Diseases of the Jawbones

DENS 3702, Spring Semester

Basic objectives for individual lesions:
1. Identify the cause (etiology; pathogenesis), cell or tissue of origin, and frequency (prevalence
rate)
2. List the predilection GAL (Gender predilection, Age predilection, Location predilection)
3. Describe the typical clinical appearance, unusual clinical variants, and look-alike lesions
4. Describe the basic microscopic features
5. Describe the usual biologic behavior (pathophysiology) and prognosis without treatment, and
describe the typical treatment(s) and the prognosis with such treatment(s)
6. Describe unique variants, special features, or unique problems
Osteogenesis imperfecta:
1. Etiology: mutation in genes of type I collagen formation (autosomal dominant, some autosomal
recessive); 1/8,000 births
2. GAL:
None
Infant and young child
Teeth (opalescent dentin)
3. Clinical: Bowing, angulation, deformity of long bones; pathologic fracture; Wormian skull;
osteopenia;
Blue or gray or brown translucent crowns identical to dentinogenesis imperfecta
Maybe shell teeth
Fracture of crowns; maxillary hypoplasia
Rarely, mixed radiolucent/opaque areas of jaws; hearing deficits
Hypermobile joints; blue sclera; capillary fragility (pathologic bleeds)
4. Micro: Immature, irregularly shaped bony trabecula in fibrous background; diminished marrow;
teeth have small pulps (shell teeth have large pulps)
5. Treat: Cautious behavior to prevent fracture; C-section for birth; shorten dental crowns;
overdenture
6. Special: 4 types of disease:
Type I: most common, mildest form; blue sclera throughout life; AD inheritance
Type II: most severe (90% are stillborn or die shortly after birth); both AD & AR inheritance
Type III: second most severe form; usually noticed after 6 months; sclera often normal; most
die before adulthood (usually from cardiopulmonary problems from kyphoscoliosis);
both AD & AR inheritance
Type IV: fractures in 50% at birth; blue sclera usually fades with time; AD inheritance
Osteopetrosis:
1. Etiology: inherited failure of osteoclastic function (number of osteoclasts is normal or high) >>
no bone resorption >> gradual thickening of trabecula and cortex & anemia from less marrow
space; prevalence rate: 1/100,000 persons
2. GAL: none; infancy (except adult onset type); none
3. Clinical: Slow opacification and decreased blood flow to bone (painful?), often with
osteomyelitis which fails to heal (primarily a jaw problem), hearing loss and vision loss and

facial palsy from crimping of nerves as they pass thru foramina; delayed or stopped tooth
eruption; pathologic fractures
4. Micro: Thick lamellar bone forming concentric rings as it fills marrow spaces; thick cortex
5. Treat: Antibiotics to counter fewer hematopoietic cells; treat anemias if possible; try to prevent
dental infection; hyperbaric therapy; a variety of medical therapies are tried.
6. Special: Two major types:
Infantile osteopetrosis (malignant osteopetrosis): severe (usually die in first decade);
most common form; AR inheritance.
Adult osteopetrosis (benign osteopetrosis): not severe (usually no marrow deficit);
bone ain is common; AD inheritance
Cleidocranial dysplasia:
1. Etiology: defective CBFA1 gene (chromosome 21) which guides osteoblastic differentiation and
appropriate bone formation; AD inheritance with 40% spontaneous mutations
2. GAL: none; childhood and teenage years; clavicle
3. Clinical: missing or partially missing clavicles; drooping shoulders; frontal and parietal bossing;
delayed closure of skull sutures (wormian bones); failure of permanent teeth to erupt;
supernumerary teeth; hypoplastic alveolar development.
4. Micro: Bone looks normal; permanent teeth lack secondary cementum.
5. Treat: Surgical exposure and orthodontic repositioning of teeth; extraction of teeth with denture
construction.
Focal osteoporotic marrow defect:
1. Etiology: Unknown, perhaps chronic local ischemia, perhaps demands of body for blood cells
2. GAL: female; middle-aged and older; third molar and retromolar areas, especially mandible,
especially in old extraction sites
3. Clinical: poorly defined radiolucency, perhaps with portions of residual socket; may be tender or
painful; no cortical expansion.
4. Micro: marrow is usually fatty, may be hematopoietic, and bony trabecula are thin and widely
spaced.
5. Treat: None required unless painful, but usually conservative curettage is done to rule out
lymphoma or sarcoma of bone.
Massive osteolysis (Gorham disease; phantom bone disease):
1. Etiology: unknown, perhaps from vascular proliferation in marrow spaces (hemangiomatosis of
bone), many cases have traumatic episode to start
2. GAL: none; young adults; mandible, pelvis, humerus, clavicle
3. Clinical: Bone starts to dissolve, showing poorly demarcated radiolucencies around and
between the teeth, continues until much or all of the mandible and maxilla are gone; painless
4. Micro: Immature bone with osteoclastic and osteoblastic activity, with fibrosis of marrow spaces
often containing many dilated capillaries
5. Treat: None is effective; surgical curettage is usually tried
Idiopathic osteosclerosis (bone scar; enostosis; bone island):
1. Etiology: by definition, unknown
2. GAL: none; 5-20 years of age; mandible, especially first molar and premolar region
3. Clinical: Irregular, relatively well defined and uniform radiopacity without capsule slowly

enlarges between or at apex of teeth; asymptomatic; no cortical expansion; growth stops with
adulthood
4. Micro: Dense lamellar bone with fibrous tissue in small spaces
5. Treat: none required unless secondarily infected, then conservative surgical removal
Pagets disease of bone (osteitis deformans):
1. Etiology: abnormal, enhanced resorption and deposition of bone, possibly from a slow virus,
such as paramyxovirus (detected in osteoclasts); 1/100 persons over 45 years of age, but most
disease is subclinical
2. GAL: men; late middle age and older; maxilla and skull
3. Clinical: irregular radiolucent/radiopaque regions become more radiopaque over time (cotton
wool appearance); early stage is radiolucent (osteoporosis circumscripta); jaws involved in
17%; may get anemia and bleeding (no hematopoietic tissue or platelets), deafness and visual
loss (pinched nerves as they traverse foramina in skull base); Lincolns sign (black beard) with
technetium bone scan (scintigraphy) when mandible is involved; enlargement of maxilla, small
sinuses; bowed legs; elevated alkaline phosphatase (25%+ above normal); may be bone pain
4. Micro: classic appearance of Chinese character (mosaic; jig-saw) bone with immature trabecula
and abundant osteoblastic but lesser osteoclastic activity, with fibrous background stroma;
many reversal or cement lines in the bone
5. Treat: seldom causes death; parathyroid hormone antagonists (calcitonin, bisphosphonates),
aspirin for pain; may do skull base surgery to relieve nerves; new dentures or bridgework may
be required as maxilla expands. Up to 13% risk of osteosarcoma or giant cell tumor, the
former seldom in jaws, the latter often in jaws.
Langerhans cell histiocytosis (Langerhans cell disease; histiocytosis X):
1. Etiology: unknown, proliferation of Langerhans cells (dendritic mononuclear cells normally
found in epidermis, mucosa, lymph nodes, bone marrow, which process antigens to T cells)
2. GAL: none; first 2 decades of life; posterior mandible
3. Clinical: 3 basic types:
Acute disseminated histiocytosis (Letterer-Siwe disease): severe visceral involvement
and dermal involvement, with death in the first two years of life
Chronic disseminated histiocytosis (Hand-Schller-Christian disease): bone, viscera and
cutaneous involvement; bone usually shows well demarcated radiolucency with no sclerotic
rimming (punched our radiolucency); perforation rather than expansion of cortex; may have
superficial alveolar destruction mimicking periodontitis; teeth become loose and exfoliate or
appear to be floating in air radiographically; skull radiolucencies are frequent
Eosinophilic granuloma: single alveolar punched out radiolucency or periodontitis-like
alveolar destruction; asymptomatic
4. Micro: eosinophils, macrophages, lymphocytes, multinucleated giant cells
5. Treat: curettage; earlier the onset, worst the prognosis; may be fatal
Central giant cell granuloma (giant cell lesion):
1. Etiology: unknown, but not thought to be neoplastic...perhaps reparative?
2. GAL; females; before 30 years of age; mandible, especially anterior
3. Clinical: two variants: the nonaggressive and more common type, and the aggressive lesion. Well
defined radiolucency, usually with thin sclerotic rim and scalloped borders; may expand cortex
and push teeth; may be multilocular or unilocular; usually <1 cm but may be up to 10 cm

diameter. Rarely: may be painful or tender; may produce paresthesia, may perforate cortex.
4. Micro: multinucleated osteoclast-like cells in cellular stroma of spindled and oval mesenchymal
cells with nuclei similar to those of the giant cells; extravasated erythrocytes; hemosiderin
deposits (old hemorrhage); reactive new bone formation near periphery; not encapsulated but is
well demarcated
5. Treat: surgical curettage; some respond to corticosteroid injections, some to calcitonin or
interferon alfa-2a; up to 10-20% recur.
6. Special: the giant cell tumor of long bones is quite different and much more aggressive, often
with a malignant biological behavior. The brown tumor of hyperparathyroidism looks
exactly like it radiographically and microscopically (think of this if multiple or aggressive).
Cherubism (familial fibrous dysplasia):
1. Etiology: developmental anomalies; AD inheritance, defective gene on chromosome 16
2. GAL: none; first and second decades of life; posterior jaws, usually bilateral, often all four
quadrants
3. Clinical: Greatly expansile radiolucencies, usually multilocular, begin prior to 5 years of age,
enlarging until puberty, after which they usually stabilize and slowly regress. Face appears
greatly enlarged, with eyes toward heaven because of pressure on infraorbital bone. Painless;
tooth buds often pushed out of position; wide alveolus (speech problem?). Rarely: ribs and
humerus involved. May have multiple multinucleated giant cell granulomas.
4. Micro: like giant cell granuloma, although often more loose tissue; eosinophilic cuffing around
small vessels; old lesions: densely fibrous, fewer giant cells
5. Treat: none, unless pathologic fracture; usually facial features are normal by 25-40 years of age;
surgical curettage can be performed; irradiation works, but risk of future sarcomas, so not done
Simple bone cyst (traumatic bone cyst; solitary bone cyst; idiopathic bone cavity):
1. Etiology: unknown, probably chronic ischemic bone disease
2. GAL: males; 10-25 years of age; posterior mandible
3. Clinical: poorly-demarcated to well-demarcated radiolucency, often with scalloped borders and
often scalloped between tooth roots (teeth remain viable); 20% with expanded cortex; rarely:
tender or painful; intramedullary void or cavitation
4. Micro: very little tissue available, usually with normal bone (maybe immature), fibrous tissue
and a few lymphocytes
5. Treat: create cortical window, then curette walls of cavitation to stimulate fresh hemorrhage.
Usually defect fills in with new bone in less than 6 months.
Aneurysmal bone cyst:
1. Etiology: unknown, but perhaps reactive response to trauma; some think it is an atypical central
giant cell granuloma or similar to that lesion
2. GAL: none, teenagers and young adults; posterior mandible, shafts of long bones
3. Clinical: Multilocular, well-demarcated radiolucency, often with thin sclerotic rim; usually thins
and expands cortex; often painful; may be compressible; may have paraesthesia; rarely:
crepitus
4. Micro: thin fibrous trabecula with scattered multinucleated giant cells separate large blood-filled
cavities; endothelial cells are not seen lining the cavities; erythrocyte extravasation may be
seen in stroma; large areas of fibrous tissue may be seen; 20% are associated with another
lesion, usually giant cell granuloma or benign fibro-osseous lesion.

5. Treat: curettage or enucleation, usually heals in 6-12 months; at least 8% recur

Fibrous dysplasia of bone:
1. Etiology: developmental anomaly from postzygotic mutation of GNAS 1 (guanine nucleotidebinding protein, alpha-stimulating activity polypeptide 1) gene
2. GAL: none; 7-20 years; posterior maxilla
3. Clinical: two basic types:
Monostotic fibrous dysplasia: 85% of cases; jaws are among most common sites;
painless bony enlargement of diffuse alveolar or other maxillofacial area; growth is slow;
teeth become separated but remain viable; ground-glass radiopacity, or irregular opacities,
or mixed radiolucent-radiopaque regions; poorly demarcated from surrounding normal
one; cortical expansion and thinning; lamina dura may be hard to see; PDL may be thin
Craniofacial fibrous dysplasia: adjacent maxillary bones are involved (only)
Polyostotic fibrous dysplasia (Jaffe-Lichtenstein syndrome; McCune-Albright
syndrome): relatively uncommon; may involve most of skeleton; caf au lait spots;
sexual precocity, hyperthyroidism, pituitary adenoma; hockey stick deformity of hip;
if only caf au lait spots = Jaffe-Lichtenstein syndrome.
4. Micro: irregular immature bony trabecula in a fibrous background stroma, with no osteoblasts
and no osteoclasts; no capsule; jaw lesions become more ossified with time
5. Treat: surgical recontouring; usually burns out with adulthood; may require multiple
recontouring procedures during teen years.
6. Similar lesion: segmental odontomaxillary dysplasia: single maxillary quadrant shows
radiopaque pattern of vertical stripes
Cemento-osseous dysplasia:
1. Etiology: developmental anomaly; may be familial
2. GAL: Female; young adults and early middle-aged; mandible; some lesions have racial
predilection
3. Clinical: three basic groups:
Focal cemento-osseous dysplasia: single site involved; 90% females; mean age 38 years;
more frequent in whites than blacks; posterior mandible; asymptomatic mixed
radiolucent/opaque areas less than 1.5 cm., becoming more sclerotic over time;
moderately well demarcated; nonexpansile
Periapical cemento-osseous dysplasia (periapical cemental dysplasia): anterior mandible,
at apex of viable teeth; 14:1 female;male ratio; 70% in blacks; 30-50 years old;
asymptomatic; nonexpansile; lesions are similar to focal variant in appearance and
behavior
Florid cemento-osseous dysplasia: multiple quadrants involved, usually mandible, usually
periapical locations; lesions are larger than focal or periapical variants, and can expand
cortex and produce tenderness or pain; may become exposed to surface (calcified material is
rather avascular)
4. Micro: globular masses of dark calcified material (osseous or cementoid or both) with minimal
cellularity, in a background stroma of immature fibrous tissue; encapsulated; may have one or
more traumatic bone cysts
5. Treat: none required unless symptomatic, then conservative surgical curettage; try to prevent
dental infections, since lesion is rather avascular

Familial gigantiform cementomas:

1. Etiology: unknown, but appears to be an adult onset developmental anomaly; AD inheritance
2. GAL: none; first and second decades; posterior mandible; racial predilection for whites
3. Clinical: Multiple, well demarcated, expansile, mixed radiolucent/radiopaque intraosseous
lesions can become very large; may affect all four quadrants; impaction of teeth; facial
deformity
4. Micro: same as for cemento-osseous dysplasia
5. Treat: continues to enlarge until fifth decade; once lesions are predominantly radiopaque surgical
resection and recontouring can be done, may have to be repeated
Central ossifying fibroma (central cementifying/ossifying fibroma):
1. Etiology: benign neoplasm
2. GAL: none; young adults and early middle-age; mandibular molar and premolar region
3. Clinical: well demarcated unilocular radiolucency, sometimes with thin sclerotic rim; can be
expansile and can become very large; asymptomatic; older lesions show irregular radiopacities
in the radiolucency; can push roots aside
4. Micro: islands and irregular trabecula of immature bone in a background of immature fibrous
tissue; often areas with dark cementoid calcified globules
5. Treat: Conservative surgical removal or curettage
6. Special variant: juvenile ossifying fibroma (juvenile aggressive ossifying fibroma): more rapid
growth, larger growth capacity, high recurrence rate, younger patient (first 2 decades of life);
two microscopic types: trabecular and psammomatoid
Osteoma:
1. Etiology: benign neoplasm; rare
2. GAL: none; teens and young adults; mandible, only found in H&N bones
3. Clinical: asymptomatic bony mass of cortex with normal overlying mucosa; radiopaque, maybe
lobulated; may project into sinus; may be completely intramedullary
4. Micro: dense lamellar bone (compact osteoma) with small fibrous tissue-filled spaces,
occasional marrow; some masses have normal marrow space (cancellous osteoma)
5. Treat: conservative surgical removal, otherwise will slowly continue to enlarge
Gardner syndrome:
1. Etiology: AD inheritance (mutation on chromosome 5); prevalence rate: 1/8,000 births
2. GAL: none, second and third decades; mandible
3. Clinical: multiple osteomas (usually compact type) of maxillofacial bones; adenomatous
intestinal polyposis, with at least 50% risk of adenocarcinoma transformation; sometimes
odontomas; supernumerary teeth; impacted teeth; epidermoid cysts of skin; desmoid tumors
of skin; rarely: thyroid carcinoma; pigmented lesions of ocular fundus
4. Micro: osteomas are as above, intestinal polyps are adenomatous in nature
5. Treat: osteomas can be conservatively removed via surgery; polyps are monitored carefully by
internist and removed when too large or too numerous (prophylactic colectomy is frequent);
skin cysts and fibrous tumors can be conservatively removed as needed
Osteoblastoma:
1. Etiology: benign neoplasm of osteoblasts
2. GAL: slight male; 10-30 years of age; posterior mandible

3. Clinical: 2-4 cm well demarcated radiolucency with sclerotic rimming of periphery; often patchy
irregular radiopacities; may expand cortex; painless
4. Micro: irregular trabecula of immature bone with abundant osteoblastic rimming and with
numerous osteoblasts seen in background fibrous stroma
5. Treat: conservative surgical excision or curettage; small recurrence rate
6. Special variant: aggressive osteoblastoma: has atypical cells and is very cellular, occurs in older
persons, often painful, may become very large
7. Similar lesion: osteoid osteoma: identical histology but center has plexus of nerves and there is
usually a thick sclerotic rimming around lesion; very painful but pain disappears with aspirin or
other prostaglandin inhibitors
Chondroma:
1. Etiology: benign neoplasm of hyaline cartilage and chondrocytes
2. GAL: none; third and fourth decades; anterior maxilla, condyle, usually hands and feet
3. Clinical: asymptomatic cortical expansion, slow enlargement; well demarcated radiolucency with
scattered globular radiopacities.
4. Micro: mature hyaline cartilage, encapsulated, small chondrocytes in well-formed lacunae
5. Treat: conservative surgical excision or curettage; low recurrence outside facial bones, but in
facial bones recurrence should be suspected as being a low-grade chondrosarcoma (which can
look microscopically very similar)
6. Special disease: multiple chondromas are seen in Ollier disease and Maffucci syndrome (also
has soft tissue angiomas)
Osteosarcoma:
1. Etiology: malignant neoplasm of osteoblasts; the most common primary malignancy of bone; 7%
of osteosarcomas occur in jaws
2. GAL: none; 20-40 year olds (jaw patients are more than a decade older than the average patient
with extragnathic osteosarcoma; none
3. Clinical: Painful, bony-hard or firm mass, sometimes with surface ulceration, sometimes
lobulated; may be associated with paresthesia. Often very radiodense, but may be mixed
radiolucent-radiopaque lesion and may be completely radiolucent. Borders are poorly defined
or moth-eaten, and cortex becomes perforated, often with overlying sunburst radiopaque
pattern. Teeth are destroyed and periodontal ligament may be quite widened.
4. Micro: Background fibrous stroma with many enlarged and plump osteoblastic cells, often with
bizarre shapes and often with pleomorphic nuclei. Immature bone and osteoid are being created
from the stroma, often de novo. Osteosarcomas of the jaws tend to appear more mature or
better differentiated than extragnathic lesions; cartilage may be formed. Tumors are
microscopically classified into 3 types: osteoblastic osteosarcoma, fibroblastic osteosarcoma
and chondroblastic osteosarcoma. Very well differentiated lesions may closely resemble a
benign fibro-osseous lesion, such as ossifying fibroma.
5. Treat: Radical surgical excision. Lesion tends to metastasize late, via blood stream; main problem
is local recurrence and destruction. Chemotherapy and radiotherapy are often used as
adjunctive therapies. Jaw osteosarcomas have a much better prognosis than extragnathic
osteosarcomas, but remains a bout 50% survival at 5 years.
6. Special types:
Small cell osteosarcoma: resembles Ewing sarcoma microscopically, but osteoid is
produced; occurs in young persons; very poor prognosis.

Peripheral (juxtacortical) osteosarcoma: develop outside bone, grow outward, have

better prognosis than intramedullary lesions; two types: parosteal osteosarcoma
(usually very well differentiated, may be mistaken for a benign fibro-osseous lesion,
such as ossifying fibroma) and periosteal osteosarcoma (usually with abundant
cartilage in tumor)
Post-irradiation osteosarcoma: develops years after radiotherapy for another
malignancy; fibrosarcoma and chondrosarcoma (dedifferentiated chondrosarcoma),
and giant cell tumor many also occur in this setting

Chondrosarcoma:
1. Etiology: malignant neoplasm of chondroblasts/chondrocytes; less than 1% of all
chondrosarcomas are in jaws
2. GAL: none; none, but average age is 33 years; none
3. Clinical: Asymptomatic (although more than 1/3 are tender or painful), slowly enlarging bonyhard mass which may be lobulated and has normal overlying mucosal coloration. Maxillary
lesions may cause epistaxis and nasal obstruction. Mixed radiolucent/radiopaque appearance,
poorly circumscribed, but may show sclerotic rimming. Cortical expansion and/or perforation
occurs in large lesions, sometimes with sunburst radiopaque pattern. Root resorption or
widening of periodontal ligament may be seen.
4. Micro: Background of hyaline cartilage (sometimes fibrocartilage) with enlarged,
hyperchromatic chondrocytes with lacunae, often with multiple cells in the same lacuna.
Lobules of tumor cartilage (blue balls) are separated by fibrous trabecula, often with
concentration of lesional cells are the periphery of the lobules. Osteoid may be seen. Tumors
are graded, with Grade I showing an appearance very similar to chondroma, and grade III
showing many lesional cells, often bizarre in shape. Almost all jaw chondrosarcomas are grade
I or II
5: Treat: Radical surgical excision; prognosis is correlated with histologic grade. Prognosis is worse
than for osteosarcoma, which is contrary to the pattern in extragnathic tumors, where
osteosarcoma carries a much worse prognosis than chonrdosarcoma.
6. Special types:
Clear cell chondrosarcoma: low-grade variant, with numerous lesional cells showing
abundant clear cytoplasm
Dedifferentiated chondrosarcoma: combination of well differentiated chondrosarcoma
and poorly differentiated fibrosarcoma, possibly arising from an irradiated
chondrosarcoma; prognosis is poor
Mesenchymal chondrosaroma: very cellular (moderate-sized, dark spindled and round
cells) with only focal cartilage production; 10-30 year olds; well-demarcated margins
with focal moth-eaten destruction; rapidly growing and painful; only 30% 5-year survival

Ewing sarcoma:
1. Etiology: malignant neoplasm, probably of primitive neuroectodermal cells; 10% of all primary
bone tumors; 3% of all Ewing sarcomas occur in jaws
2. GAL: males; first and second decades of life; posterior mandible (usually in the hip); racial
predilection for whites
3. Clinical: Irregular radiolucency with moth-eaten margins and minimal osteosclerotic reaction.

May show parallel sclerotic lines along cortex (onion-skinning); may show cortical perforation.
Painful lobulated mass, perhaps with leukocytosis and fever, can lead to a mistaken diagnosis
of osteomyelitis
4. Micro: Sheets and lobules of small, dark cells with large nuclei and ill-defined borders show
dense collagen trabecula between them, and often show focal hemorrhage and necrosis. 75%
show glycogen granules, which can be stained with PAS. Diagnosis is extremely difficult, as
tumor cells may look like those in: metastatic neuroblastoma, malignant lymphoma, small
cell osteosarcoma, embryonal rhabdomyosarcoma, the primitive neuroectodermal tumor,
and metastatic small cell carcinoma
5. Treat: Radical surgical excision and chemotherapy; with chemo the 5-year survival has increased
from 5% to almost 80%
6. Special type: Large cell Ewing sarcoma: lesional cells are much large and more open than
normal Ewing sarcoma; no difference in prognosis
Metastasis to the jawbones:
1. Etiology: malignant neoplasm from extragnathic site, usually breast, prostate, colon, lung;
represents more than 3% of all oral cancers; spread via blood stream. Metastatic cancers are, by
far, the most common bone tumors in humans (not primary bone tumors); usual bones affected
= vertebrae, ribs, pelvis, skull
2. GAL: none, late middle age, posterior mandible (apical region) and tongue
3. Clinical: Poorly demarcated, moth-eaten, painful radiolucency, usually near apex of a tooth; may
show widened periodontal ligament, often perforates cortex but seldom resorbs or moves teeth.
Breast and prostate cancers often stimulate a strong radiodense reaction in the bone.
Technetium scintigraphic bone scan will show hot spot. Tumor often mimics toothache, with
delayed cancer therapy while endodontic treatment and extraction are done; tumor then is seen
to bubble out of extraction socket.
4. Micro: The histology corresponds to that of the original tumor
5. Treat: Radical surgical excision, look for primary tumor and treat accordingly. Jaw lesion may
not be treated if it represents just one of many metastases, however, half of jaw metastases
represent the first sign of malignancy in the patient.