Osteosarcoma is a malignant bone tumor that arises from primitive bone-forming cells. It most commonly occurs in adolescents and young adults. The most frequent sites are the distal femur, proximal tibia, and proximal humerus. Treatment involves preoperative chemotherapy, surgical resection with wide margins, and postoperative chemotherapy. Prognosis depends on the stage, with 5-year survival rates of 60-80% for localized tumors and 15-30% for those that have metastasized.

1. Presented by:
SANA ARMAN 

2. • OSTEO = Bone
• SARCOMA = Malignant tumour of
connective tissue

3. OVERVIEWOVERVIEW
• Introduction
• Epidemiology
• Classification
• Skeletal Distribution
• Etiology
• Clinical and Radiographic features
• Histopathology
• Staging
• Treatment and Prognosis

4. INTRODUCTIONINTRODUCTION
• 2nd
most common primary malignant bone
tumor after multiple myeloma.
• Arise from primitive mesenchymal bone
forming cells
• Formation of osteoid directly by sarcoma
cells.

6. EPIDEMIOLOGYEPIDEMIOLOGY
 Involves any age but highest occurrence
in adolescence i.e,10 to 25 yrs
 Males > Females
 Blacks > Whites

7. OSTEOSARCOMA
Primary Secondary
Central
(intra-
medullary)
Intra
Cortical
Peripheral
(juxta-cortical)
High
Grade
Low
Grade
• Paraosteal
• Periosteal
• High grade
surface OS
• Conventional OS
• Telangiectactic OS
• Small cell OS
Sequelae of .
•Pagets Disease
•Chemotheraphy
•Chondrosarcoma-
dedifferentiation
CLASSIFICATICLASSIFICATI
ONON

8. INTRA CORTICALINTRA MEDULLARY
(central)
JUXTA CORTICAL
(surface)
• 95%
• Metaphysis
• Fast growing
• Very rare
• Diaphysis
• 5%
• Metaphysis or Diaphysis
• Slow growing

9. ETIOLOGYETIOLOGY
• Exact cause is unknown.
• Risk Factors
– Rapid bone growth
– Environmental
 Radiation
 Oncogenic virus
– Genetic
 Mutation of RB gene
 Li Fraumeni syndrome – Mutation in p53 tumour suppressor gene
 Rothmund Thomson syndrome (Autosomal Recessive)
– Pre existing lesions – Ex: Fracture of bone, Infarcts, Pagets disease etc

10. SKELETAL DISTRIBUTIONSKELETAL DISTRIBUTION
• Sites
– Metaphysis > Diaphysis > Epiphysis
[89%] [10%] [1%]
• Distal Femur [40%]
• Proximal Tibia [20%]
• Proximal Humerus [10%]
• Others – Jaw [8%] or
Pelvis [8%]

11. CLINICAL ANDCLINICAL AND
RADIOGRAPHIC FEATURESRADIOGRAPHIC FEATURES
 Clinically
• Pain
• Swelling
• Loosening of teeth
• Paresthesia
• Nasal obstruction

12.  Radiographically
• Codmans triangle
• Sunburst appearance
• Symmetric widening of periodontal
ligament.

13.  Radiographically
• Codman’s triangle :
Formed at the angle between
the elevated periosteum and
underlying surface of cortex.

14. • Sunburst appearance: Due to
osteogenesis within the tumour.
 Radiographically

15. • Symmetric widening of periodontal
ligament space: Due to tumour infiltration.
 Radiographically

16. PATHOLOGYPATHOLOGY
 GROSSLY :
• Grey white
• Bulky mass
• Codmans triangle
• Cut surface shows areas of
hemorrhages and necrotic
bone.

18. g
HISTOLOGICALLYHISTOLOGICALLY :
• Sarcoma cells - Undifferentiated mesenchymal
stromal spindle shaped cells with hyperchromatic
nuclei.
• Osteogenesis – Osteoid matrix and bone is found
interspersed in the areas of tumour cells.
Osteiod
production
Spindle cells with
hyperchromatic
nuclie

19. CONVENTIONAL OSTEOSARCOMACONVENTIONAL OSTEOSARCOMA
 Osteoblastic
 Chondroblastic
 Fibroblastic

20.  OSTEOBLASTIC OSTEOSARCOMAOSTEOBLASTIC OSTEOSARCOMA

21.  CHONDROBLASTIC OSTEOSARCOMACHONDROBLASTIC OSTEOSARCOMA

22.  FIBROBLASTIC OSTEOSARCOMAFIBROBLASTIC OSTEOSARCOMA

23.  Histologic variants
• Telangiectactic: Large,cavernous,dilated
vascular channels.
• Small cell: Small,uniform tumour cells.
• Fibrohistiocytic: Resembles malignant fibrous
histiocytoma
• Anaplastic: Marked anaplasia
• Well differentiated: Minimal cytologic atypia

25. EVALUATIONEVALUATION
Medical history and physical examination
Confirmed by investigations
• Plain x ray
• MRI scan
• CT scan
• Angiogram
• Bone scan
• Laboratory studies
• Biopsy

26. STAGINGSTAGING
• To stratify risk groups
 Stages :
• Stage I - Low grade lesions
• Stage II - High grade lesions
• Stage III - Metastatic disease
 Substages :
• A - Intramedullary lesions
• B - Local extramedullary spread

27. TREATMENT (plan)TREATMENT (plan)
• Radiological staging
• Biopsy to confirm diagnosis
• Preoperative chemotherapy
• Repeat radiological staging (access chemo response, finalize
surgical treatment plan)
• Surgical resection with wide margin
• Reconstruction using one of many techniques
• Post op chemotherapy based on pre op response

28. ChemotherapyChemotherapy
• Preoperatively - Neoadjuvant
chemotherapy (to decrease spread of
tumour cells during surgery; treat
micrometastasis)
• Postoperatively - Adjuvant chemotherapy

29. SurgerySurgery
For safe and complete removal of tumor
 Methods :
a.Amputation
b.Limb savage procedure
c. Rotationplasty

30. • In mandible - Hemimandibulectomy
• Maxillectomy is difficult to perform due to
the involvement of adjacent structures like
maxillary sinus, pterygopalatine fossa and
orbital fossa.

31. PROGNOSISPROGNOSIS
5 year survival rate
• Localised tumours : 60-80%
• Metastatic tumours : 15-30%