular bones of the hands and feet : 50% • large tubular bones e.g. femur, tibia, humerus UMY
  • 35.
    ENCHONDROMA UMY • Rarely anenchondroma may extend through the cortex and demonstrate a exophytic growth pattern. This is known as an enchondroma protuberans, and may either be seen sporadically or as part of Ollier disease. • Almost all enchondromas are located in the medullary cavity of tubular bones. D/ds: • bone infarct , chondrosarcoma, intraosseous ganglion • other benign lytic bone lesions, • metastases • granulomatous disease : sarcoidosis, tuberculosis
  • 36.
    IMAGING • X-ray &CT Typically enchondromas are small 1 - 2cm lytic lesions with non-aggressive features. narrow zone of transition sharply defined scalloped margins : may have mild endosteal scalloping expansion of the overlying cortex may be present but there should not be cortical breakthrough unless fractured Chondroid calcifications may be present : rings and arcs calcification-STIPPLED/PUNCTATE/POPCORN no periosteal rxn. • The majority of enchondromas more frequently arise in the metaphyseal region,. A cartilaginous lesion in an epiphysis is more likely to be a chondrosarcoma . UMY
  • 37.
  • 38.
  • 39.
    IMAGING UMY • MRI • MRIis useful in evaluating for soft tissue extension and for confirming the diagnosis. • Enchondromas appear as well circumscribed somewhat lobulated masses replacing marrow. • T1 Intermediate to low signal • T1 C+ (Gd) enhancement is variable, and may be seen both peripherally or of translesional septae. Similar pattern of enhancement may be seen in chondrosarcomas. • T2 Typically of background intense high signal
  • 40.
  • 41.
    OLLIER”S DISEASE • Ollierdisease also known as enchondromatosis, is a non- hereditary, sporadic, skeletal disorder characterised by multiple enchondromas that are principally located in the metaphyseal regions. • Plain films show multiple enchondromas. Larger lesions can show cartilage calcification in a typical rings and arcs pattern. • Imaging characterestics are of same as ENCHONDROMAS UMY
  • 42.
    MAFUCCI’S SYNDROME UMY • Maffuccisyndrome is a congenital non hereditary mesodermal dysplasia characterised by multiple enchondromas with soft-tissue cavernous haemangiomas. • Imaging findings are multiple enchondromas seen associated with soft tissue swelling and phleboliths. • Enchondromas degenerate into chondrosarcomas in 15-51% of cases and soft- tissue haemangiomas to vascular sarcomas in 3-5%.
  • 43.
  • 44.
    Chondroblastoma UMY • Rare benigncartilaginous neoplasms( CODMAN TUMOR ) • Less than 1% of all primary bone tumours, occurring predominantly in young patients (< 20 years of age). There is a male predilection. • Pathologically composed of chondroblasts, chondroid matrix, cartilage with occasional giant multi-nucleated cells.* with surrounding chondroblasts. • Aneurysmal bone cysts can be seen secondarily to underlying chondroblastoma. • Patient may present as synovitis of knee.
  • 45.
    SITE • Epiphysis ofa long bone (70% occurring in the humerus (most frequent), femur and tibia, ~ 10% are found in the hands and feet) UMY
  • 46.
    IMAGING • X-rays • epiphyseal •well defined lytic lesions; either smooth or lobulated margins with a thin sclerotic rim • Internal calcifications can be seen in up to 40-60% of cases • They range in size from 1-10cm, with most being 3-4cm at diagnosis • CT • better delineation of the relationship to the growth plate and articular surface • Solid periosteal reaction (seen in up to 50% of cases) and internal calcification (calcified matrix seen in ~ 1/2 of cases) and cortical breach are also more easily appreciated. • Endosteal scalloping may be UMs Y een
  • 47.
  • 48.
  • 49.
    IMAGING UMY • MRI • Idealfor the evaluation of transphyseal or transcortical extension. • Demonstrating associated surrounding bone marrow oedema. •These lesions have signal typical of cartilage: T1 - lesion itself is of low to intermediate signal T2 / STIR - lesion is of intermediate to high signal • Fluid-fluid levels may occasionally be seen .
  • 50.
  • 51.
    MICROSCOPY UMY • Sheets ofchondroblasts with background of chondroid matrix. • Polygonal cells with distinct cytoplasm. • Dystrophic calcification surrounding individual cells – “CHICKEN WIRE “ appearance. • Abundant Giant cells • Secondary ABC in 20 % cases.
  • 52.
    TREATMENT • The goalfor treatment of chondroblastoma is to remove the tumor and prevent damage to the end of the affected bone. • Treatment may include: Surgical removal of the tumor - Biopsy and curettage with possible use of adjuvant liquid nitrogen or phenol, or a mechanical burr. It may be necessary to reconstruct articular surfaces due to subchondral erosion. Bone grafting /bone cement used Any joint invasion is usually secondary to previous instrumentation. UMY
  • 53.
    BONE FORMING TUMORS UMY Osteoidosteoma Osteoblastoma Bone island
  • 54.
    OSTEOID OSTEOMA UMY - Osteoblasticmass called nidus surrounded by zone of reactive sclerosis - 2nd decade - M > F - Site : proximal femur ( mc ) , tibia , spine ( posterior elements ) Not seen in bones of membranous origin C/F : Dull pain , worse at night , relieved with NSAID s , not related to position or function , often aggravated by alcohol
  • 55.
    - Pain iselicited by local pr. - O.O is suspected in spine when a pt < 30 yrs complains of constant back pain , when spine is stiff and scoliotic & SLRT is positive with no signs of nerve root compression. Radiological findings : Radiolucent nidus ( 1.5 cm) with reactive sclerosis in cortex , DD : Osteoblastoma , Non-suppurative osteomyelitis of garre , Brodies abscess, Stress # , Diagnosis : Tc99 bone scan – Inc uptake “Headlight in fog “ & “Double – density sign “ CT – BULLS EYE appearance UMY
  • 56.
  • 57.
  • 58.
    Pathology : Nidus –osteoblasts & nonmyelinated axons Stroma – osteoblasts , osteoclasts , fibroblasts & blood filled capillaries - Transform into osteoblastoma but no malignant transformation. Treatment : Self limiting lesions – conservative treatment with NSAIDs – not well tolerated - Surgery : to eradicate pain producing nidus ( accurate localization is hence crucial ) methods : - en bloc resection or burr down tech. Latest is percutaneous radiofrequency ablation UMY
  • 59.
    OSTEOBLASTOMA UMY - Histologically similarto O.O but differing in progressive growth & absence of reactive perifocal bone formation. - Potentially malignant - Mc site : vertebral column ( post. Elements) - C.F : pain of varying intensity pathological # neurological problems Radiographic features : nothing particularly distinctive well circumscribed lesion , CT – COTTON WOOLappearance due to irregular opacities
  • 60.
    - Radiopacity expressionof quantity & degree of maturation of osteoid substance. Bone scan – localizing smaller lesions esp in spine Pathology : very vascular DD : Osteoid osteoma Osteosarcoma ( increase in sr.ALP). Treatment : curettage & bone grafting UMY
  • 61.
  • 62.
  • 63.
    FIBROUS LESIONS UMY Nonossifying fibroma Corticaldesmoid Benign fibrous histiocytoma Fibrous dysplasia Osteofibrous dysplasia
  • 64.
    NON OSSIFYING FIBROMA UMY -Also called Fibrous cortical defect or Metaphyseal cortical defect or Fibrous xanthomas - Mc musculoskeletal tumor - Occurs in 30 % of children - 1st two decades - Site : femur , tibia , humerus ( 8 % - multiple lesions) - Asymptomatic - X ray : well defined , eccentric , radiolucent lesion in metaphysis ,multilocular app or rim of sclerosis , doesn’t expand the cortex & no periosteal reaction. - Treatment : observation
  • 65.
  • 66.
    FIBROUS DYSPLASIA UMY -intrinsic defectof endochondral bone maturation  immature ossification pattern -Characterized by replacement of normal bone & marrow by fibrous tissue & small woven spicules of bone  weakbone . - Solitary or multifocal - ALBRIGHT ‘ S SYN : polyostotic F.D + café au lait spots + endocrinopathies . - MAZABRAUD SYN- Polyostotic FD+ Intramuscular myxomas - Site : rib , femur , humerus , tibia , maxilla - C.F : monostotic – asymptomatic bone pain , skeletal deformities .
  • 67.
    RADIOGRAPHIC APPEARENCE Radiographic features: - Epiphysis or metaphysis or diaphysis - Well defined geographic lytic lesions - Ground glass matrix : intramedullary radiolucencies - Cortical thinning - Secondary deformities esp. in wt , bearing bones - Shepherd’s crook deformity ( microfractures – on tension side of bone ) - Poorly defined areas of osteolysis - Cortical destruction - Soft tissue involvement suspect malignant transformation UMY
  • 68.
  • 69.
    Shepherd's crook deformity UMY •Coxa varus angulation of the proximal femur, classically seen in femoral involvement by fibrous dysplasia, although may be seen in other disorders such as Paget disese of bone and osteogenesis imperfecta. • The shape of the proximal femur resembles that of the staff carried by herders (shepherds), which is known as a crook.
  • 70.
  • 71.
    TREATMENT UMY - Monostotic lesions asymp  no Rx Indications : severe deformity persistent pain pathological # - Curettage & grafting ( cortical allograft prfrd. d/t slower absorption) - Internal fixation +/- osteotomy - Bisphosphonates : beneficial
  • 72.
    CYSTIC LESIONS UMY Unicameral bonecyst Aneurysmal bone cyst Intraosseous ganglion cyst
  • 73.
    UNICAMERAL BONE CYST UMY -Developmental anamoly of physis - Transient failure of ossification of physeal cartilage & cyst formation - < 20 yrs age , M > F - Spontaneously resolve in late adolescence , rarely persist into adulthood - Site : proximal humerus , proximal femur , calcaneum . Active cysts are juxtaposed to physis (within 1 cm) C.F : usually asymptomatic , pathological #
  • 74.
    - Cysts progressfrom active to quiescent to involutional UMY - stage . cysts usually shrink as patient approaches skeletal maturity. - Radiographic features : metaphysis of immature skeleton , DIGNOSTIC- well marginated , centrally located ,purely lytic lesion. radiolucent that expand and thin the cortex . FALLEN FRAGMENT SIGN - # fragment in the cyst DD :ABC & fibrous dysplasia
  • 75.
  • 76.
  • 77.
    Bone cyst of humerus Pathologicfracture “Falling Fragment Sign” UMY
  • 78.
    MRI MR signal characteristicsfor an uncomplicated lesion include T1 - low signal T2 - high signal Usually there no fluid-fluid levels unless there has been a complication with haemorrhage. CT and MRI add little to the diagnosis, but are however helpful in eliminating other entities that can potentially mimic a simple bone cyst UMY
  • 79.
  • 80.
    TREATMENT Small asymp lesionsin upper extremities- observation & follow up Larger lesions need Rx Symptomatic lesions Lesions in lower extremities Various options are Curettage +/ - bone grafting +/- int. fixation Aspiration & inj of steroids or bone products UMY
  • 81.
    Aneurysmal bone cyst(ABC) • Benign , Expansile • Primarily seen in children and adolescents (80% l <20yrs of age) • Blood-filled spaces of variable size separated by connective tissue (trabeculae of bone or osteoid tissue) and osteoclast giant cells •Not lined by endothelium. Types • Primary • Secondary (e.g chondroblastoma, fibrous dysplasia, giant cell tumour (GCT), osteosarcoma UM )Y
  • 82.
    • Location Long bones– tibia & fibula (24%), femur (13%), Spine 20-30% (posterior elements). sacrum • A variant of ABCs is the giant cell reparative granuloma.( SOLID ABC) • seen in the tubular bones – hand , feet craniofacial skeleton. UMY
  • 83.
    Radiographic features • Xray sharply defined, expansile osteolytic lesions, with thin sclerotic margins. Eccentricity is typical. But very often missed out due to cortical thinning due to ballooning. CT Demonstrates these findings to a greater degree, and is also better at assessing cortical breach and extension into soft tissues. Fluid fluid levels (better than MRI) UMY
  • 84.
  • 85.
  • 86.
    MRI UMY • MRI Demonstrate FluidFluid level in lesion. To distinguish between Primary and secondary (if solid component Is present.) The cysts are of variable signal, with surrounding rim of low T1 and T2 signal. Focal areas of high T1 and T2 signal are also seen presumably representing areas of blood of variable age. SBC vs ABC on MRI- Presence of double density fluid level & intralesional septations- ABC
  • 87.
    BONE SCAN • Doughnutsign - increased uptake peripherally with a photopenic centre. UMY
  • 88.
    TREATMENT UMY Excision – corticalbased or surface tumors Extended intralesional curettage & grafting – central lesions Embolisation – vertebral & pelvicABC Low dose radiation – effective method but not used d/t malignant transformation.
  • 89.
    ANJALI ,20F,ABC Rx-Curettage+ GBone grafting PRE OP IMMEDIATE POST OP FOLLOW UP UMY
  • 90.
    DHRUV 8/M ABC Rx-curettage+Chron os grafting UMY
  • 91.
    DEFINITION: Distinct neoplasm arisingfrom non-bone forming supportive connective tissue of marrow with network of stromal cells regularly interspersed with giant cells. ( Jaffe & Liechtenstein ) -75-80% OF PATIENTS 20-50 YRS Male:Female- 1:1.3 (Benign) -3:1 (Malignant) UMY
  • 92.
    Site • 55% AROUNDTHE KNEE • 10% in the distal radius • 6% in the proximal humerus • SPINE rarely involved (commoner in the sacrum) • In the head and neck region the maxilla and mandible are more commonly involved. • SIGNS&SYMPTOMS 1. PAIN 2. SWELLING 3. JOINT RESTRICTION 4. MUSCLE WASTING 5. NEUROLOGICALSIGNS 6. PATHOLOGICAL# 7. PULMONARYMETS- 3 % UMY
  • 93.
    Pathology GROSS-  End ofbone is expanded.  Eccentric lesion at the epiphyseo-metaphyseal region.  Thin periosteum.  Fleshy dark brown, soft, friable mass.  Cystic spaces seen. UMY
  • 94.
    Pathology Microscopy-  Vascularized networkof round,oval or spindle shaped stromal cells and multinucleated giant cells( 40-60 nuclei /cell) with numerous centrally placed nuclei UMY
  • 95.
    GRADING SYSTEM Jaffe,Lichenstein and Portis(1940) GRADE1- o Conventional GCT GRADE 2- o Boderline tumours GRADE 3- o Sarcomatous type of stroma Modified grading Sannerkin et al(1980) • Malignant GCT- with frank sarcomatous changes and full metastatic potential • Borderline GCT- without sarcomatous changes but with abnormal mitoses or vascular permeation or both • Conventional GCT- without features of any of the above two types No correlation exists between histological grading and clinical behavior of the tumour. Hence grading not widely accepted. UMY
  • 96.
    RADIOLOGY Type of Osteolysis •Geographic destruction (I) • Moth-eaten (II) Permeative(III) Lodwick 1A 1B 1C UMY
  • 97.
  • 98.
    RADIOLOGY • TRABACULATION PURE LYTIC(60%) FINE TRABACULTION(40%) UMY
  • 99.
    SCINTI GRAPHY Less useful Inconsistentuptake “Doughnut sign” M.R.I. Soft tissue spread Joint breach Locate N.V. bundle T1-Dark,T2-Bright ABC-20% C.T Intraossous content Intra articular spread Cortical breach Site of window ANGIO GRAPHY Locate vessels type of feeders For embolisation INVESTIGATIONS UMY
  • 100.
    SURGICAL TREATMENT Stage1& Stage2--- Intralesional or Marginal Excision Stage3 --- Wide resection with Reconstruction Radiation, Embolaisation UMY
  • 101.
    Curettage & BoneGrafting INDICATION STAGE-1&2 ADEQUATE WINDOW MOTORISED BURR ( 20,000 rpm ) BISPHOSPHONATES- Locally or systemically prevent recurrence. IV ZOLENDRONIC ACID USE FOR PRIMARY GCT UNDER STUDY UMY
  • 102.
    DEPENDING ON SITE UMY •AROUND KNEE-Hemicondylar osteoarticular allograft reconstruction / rotation hinge endoprosthesis. • AGGRESSIVE LESION OF DISTAL RADIUS- Primary resection & reconstruction with proximal fibular autograft( arthroplasty or arthrodesis) • EXPENDABLE BONES( DISTAL ULNA/PROX. FIBULA)- Priamry resection without reconstruction. • Spine /pelvis- Irradiation/embolization/both • PULMONARY METS- Resection
  • 103.
    ‘E’ OF GCT UMY •EPIPHYSEAL • ECCENTRIC • EXPANSILE • EXTENDED CURETTAGE • EXCISION –IF EXTENDED CURETTAGE FAILS
  • 104.