Fractures

Fracture
• Loss of bone integrity due to mechanical injury and/or diminished
bone strength.
Types of Fracture
 Simple Compound

-overlying skin is intact -bone communicates with the skin

 Comminuted Displaced

-bone is fragmented -ends of the bone at fracture site

are not aligned
 Stress “Greenstick”

-slowly developing -extending partially through the

-follows a period of ↑ physical bone
activity; bone is subjected to -common in infants
repetitive loads
Pathologic

-bone weakened by underlying disease process (e.g. tumor)

 Healing of Fractures

fracture

• seals off fracture hematoma • degranulated

site plts and Osteoclastic
migrating activty
• influx of inflammatory
inflammatory Fibrin mesh cells release
cells and factors Osteoblastic
ingrowth of activating activity
fibroblasts and osteoprogenitor
new capillaries cells
End of 1st week…
• Major changes:
• Organization of hematoma
• Matrix production in adjacent tissues
• Remodeling of fractured ends of the bone.

• Soft tissue or procallus

– uncalcified bone
- provides anchorage ONLY between ends of fractured
After 2 weeks…
• Soft tissue callus -> bony callus (max. girth at the end of 2nd week or
3rd week)
• Newly formed cartilage -> endochondral ossification -> fractured ends
are bridged and mineralized -> increasing its stiffness and strength
Healing of Fractures
• Healing process is complete with the restoration of medullary cavity.

*inadequate immobilization -> movement of callus -> delayed union or

non-union

• Non-union – persistence causes cystic degeneration -> luminal surface

lined by synovial like cells -> pseudoarthrosis
Osteonecrosis (Avascular Necrosis)
• Infarction of bone and marrow
• Stem from fractures or corticosteroid administration
CLINICAL COURSE: Osteonecrosis
• Symptoms depend on the location and extent of infarction

• Subchondral infarcts
– a triangular or wedge-shaped segment of tissue that has
the subchondral bone plate as its base undergoes necrosis.

• Medullary infarcts – small and clinically silent

Osteomyelitis
• Inflammation of bone and marrow secondary to infection.

• All types of organism can produce osteomyelitis but certain pyogenic

bacteria and mycobacteria are the most common.

• Types:
• Pyogenic osteomyelitis
• Mycobacterial osteomyelitis
• Skeletal syphilis
Pyogenic Osteomyelitis
• Almost always caused by bacterial infections
• Organisms reach the bone via:
1. Hematogenous spread
– (healthy children: develops in long bones)
- (adults: complication of open fractures, surgery, and diabetic
infections of the feet)
2. Extension from contiguous site
3. Direct implantation
Pyogenic Osteomyelitis

• Staphylococcus aureus
– 80% - 90% of the cases of pyogenic osteomyelitis

• Escherichia coli and Klebsiella

– GUT infections or IV drug abuser

• Haemophilus influenza and group B streptococci

– neonatal

• Salmonella
– sickle cell disease
Pyogenic Osteomyelitis
• Location of bone infection is influenced by osseous vascular
circulation, which varies with age.

• Neonate: infection of metaphysis and/or epiphysis

• Children: metaphysis
• Adult: Epiphysis and subchondral regions
CLINICAL COURSE: Pyogenic Osteomyelitis
• Hematogenous osteomyelitis
• Manifests as acute systemic illness: malaise, fever, chills, leucocytosis, and
marked-to-intense throbbing pain over affected region

• Others: subtle, with only unexplained fever (infants) or localized pain (adults)

• Dx: radiographic findings of a lytic focus of bone destruction surrounded by a

zone of sclerosis

• Cure: antibiotics + surgical drainage

Mycobacterial Osteomyelitis
• 1% to 3% of individuals with pulmonary or extrapulmonary
tuberculosis have osseous infection

• Blood-borne and originate from active visceral disease

• Tuberculous spondylitis (Pott disease)

• Spine is involved
• Destruction of discs and vertebrae result in scoliosis or kyphosis and
neurologic deficits secondary to spinal cord and nerve compression
Complications of Tuberculous osteomyelitis

• Tuberculous arthritis
• Sinus tract infection
• Psoas abscess
• Amyloidosis
Skeletal Syphilis
• Syphilis (Treponema pallidum)
• Yaws (Treponema pertenue)
• Congenital syphilis
– bone lesion appear about the 5th month of gestation
and are fully developed at birth.

• Organisms localize in areas of

• endochondral ossification (osteochondritis)
• periosteum (periostitis)
Skeletal Syphilis
• Saber shin – produced by massive reactive periosteal bone deposition
on the medial and anterior surfaces of tibia

• Acquired syphilis – bone disease may begin in tertiary stage (2 to 5

years after initial infection)

• Bones most frequently involved: Nose, palate, skull, and extremities

Thank you!
Bone Tumor and Tumor-like
Lesions
Overview
• Bone-forming Tumors
• Osteoid osteoma and Osteoblastoma
• Ostaeosarcoma

• Cartilage-forming Tumors
• Osteochondroma
• Chondroma
• Chondrosarcoma
Bone-Forming Tumors
-Tumors produce unmineralized osteoid or mineralized woven bone

• Osteoid osteoma and osteoblastoma

• Osteosarcoma
Bone-Forming Tumors
-Tumors produce unmineralized osteoid or mineralized woven bone

• Osteoid osteoma and osteoblastoma

• Osteosarcoma
Osteoid osteoma and Osteoblastoma

Osteoid osteoma Osteoblastoma

size < 2cm in diameter > 2 cm
Bone location Any. More on appendicular Posterior spine (laminae
skeleton (50% femur or and pedicles)
tibia)
Drug for pain Aspirin and NSAIDs for Unresponsive to aspirin
severe nocturnal pain
(PGE2 by osteoblast)
Radiograph Thick rind of reactive Does not induce a marked
cortical bone bony reaction
Tx Radiofrequency ablation Curetted or excised en
bloc
Others Occur in young men in
their teens and 20s
Osteoid osteoma Osteoblastoma
Osteoid osteoma Osteoblastoma
Bone-Forming Tumors
-Tumors produce unmineralized osteoid or mineralized woven bone

• Osteoid osteoma and osteoblastoma

• Osteosarcoma
Osteosarcoma
• Malignant
• Most common primary malignant tumor of the bone
Male-to-female ratio 1.6:1
Bone involved Any
Radiograph Large destructive, mixed lytic and blastic mass with
infiltrative margins
Osteosarcoma
Osteosarcoma
Osteosarcoma
• Codman triangle
-Triangular shadow between the cortex and periosteum
-Indicative of aggressiveness
-Characteristic but NOT diagnostic
Osteosarcoma Pathogenesis
Acquired genetic abnormalities:
• RB
• TP53
• INK4a
• MDM2 and CDK4
Osteosarcoma: Clinical course
• Tx: Neoadjuvant chemotherapy followed by surgery

• Prognosis: 5-year survival rates in px without overt metastases at

initial dx

• Spread hematogenously to the lungs

Cartilage-forming tumors
• Account for the majority of primary bone tumors (both benign and
malignant)

• Formation of hyaline or myxoid cartilage; fibrocartilage and elastic

cartilage are rare
Cartilage-forming tumors
• Osteochondroma
• Chondroma
• Chondrosarcoma
Osteochondroma (Exostosis)
• Benign
• Most common benign bone tumor
Male-to-female ratio 3:1
Bone involved Only in bones of endochondral origin
Radiograph Cartilage-capped tumor attached to the underlying skeleton
by a bony stalk
Osteochondroma Pathogenesis
Germline loss-of-function mutations in either
EXT1 or the EXT2 gene
-encode for enzymes that synthesize heparin sulphate
glycosaminoglycans
Osteochondroma Clinical Course
• Usually stop growing at the time of growth plate closure

• Symptomatic tumors are cured by simple excision.

• 5% to 20% osteochondromas -> chondrosarcoma.

Cartilage-forming tumors
• Osteochondroma
• Chondroma
• Chondrosarcoma
Chondroma
• Benign
• Tumors of hyaline cartilage that usually occur in bones of enchondral
origin

• Type based on location:

• Enchondromas = medullary cavity growth
• Juxtacortical chondromas = growth on surface of bone.
Enchondromas
• most common of the intraosseous cartilage tumors
• appear as solitary metaphyseal lesions of tubular bones of the hands
and feet
• Radiographic:
Circumscribed lucencies with central irregular
calcifications, a sclerotic rim and an intact cortex
Enchondromas
• Ollier disease and Maffucci syndrome are nonhereditary disorders
characterized by multiple enchondromas.
Enchondroma: Maffucci Syndrome
Enchondromas Pathogenesis

• Heterozygous mutations in the IDH1 and IDH2 genes

Enchondromas Clinical course
• Treatment depends on the clinical situation and is usually observation
or curettage
Cartilage-forming tumors
• Osteochondroma
• Chondroma
• Chondrosarcoma
Chondrosarcoma
• Malignant tumors that produce cartilage.
• Histologic variants:
-Conventional (hyaline cartilage-producing)
1. Central (intramedullary)
2. Peripheral (juxtacortical)
-Clear cell
-Dedifferentiated
-Mesenchymal
Clear cell chondrosarcoma
Chondrosarcoma
• Malignant tumors that produce cartilage.
• Histologic variants:
-Conventional (hyaline cartilage-producing)
1. Central (intramedullary)
2. Peripheral (juxtacortical)
-Clear cell
-Dedifferentiated
-Mesenchymal
Mesenchymal Chondrosarcoma
Chondrosarcoma
• 2nd most common malignant matrix-producing tumor of bone
• Commonly arise in the axial skeleton
• Imaging: calcified matrix appears as foci of flocculent densities
Chondrosarcoma Pathogenesis
• Chondrosarcomas arising in
-Multiple osteochondromasyndrome = EXT mutations
-Chondrosarcomas = IDH1 and IDH2 mutations
Chondrosarcoma Clinical Course
• Usually present as painful, progressively enlarging masses.
• Treatment:
-Conventional chondrosarcoma = wide surgical excision
-Mesenchymal and dedifferentiated = excised + chemotherapy
Tumors of Unknown Origin
• Ewing Sarcoma Family Tumors
• Giant Cell Tumor
• Aneurysmal Bone Cyst
Ewing Sarcoma
• Malignant
• characterized by primitive round cells without obvious
differentiation
Ewing Sarcoma
• Ewing sarcoma + primitive neuroectodermal tumor (PNET)
=Ewing sarcoma family tumors (ESFT)

• Pathogenesis: Most ESFT contain a (11;22) (q24;q12) translocation

generating in-frame fusion of the EWS gene on chromosome 22 to
the FLI1 gene.
ESFT
• Follow osteosarcoma as the second most common group of bone
sarcomas in children

• Usually arise in the diaphysis of long tubular bones, especially the

femur and the flat bones of the pelvis
ESFT
ESFT
Ewing Sarcoma Clinical Course
• Treatment:
-neoadjuvant chemotherapy followed by surgical excision with
or without irradiation.

**The amount of chemotherapy-induced necrosis is an important

prognostic finding.
Giant Cell Tumor
• Histology: multinucleated osteoclast-type giant cells (osteoclastoma)

• Uncommon benign, but locally aggressive neoplasm.

• Usually arises in individuals in their 20s to 40s.
Giant cell tumor
• Arise in the epiphysis but may extend into the metaphysis
• The typical location of these tumors near joints frequently causes
arthritis-like symptoms.
Aneurysmal Bone Cyst
• Character: by multiloculated blood-filled cystic spaces
ABC
• Radiograph: eccentric, expansile lesion with well-defined margins

Pathogenesis. Rearrangements of chromosome 17p13

ABC clinical course

• Treatment:
-Surgical, usually curettage or, in certain situations, en bloc
resection
Lesions Simulating Primary Neoplasms
• Fibrous Cortical Defect
• Nonossifying Fibroma
Fibrous Cortical Defect and Non-Ossifying
Fibroma
• Fibrous cortical defects (metaphyseal fibrous defects) are extremely
common, present in 30% to 50% of children older than 2 years.
• Asymptomatic and are detected incidentally on radiographic studies.
Fibrous Dysplasia
• Benign
• Localized developmental arrest; all of the components of normal
bone are present, but they do NOT differentiate into mature
structures.
Fibrous Dysplasia
• lesions arise during skeletal development, and appear in several
distinctive but sometimes overlapping clinical patterns:

• Monostotic: involvement of a single bone

• Polyostotic: involvement of multiple bones
• Mazabraud syndrome: fibrous dysplasia (usually polyostotic) and soft tissue
myxomas
• McCune-Albright syndrome: polyostotic, associated with café-au-lait skin
pigmentations and endocrine abnormalities, especially precocious puberty.
McCune Albright Syndrome
Fibrous Dysplasia Pathogenesis
• Somatic gain-of-function mutation during development in GNAS1
Metastatic Tumors
• most common form of skeletal malignancy
• pathways of spread:
(1) direct extension
(2) lymphatic or hematogenous dissemination
(3) intraspinal seeding (via the Batson plexus of veins).
Metastatic Tumors
• Radiographic appearance of metastases may be:

lytic (bone destroying)

purely blastic (bone forming)
mixed lytic and blastic
Metastatic Tumors
• Tumor cells do NOT directly resorb bone in lytic lesions. Rather, they
secrete substances that upregulate RANKL on osteoblasts and
stromal cells thereby stimulating osteoclast activity.

• Treatment:
• Systemic chemotherapy, localized radiation and bisphosphonates
• Surgery to stabilize pathologic fractures
Thank you!