Bone Lesions Oral Pathology

BONE LESIONS
S A N A R A S H E E D
A K H TA R S A E E D M E D I C A L A N D D E N TA L C O L L E G E

GENERAL HEADINGS
• (1) benign fibro-osseous lesions
• (2) metabolic conditions
• (3) benign tumors
• (4) malignant tumors

BENIGN FIBRO-OSSEOUS
LESIONS
• Lesions that develop within the jaws by replacing normal trabecular bone and marrow
with cellular fibrous tissue and randomly oriented mineralized structures.
• cemento-osseous dysplasias: in the maxilla and mandible. they all contain a
• Combination of spherical calcifications believed to be of cemental origin (cementicles)
and
• Randomly oriented osseous structures resembling detached fragments of trabecular
bone.

PERIAPICAL CEMENTAL DYSPLASIA
• Other names:
• “multiple cementoma”
• “periapical fibrous dysplasia”
• “periapical osteofibrosis”
• “localized fibro-osteoma”

• PCD is not a true neoplasm but a dysplastic condition in which multiple focal areas of
normal bone and marrow are replaced by
• Cellular connective tissue lesions with limited growth potential.
• The lesions attain a fixed size and later undergo a
• maturation process that culminates in the formation of
• multiple dense calcified (sclerotic) intraosseous nodules

• CLINICAL FEATURES
• No symptoms or visible external alterations of the involved bone occur.
• Gender: Middle aged women, African American
• Age: More than 20 years
• Location: located below the apices of the mandibular incisors,
• Or, other areas of the arch or the opposing arch
• The teeth overlying the lesions remain vital.
• Buccal or lingual expansion of the cortices is usually absent.

• RADIOGRAPHIC FEATURES
• PCD has three radiographic features that indicate stages from early formation to
maturation:
• (1) osteolytic
• (2) cemetoblastic
• (3) mature

• Osteolytic Stage
• Well-defined radiolucencies at the
apex of one or more teeth.
• The radiolucencies surround the tip of
the root and are usually
indistinguishable from an
inflammatory periapical lesion of
pulpal origin.
• Vital teeth, free from caries or
restorations.

• Cementoblastic Stage
• The cementoblastic stage displays
similarly sized lesions
• and a demarcated border with
radiolucencies containing
• nodular radiopaque deposits

• Mature Stage
• well-defined,
• dense radiopacities that usually exhibit some
• nodularity.
• The periodontal membrane can be seen
separating the lesion from the tooth.
• Each radiopaque nodule has a thin radiolucent
zone around its periphery that separates it
the surrounding bone and nearby teeth.

• HISTOPATHOLOGY
• The osteolytic stage consists primarily of cellular connective tissue replacing the
normal trabecular bone with calcified structures of insufficient size to be observed
radiographically.

• The cementoblastic stage
• has the same connective tissue
component, but displays
• a mixture of spherical calcifications and
irregularly shaped deposits of osteoid
and mineralized bone.
• These calcified and mineralized
structures are surrounded by
osteoblasts containing osteocytes.

• Tissue from the matured stage is
composed almost entirely of
coalesced spherical calcifications
and
• sclerotic mineralized bone with
little connective tissue
• TREATMENT
• After a diagnosis of PCD is made,
no further treatment is necessary.

FLORID CEMENTO-OSSEOUS DYSPLASIA

FLORID CEMENTO-OSSEOUS
DYSPLASIA
• Florid cemento-osseous dysplasia (FCOD) is a more extensive form of PCD.
• It may be confined to one quadrant or involve all four quadrants.
• It has been added to the classification of oral disease, replacing the previous diagnosis
of diffuse sclerosing osteomyelitis when no evidence of infection or other bone
inflammation is present.

• Age: middle-aged
• Gender: African-American women
• External signs or symptoms are generally absent with lesions found on routine
radiographic evaluation.
• Patients will experience pain or discomfort if involved areas become secondarily
infected as a result of periapical infection or after an extraction.
• The areas of dense bone have reduced vascularity and are less able to cope with the
usual transient infection.

DYSPLASIA
• On occasion, after patients become
• edentulous, some of the dense sclerotic bone nodules break through the surface,
because they do not resorb at the same rate as normally vascularized alveolar bone.
• These sequestra cause much discomfort and act
• as a portal of entry for bacteria that can cause an acute
• osteomyelitis.

• Multiple radiolucent and radiopaque
lesions
• “Cotton ball” appearance of lesions.
• Some large, purely radiolucent areas may be
interspersed among the radiopacities.
• Lesions occupy the complete thickness of the
bone and are found from the alveolar crest to
inferior border.
• A solitary lesion is occasionally present,
• usually in a molar area. Such a lesion has
• been designated as focal cemento-osseous
dysplasia

DYSPLASIA
• HISTOPATHOLOGY
• Cellular connective tissue
• Containing many small and large
spherical calcifications
• And, large nodules of dense bone
• A zone of connective tissue usually
separates
• the lesions from the surrounding bone.
Occasionally,
• areas of traumatic (hemorrhagic) bone
cyst can be observed in the connective
tissue of the lesions

• TREATMENT
• FCOD lesions are not treated unless the dense bone
• nodules become secondarily infected and produce osteomyelitis
• in the area.
• Treatment of the complicating
• osteomyelitis consists of débridement, drainage, and
• antibiotics.

FIBROUS DYSPLASIA
• It may involve only a single bone (monostotic) or multiple bones (polyostotic).
• Fibrous dysplasia is not considered a true neoplasm, because it is self-limiting.
• It begins as a fibrous replacement of the medullary bone, which in turn is gradually
replaced by a metaplastic woven bone that eventually matures into dense lamellar
bone.

FIBROUS DYSPLASIA
• Juvenile Fibrous Dysplasia
• Juvenile fibrous dysplasia is the most common type of monostotic regional deformity
in the head and neck.
• Slow-growing regional distortion that usually enlarges proportionately with the
affected bone.
• The regional overgrowth continues until general body growth ceases in the late teens
or early twenties.
• aggressive juvenile fibrous dysplasia grows at a faster rate than the affected bone,
producing major, often grotesque deformity that results in loss of function.

CLINICAL FEATURES
• Age: early to late childhood
• Site: The maxilla is affected more often than the mandible.
• pain or discomfort is absent.
• Teeth are often displaced, rotated, or malaligned.
• The aggressive form of juvenile fibrous dysplasia becomes symptomatic if the lesion is
traumatized and ulcerated because of impingement by the teeth during mastication.
• In the maxilla the aggressive form often extends to the floor of the orbit and the nasal
passages, interfering with both sight and breathing. Treatment to alleviate gross
distortion and to restore function is often required in these lesions.

JUVENILE FIBROUS DYSPLASIA
• In early lesions the area may be radiolucent, becoming more radiopaque as more bone is
formed.
• A mature lesion retains none of the normal architecture of trabecular bone, having
replaced it with abnormal bone that produces a “ground glass” or “orange peel” pattern
radiographs.
• No line of demarcation exists, because the lesion blends with the surrounding bone.
• Expansion of the cortical plates and displacement of tooth roots is common.
• The lamina dura is usually obscured and the cortical plates thinned.

JUVENILE FIBROUS DYSPLASIA
• HISTOPATHOLOGY
• Initially it is composed of cellular connective tissue that has replaced the normal
trabeculae and marrow. Gradually, irregular islands of osteoid and bone emerge from
the fibrous tissue background.
• The new bone has a woven pattern when viewed with polarized light.
• In the jaws, some spherical calcifications may be included with the abnormal bone
formation.
• lamellar pattern is seen eventually.
• By adulthood the lesion usually matures, and bone may be somewhat normal.

FIBROUS DYSPLASIA
• Adult Monostotic Fibrous
Dysplasia
• The affected area presents as an
asymptomatic diffuse expansion of
the cortices.
• Some movement of teeth within the
area may occur.

• Mixed radiolucent and radiopaque “cotton ball” pattern.
• Expansion and thinning of the cortical plates.
• HISTOPATHOLOGY
• Some areas in which cellular fibrous connective tissue predominates and other areas
dominated by immature metaplastic bone with a woven pattern.
• Of diagnostic importance is the blending of lesional tissue with surrounding normal
bone and the cortical plates—a feature that separates it from ossifying fibroma.

POLYOSTOTIC FIBROUS DYSPLASIA
• Polyostotic fibrous dysplasia is usually accompanied by skin pigmentation and
endocrine dysfunction.
• Bone lesions may be confined to the craniofacial area or distributed diffusely
throughout the skeleton.
• The presence of expansile lesions in multiple bones.
• Many patients will also have large light-brown pigmentations termed café au lait spots
on the torso, particularly the back, buttocks, and sacral areas.
• The pigmented areas have a jagged periphery, in contrast to pigmented skin areas
found in multiple neurofibromatosis, where the periphery is smooth.
• The bones most commonly involved are the ribs, cranium, maxilla, femur, tibia, and
humerus.

• When endocrine dysfunction is present (McCune-Albright syndrome), manifestations
often begin in early childhood.
• Without endocrine dysfunction, (Jaffe syndrome)
• The most notable and concerning is precocious sexual development in young women,
consisting of premature vaginal bleeding, breast development, and emergence of
axillary and pubic hair.
• Other endocrine dysfunctions include
• thyrotoxicosis, pituitary gigantism, and Cushing syndrome.
• HISTOPATHOLOGY
• The microscopic appearance of bone lesions of polyostotic
• fibrous dysplasia is identical to that of monostotic
• disease.

CHERUBISM
• Hereditary.
• Autosomal dominant trait.
• It has been mapped to the 4p16.3 gene locus,
• Found only in the jaws, it mainly involves the mandible in a bilateral symmetrical
manner. The maxilla is less commonly involved.
• a “chubby” appearance and often
• produce some elevation of the floor of the orbits, causing
• the pupils to be elevated upward.
• “Angel like face”

CHERUBISM
• Lesions begin in early childhood as slow-growing expansions of the posterior
of the mandible or maxilla.
• Expansion is asymptomatic and not limited to the buccal and lingual cortical plates.
The ramus may be expanded anteriorly and the other arches superiorly and inferiorly.
• In addition to obvious facial deformity, there is
• interference in mastication
• speech development,
• random alignment of teeth,
• and resultant severe malocclusion

• Lesions continue to enlarge until the patient reaches puberty, at which time the lesions
stabilize. In some patients, rib lesions have been found. Eventually the involved bones may
undergo some reduction in size. At this time surgical recontouring can make the
disfigurement less noticeable.
• Large areas of radiolucency in the bones that exhibit massive expansion.
• Both erupted and unerupted teeth are randomly distributed within the enlarged arches.
• Faint radiopacities resembling residual or new bone are sometimes present.
• As the lesion matures the radiographic appearance gradually changes, with more
radiopaque structures becoming evident.
• After stabilization the involved areas exhibit a “ground glass” radiographic appearance
similar to that found in stabilized fibrous dysplasia.

• HISTOPATHOLOGY
• In the early stages, lesions are composed almost entirely of giant cell tissue in which
numerous multinucleated giant cells are present in a background of mononuclear
• As individual lesions mature, the giant cell component is gradually replaced by
cellular fibrous tissue in which randomly oriented spicules of metaplastic woven bone
develop that resemble those found in fibrous dysplasia.
• After lesions become stabilized, the bone dominates the lesion, becoming lamellar
and reoriented for structure and function.

• Skeletal bones provide structure and strength to the anatomy and determine overall
body size. Of equal importance are their roles as reservoirs for essential metabolic
minerals and as envelopes to house the tissues for blood and immune cell production.
To carry out these roles, bone cells and their precursors react to the influences of
circulating hormones and other body-regulating molecules. Thus bones are particularly
sensitive to physiologic and genetic derangement that can result in alterations to their
structure and mineral content
• Four metabolic bone diseases that are capable of producing changes in the jaws and
other craniofacial bones are discussed in this chapter:
• (1) Paget disease,
• (2) hyperparathyroidism,
• (3) osteopetrosis, and
• (4) osteogenesis imperfecta

PAGET’S DISEASE
• Paget disease (osteitis deformans) is an alteration in the histology and morphology of
bone. It can be confined to one bone or be distributed in multiple regions throughout the
body. It consists of a simultaneous increase in the resorption and apposition mechanisms of
bone.
• Initially the process is dominated by bone resorption, primarily mediated by hyperactivity
of osteoclasts. Excessive bone formation follows, with a net increase in volume but a
decrease in bone strength.
• Both osteoclastic resorption and osteoblastic apposition can be often found to occur
simultaneously on the same side of a section of bone.
• This uncoordinated function of osteoclastic and osteoblastic activity results in numerous
tortuous “cement" or “reversal” lines that give the bone a characteristic mosaic pattern
when viewed microscopically.

PAGET’S DISEASE PATHOGENESIS
• A genetic predisposition for Paget disease of bone with locus identified on chromosome
18q-21-22 (PDB2).
• One of the main mechanisms of osteoclast formation and activation involves the OPG,
RANK, and RANKL pathways, where binding of RANKL to RANK results in the differentiation
of osteoclast precursors. Malfunction of this pathway results in either too much or too little
total bone formation.
• Interleukin-6 (IL-6) has been found to play a part in patients with Paget disease by
increasing the hyperresponsivity of the osteoclast and its precursor cells. Changes in the
osteoclast, in turn, produce secondary effects on the other bone cells and the vascularity of
the region.
• The virus inclusion bodies within some of the multiple nuclei of pagetic osteoclasts appear
to be paramyxoviral transcripts and antibodies against two of the paramyxoviruses—the
measles and canine distemper virus have been found.

PAGET’S DISEASE
• Age: 60 years
• The disease may be confined to one bone (monostotic) or simultaneous in multiple
bones (polyostotic). When multiple bones are involved, most patients develop some
degree of incapacity, altered physical appearance, pain, and joint disease.
• In the skull, there is a net increase in head size and shape and in the thickness of the
cranial bones, presenting symptom is a gradual increase in hat size caused by
increased cranial circumference.
• In the involvement of the base of the skull, encroachment on the various foramina
can result in compression of the spinal cord and cranial nerves and lead to paralysis
and loss of hearing and sight.

PAGET’S DISEASE
• In the jaws the maxilla is more
commonly involved than the
mandible. The arch may exhibit
complete or partial involvement,
giving it either a diffuse
enlargement or tumorous
appearance.
• Because symptoms are absent,
first sign of involvement may be
the gradual appearance of
or generalized spaces between
teeth.
• In the edentulous patient a
denture may become tight and

PAGET’S DISEASE
• Serum level of alkaline phosphatase increases : Normal alkaline phosphatase levels
are approximately 63 IU/L, but in Paget disease they may approach 1000 to 5000 IU/L
in patients with a polyostotic distribution and 200 to 500 IU/L when a monostotic
lesion is present.
• Elevated levels of urinary hydroxyproline are indicative of increased resorptive activity
activity of osteoclasts.
• Serum calcium usually remains within normal levels.

PAGET’S DISEASE
• When bones are seriously affected, they often become painful and subject to fracture.
• Complications
• High-output heart failure can occur as a result of increased peripheral bone vascularity.
• Sarcoma
• Fibrosarcoma
• Benign and malignant giant cell tumors.

PAGET’S DISEASE
• In early osteolytic stage, radiolucency is
seen.
• Then bone density increases.
• The most common radiographic
appearance is a combination of
radiolucent and radiopaque lesions
resembling cotton balls in a diffusely
defined radiolucent area.
• This bone is enlarged and has less dense
outer cortices.

PAGET’S DISEASE
• The maxilla and mandible are
often greatly enlarged and
exhibit loss of the lamina dura.
• Often teeth in the area exhibit
hypercementosis of their roots

• Scintigraphy
• The scanning agents are
isotopes that are taken up by
cells that are actively
metabolizing or undergoing
rapid mitotic activity. In some
cases “hot spots” are found,
they often indicate early lesions
of Paget disease that have not
produced enough osteolysis to
be radiographically apparent.

PAGET’S DISEASE
• HISTOPATHOLOGY
• an increase in osteoclasts, osteoblasts, and blood vessels
• a replacement of the normal dense lamellar bone with a less dense bone having a
mosaic pattern.

PAGET’S DISEASE
• Osteolytic phase During the osteolytic phase,
osteoclasts are numerous and large, containing
50 to 100 nuclei. They are present throughout
bone in deep indentations of resorption, with
relatively few osteoblasts laying down new
bone within the region.
• The mixed phase consists of zones in which each
end of the spectrum is present simultaneously.
The mosaic pattern is a prominent feature of the
residual matured lamellar bone that is found in
the mixed and osteosclerotic phases of the
disease.
• When the disease is in the osteosclerotic phase,
osteoblasts predominate and the woven bone
matures to dense lamellar bone, with little
resorption taking place.

HYPERPARATHYROIDISM
• Hyperparathyroidism may be primarily caused by
excessive secretion of parathyroid hormone (PTH) or
secondarily by kidney disease. In both, resultant
hypercalcemia and hypophosphatemia can give rise to
associated disturbances in ion metabolism, depletion
of bone minerals, kidney stones, gastrointestinal
disorders, and muscle weakness.
• Causes of Primary hyperparathyroidism:
• Adenomas
• Hyperplasia
• Carcinomas

HYPERPARATHYROIDISM
• In some patients the gland may be reacting secondarily to other alterations in the body,
with the increased secretion part of a compensatory mechanism.
• This form of the disease is termed secondary hyperparathyroidism.
• The most common alteration is renal disease in which chronic loss of circulating phosphate
ion is the result of damage to the kidneys’ distal tubules. The depleted serum phosphate
ion causes a constant demand for calcium to maintain the electrolyte balance.
• Increased amounts of PTH are required to liberate calcium from the bone reservoir through
osteolysis.

HYPERPARATHYROIDISM
• Age: 60 years and over
• Gender: hyperparathyroidism is found in 1:500 women and 1:1000 men.
• Hypercalcemia is the most common manifestation of hyperparathyroidism and is
diagnosed when serum calcium is above the normal range of 8.6 to 10.4 mg/100 ml.
• Lowered serum phosphate level.
• Levels of urinary phosphate may be elevated

HYPERPARATHYROIDISM
• Bone changes consist of either a subtle
generalized reduced bone density
(osteoporosis) or mottled areas of
radiolucency with thinning of the cortical
plates and the medullary bone (osteitis
fibrosa cystica). In the mandible and
maxilla, the normal trabecular pattern may
be lost, and some lack of distinctness of
lamina dura occurs in the late stages of
chronic or severe disease
• Occasionally a large destructive
radiolucency may be present, indicative of
giant cell tumor of hyperthyroidism
(“brown tumor”).

HYPERPARATHYROIDISM
• HISTOPATHOLOGY
• Increased osteoclastic activity,
• Thinning of the trabecular bone,
• Wide zones of osteoid rimmed with activated osteoblasts.
• Some replacement of marrow with loose cellular connective tissue may occur.

OSTEOPETROSIS
• Pathogenesis
• Osteopetrosis is a generalized hereditary condition in which the bones become
substantially denser than normal.
• Other hormonal, metabolic, dietary, or hereditary disorders can also produce
osteopetrosis.
• The most common forms are hereditary, consisting of a
• 1. benign type of osteopetrosis that is autosomal dominant with a gene locus at 1p21
and
• 2. a malignant autosomal recessive osteopetrosis with gene locations at 16p13 and

OSTEOPETROSIS
• Pathogenesis
• It appears that the pathogenesis of osteopetrosis is due to a reduction in osteoclastic
activity.
• Malfunction of the OPG, RANK, and RANKL pathway results in a reduction in
osteoclastic differentiation, allowing osteoblastic function and bone formation to
proceed unabated.

OSTEOPETROSIS
• The most serious clinical features of osteopetrosis are
• 1. Lack of resorption of calcified cartilage during endochondral growth,
• 2. Reduced marrow space for red and white blood cell development, and
• 3. Overly deposited and mineralized bones.

OSTEOPETROSIS
• The defects result in patients of
• Short stature who are highly susceptible to infection and hemorrhage
• and
• who are reluctant to participate in vigorous activities because of the high frequency of
bone fracture

OSTEOPETROSIS
• Patients with the more severe form of osteopetrosis have symptoms that begin in
infancy with
• breathing and hearing difficulties because of oversized facial and mastoid bones.
• These are followed by functional defects in the ocular and trigeminal nerves as they
become compressed by sclerosis of the foramina of the base of the skull.

OSTEOPETROSIS
• Eventually the patients develop an enlarged cranium with prominent frontal bossing. The
commonly occurring delay in dental development and eruption of teeth can sometimes be
restored in a child with congenital osteopetrosis with the use of a bone marrow
transplantation that induces normal osteoclast function.
• The long bones are shortened and extremely fragile, and they exhibit replacement of
marrow with dense bone. This results in depletion of platelets, leukocytes, and erythrocytes,
which produces a tendency for spontaneous hematomas, multiple infections, and anemia.
• Complications
• Patients with severe osteopetrosis usually die from complications of marrow depletion
before they reach 10 years of age. In the more benign forms, reduced stature occurs less
commonly and nerve deficits are less severe. Teeth erupt but have a tendency for ankylosis.
Routine extraction and periapical infection from advanced caries often result in a persistent
osteomyelitis caused by dense avascular bone and limited connective tissue unable to
initiate an adequate healing response.

OSTEOPETROSIS
Radiographs exhibit a generalized increase in bone density
with obliteration of normal internal architecture.
It is particularly severe in the enchondral areas of long
bone.
The cartilaginous portion of the ribs also exhibits
an uncharacteristic increase in opacity (Figure 4-20, A).
The cranial plates are thickened, and the base is affected
to a greater degree than the other bones (Figure 4-20, B).
Sinus cavities are greatly reduced in size.
Fracture of the long bones is common.
Embedded or unerupted teeth are common in the severe forms of the
disease

OSTEOPETROSIS
• HISTOPATHOLOGY
The bone is dense and sclerotic, with most of the marrow
spaces replaced with bone or fibrous tissue.
In some forms a normal number of osteoclasts are
present but do not display a ruffled border and clear zone
that are present in normal functioning cells during
resorption.
In other forms of the disease the number of
osteoclasts is greatly reduced.
The bone is somewhat avascular; in some cases, islands
of calcified cartilage are found that should normally be
resorbed during development.

OSTEOGENESIS IMPERFECTA
• Osteogenesis imperfecta (OI) is a genetically determined disorder of connective tissue
characterized by bone fragility.
150 mutations of the COL1A1 gene on chromosome 17 and COL1A2
gene on chromosome 7.
The disorder is manifested in tissues in which the principal matrix protein is type I
collagen. These are mainly bone, ligaments, sclera, and dentin.
In contrast to osteopetrosis, OI is characterized by defective matrix formation and a
lack of mineralization rather than hypermineralization. The net result is similar to
osteopetrosis in that the patient has bone fragility, multiple fractures, and hearing
defects.
Of importance is the close association of OI with dentinogenesis imperfecta.

• Classification of OI types according to onset and lethality:
• (1) neonatal lethal;
• (2) severe nonlethal;
• (3) moderate and deforming;
• (4) mild nondeforming.
• Many patients share clinical features with other hereditary connective tissue diseases,
• such as Ehlers-Danlos syndrome and Marfan syndrome.

• The neonatal lethal form of OI occurs in 10% of cases, with patients suffering multiple
fractures during gestation and delivery. Most die within weeks if they survive birth.
• The severe nonlethal form occurs in 20% of patients; they also have multiple fractures at
birth. The patient has fragility and generalized deformity of all bones, blue sclera of the
eyes, and dentinogenesis imperfecta.
• Patients are confined to a wheelchair.
• Patients with the moderate and deforming type are less severely affected than the other
two, but have a high incidence of blue sclera and dentinogenesis imperfecta.
• The mild nondeforming type affects 60% of patients. Little evidence of the condition is
present at birth, but the ease of bone fractures appears as the child begins to walk. The
incidence of fractures declines at puberty. All patients have some degree of blue sclera,
only 25% will have dentinogenesis imperfecta. Some joint laxity is present, and 70% will
have hearing impairment.

• Radiographs exhibit shortened, deformed extremities with large areas of cystlike
radiolucencies.
• The midshaft areas are narrowed with bulbous metaphyseal and epiphyseal zones.
• Multiple fractures and healed fractures are apparent.
• Nearly all forms exhibit some spinal scoliosis.
• The teeth exhibit the usual changes of dentinogenesis imperfecta with bulbous
obliteration of the pulpal chambers, and shortened roots. Unilocular radiolucencies
that occupy both sides of the mandible have been found. They are similar surgically
and microscopically to traumatic bone cysts.

• HISTOPATHOLOGY
• The bones of patients with severe forms of OI have markedly thinned cortices
composed of immature woven bone.
• The trabeculae are short, thin, widely spaced, and disorganized.
• Bones display an increased number of osteoblasts, osteoclasts, and osteocytes, as
as decreased mineral content.

TORUS, EXOSTOSIS, AND OSTEOMA
• A torus commonly occurs in two specific intraoral locations:
• (1) on the midline of the hard palate, termed torus palatinus,
• (2) on the lingual of the mandible in the cuspid and premolar region, termed torus
mandibularis.
• Histologically identical lesions occurring on the alveolar bone of the mandible and
maxilla in other regions of the gingiva are termed exostoses.
• Similar lesions arising on the periosteal surfaces, but not in the previously mentioned
locations, are termed osteomas.
• Whereas tori and exostoses are thought to be reactions to bone stresses, the osteomas
are considered benign neoplasm.

• Torus palatinus is found on the midpalate of over 20% of adults. It is not present in
young patients, developing only after puberty in susceptible individuals.
• Once begun, lesions usually grow slowly over the patient’s entire life.
• Growths commonly consist of four evenly spaced lobes composed of dense bone with
a thin layer of mucosa tightly stretched over the surface.
• Lesions can grow large, sometimes becoming pedunculated.
• Larger tori interfere with speech, placement of prosthetic appliances, and oral hygiene
maintenance and may develop nonhealing ulcers that progress to chronic
osteomyelitis.

TORUS MANDIBULARIS
• Torus mandibularis is commonly found bilaterally in the cuspid area of the lingual
mandible.
• In some racial groups such as northern native peoples it occurs in over 30% of adults.
• The tori are slow growing, usually multiple lobed, and may become very large.
• Larger growths may interfere with tongue movement, oral hygiene maintenance, and
the ability to wear an intraoral prosthesis.
• They are easily lacerated and slow to heal.

EXOSTOSIS
• Exostoses are found randomly in adult patients, usually occurring on the attached
gingiva over the apices of teeth.
• They most commonly appear on the buccal plate over the bicuspids as multiple
rounded or oval nodules of dense bone,
• They are of little consequence to the patient unless they are cosmetically unacceptable
or interfere with the placement of a prosthesis.

OSTEOMA
• Osteomas are found at nearly any age and may be solitary or multiple.
• Location: They may be located either superficially or intraosseously on any bone of
the cranium or face or within the sinus cavities.
• When multiple, they are often associated with Gardner syndrome, a hereditary
condition with an autosomal dominant pattern and a gene locus at 5q21-q22.
• Gardner Syndrome
• The syndrome consists of
• Multiple intestinal polyps with malignant potential,
• Unerupted normal and supernumerary teeth,
• Cysts and fibromas of the skin.

OSTEOMA
• HISTOPATHOLOGY
• Each of the lesions is composed of dense cortical bone with a lamellar pattern.
• The cortical bone is sclerotic and relatively avascular.
• The medullary bone is denser than normal with reduced marrow spaces.
• The periosteal layer is often more active in osteoma than in tori or exostoses.

OSTEOID OSTEOMA
AND OSTEOBLASTOMA

OSTEOID OSTEOMA
AND OSTEOBLASTOMA
• Osteoid osteoma and osteoblastoma share many common clinical and histological features
each other and with cementoblastoma.
• All produce swelling and pain (particularly when pressure is applied), and all occur in young
patients.
• A similar histologic pattern is common to all lesions, consisting of a central nidus of increased
vascularity with extremely active osteoblasts and osteoclasts surrounded by cellular bone that
contains a wide zone of osteoid.
• They differ in that osteoid osteoma is small (0.5 to 2.0 cm), and osteoblastomas and
cementoblastomas are large (>2.0 cm).
• Cementoblastoma also differs, because it surrounds and is in continuity with the root
of a molar.
• The three lesions are considered variations of the same process.

OSTEOID OSTEOMA
AND OSTEOBLASTOMA
• The radiographic features of osteoid osteoma and osteoblastoma are distinctive and
pathognomonic.
• They are rounded, with a well-defined central radiolucency (nidus) surrounded by a
zone of increased radiopacity.

OSTEOID OSTEOMA
AND OSTEOBLASTOMA
• HISTOPATHOLOGY
• All lesions pass through several phases.
• Phase 1: Initially a small focus of active osteoblasts.
• Phase 2: a period in which wide zones of osteoid are deposited.
• Phase 3: in the matured stage, the osteoid becomes well calcified, creating an
form of bone.
• The center usually remains vascular with increased numbers of plump osteoblasts
large osteoclasts.

CEMENTO-OSSIFYING FIBROMA
• Other names
• 1. Ossifying fibroma
• calcifications in lesions.
• 2. Cementifying fibroma
• in some jaw lesions the calcifications are exclusively cementicles.
• 3. Psammomatoid juvenile ossifying fibroma
• when lesions containing the spherical calcifications occur in the sinonasal and orbital
in young patients.
• 4. Trabecular juvenile ossifying fibroma
• lesions of the maxilla and mandible with trabecular bone as the main histologic feature.

• All histologic variants is similar, causing
• 1. expansion of the cortical plates,
• 2. replacement of normal bone with neoplastic cellular fibrous tissue
• 3. formation of spherical calcifications,
• 4. irregularly oriented randomly oriented bony structures.
• The histologic features of many COFs closely resemble those of fibrous dysplasia. It is
separated from fibrous dysplasia primarily by its clinical and radiographic features and
the finding that the neoplastic tissue does not blend with the surrounding bone but is
sharply demarcated from it by a thin zone of fibrous tissue.
• A faster growing and more destructive variant of COF sometimes occurs in patients
under age 15 and is termed juvenile, or aggressive, ossifying fibroma.

• Location in the mandible posterior to the canines and only occasionally in the maxilla
and other locations.
• Gender It occurs twice as often in women
• Age primarily in the 20- to 30-year age group.
• The lesion is usually painless and grows slowly, exhibiting marked buccal and lingual
bony expansion.

• Unilocular or multilocular lesion.
• In the early stages the lesions are small and usually completely radiolucent.
• As they enlarge, increased amounts of irregularly shaped radiopacities appear within
the radiolucent area.
• In the later, more mature stage, the radiopaque structures enlarge and coalesce,
often forming a nearly radiopaque lesion with a thin rim of radiolucency separating it
from the surrounding normal bone.
• Root resorption and displacement of teeth.

• HISTOPATHOLOGY
• The more radiolucent lesions are composed of cellular fibrous connective tissue,
frequently in a whorled pattern.
• Spherical amorphous calcifications of various sizes (cementicles) are often present
randomly distributed.
• Irregularly shaped calcified structures containing osteocytes and a wide zone of
osteoid and osteoblasts are frequently intermingled.
• A thin outer zone of fibrous connective tissue is usually present, separating the
fibroosseous tissue from the surrounding normal bone.

GIANT CELL LESIONS
• In all of these lesions the giant cell
tissue has the same
histopathologic composition—
1.accumulations of multinucleated
giant cells in a background of
mononuclear fibrohistiocytic cells,
2.plump fibroblasts, and
3.extravasated red blood cells.

PERIPHERAL GIANT CELL GRANULOMA

• Age: 30- to 40-year-old age group
• Gender: Women
• Appearance: sessile focal purplish nodule on the gingiva.
• Size: 2cm
• may encompass one or more teeth
• spreads through penetration of the periodontal membrane
• Occasionally, lesions arise from the periosteum overlying edentulous areas.

• 1. Superficial erosion of the cortical bone
• 2. some widening of the adjacent periodontal space
• 3. small spicules of bone extending vertically into the base of the lesion
• 4. Saucerization beneath the lesion.

• HISTOPATHOLOGY
• 1. Nodules of multinucleated giant cells in a background of mononuclear cells and
extravasated red blood cells.
• 2. Bands of fibrous connective tissue stroma containing small sinusoidal spaces
(especially in the periphery) surround the nodules.
• 3. Osteoid deposits or spicules of new bone are often present in the base of the
lesion.
• 4. Accumulations of hemosiderin are found throughout the lesion.

CENTRAL GIANT CELL LESION
• Age: 10- to 30- year-old age group.
• Location: anterior mandible and maxilla.
with nearly 75% located in the mandible
and crossing the midline
• Expansion of the buccal and lingual
plates.
• Cortical perforation and resorption of root
apices.

• 1. Radiolucency (usually relatively large) with an indistinct line of demarcation with the
adjacent normal bone.
• 2. Buccal and lingual expansion.
• 3. Often exhibit complete cortical bone loss.
• 4. Movement of associated teeth and resorption of tooth roots.

• HISTOPATHOLOGY
• Tissue from the lesions is composed of giant cells, usually containing 5 to 20 nuclei,
against a background of mononuclear cells and fibrous tissue
• Less aggressive Giant cells are within distinct nodules separated by cellular fibrous tissue.
• Granulomatous foci of new bone evidenced by osteoid and woven bone.
• More aggressive More mononuclear cells and giant cells and less mature fibrous tissue.

ANEURYSMAL BONE CYST
• It differs primarily by containing many large blood-filled spaces separated by bands of
fibrous tissue containing giant cells.
• The most commonly associated conditions are benign and malignant bone tumors,
fibrous dysplasia, traumatic bone cyst, and intraosseous hemangioma.

• Age: 10- to 19-yearold age group.
• Location: posterior mandible and often extend into the ramus. In the maxilla,
confined to the molar area.
• Lesions are firm, diffuse swellings that produce facial deformity and malocclusion.
• ABC grows rapidly and may perforate the cortex.

• An oval or fusiform expansile radiolucency in which the cortex is thinned or eroded.
• Teeth are often moved and their roots resorbed.
• Lesions are usually unilocular, with some exhibiting faint trabeculation.

• HISTOPATHOLOGY
• ABC tissue consists of large blood-filled spaces separated by fibrous septa.
• The septa are composed of connective tissue containing osteoid deposits, spicules of
woven bone, and deposits of hemosiderin.
• Varying numbers of multinucleated giant cells may be observed.

TRAUMATIC BONE CYST
• Other names:
• simple bone cyst,
• hemorrhagic bone cyst,
• idiopathic bone cavity,
• It is an intrabony cavity that spontaneously occurs in the mandible of young patients.
• Although the cause of this lesion is unclear, it is commonly thought to occur after a
traumatic injury in which faulty resolution or lysis of the intramedullary hemorrhage
results in the formation of an empty bone cavity

TRAUMATIC BONE CYST
• Location molar and premolar region of the mandible.
• Age patients under 20 years of age.
• Gender A slight female predilection.
• Lesions are asymptomatic.
• Cavity of lesion may be empty or contain a small amount of serous or
fluid.

TRAUMATIC BONE CYST
• Traumatic bone cyst appears as a well-
circumscribed, solitary radiolucency of
variable size.
• Larger lesions frequently extend between
the roots of the associated teeth to
produce a scalloped appearance that is
characteristic of this lesion

TRAUMATIC BONE CYST
• HISTOPATHOLOGY
• A thin layer of loose and delicate connective
tissue overlying a zone of reactive bone that
exhibits remodeling.
• Soft tissue luminal surface contains a thin
layer of fibrin.
• In areas where healing is taking place, the
connective tissue will contain mineralized
deposits of new bone with a distinctive
lamellar pattern.

LANGERHANS CELL HISTIOCYTOSIS
• Other names:
• idiopathic histiocytosis,
• Langerhans cell granuloma,
• Langerhans cell disease

• Based on the clinical findings, LCH is grouped into three categories for treatment and
prognostic purposes:
• (1) chronic focal—usually a solitary lesion in one bone but occasionally in multiple
bones, with no soft tissue or organ involvement (previously designated as
granuloma”);
• (2) chronic disseminated—involving multiple bones, organs, lymph nodes, and
occasionally skin (previously designated as “Hand-Schüller-Christian disease”); and
• (3) acute disseminated—involving most organs, lymph nodes, bone marrow, and skin
of infants (previously designated as “Letterer-Siwe disease”).

Chronic focal form of LCH
(“eosinophilic granuloma”)
•occurs most frequently in teenagers
and young adults.
•May involve several teeth
•a solitary intraosseous punch out
lesion around and beneath the
teeth roots.
•appear as focal areas of advanced
periodontal disease in which the
teeth seem to be floating in space
because of the lack of surrounding
bone.
•In edentulous areas, lesion appears
as well demarcated radiolucency.
The chronic disseminated form
(“Hand-
Schüller-Christian disease”)
•tends to occur most commonly in
patients under10 years of age
the acute disseminated form
(“Letterer-Siwe disease”)
•Patients are usually infants
•extensive involvement of skin and
visceral organs by anaplastic cells.

• HISTOPATHOLOGY
• tissue contains sheets of large histiocytic cells with eosinophilic cytoplasm and
centrally placed nuclei with occasional multinucleated cells interspersed with
other inflammatory cells.
• presence of abundant focal concentrations of eosinophils.
• The presence of Birbeck granules appear either as elongated thin rods or tennis
racket–shaped when viewed with electron microscopy confirms a diagnosis of
LCH.
• Using immunohistochemistry, the mononuclear histiocytic cells are S-100 and
CD1a-positive

OSTEOGENIC SARCOMA
• Location It most commonly occurs in the long bones, having a predilection for the
distal and proximal areas of the femur, tibia, and humerus. Approximately 7% of
osteogenic sarcomas occur in the head and neck area.
• Pathogenesis
• RB1 gene (13q14.1-q14.2) causes both retinoblastoma and osteogenic sarcoma.
• Lesions also commonly develop in bones beneath soft tissue that has received prior
radiation treatments.

OSTEOGENIC SARCOMA
• Age 33 or 24 years
• Appearance Lesions of the mandible and maxilla are usually first noticed as bony,
hard swellings of the buccal and lingual cortices (with or without pain) and often
associated with separation of teeth
• juxtacortical osteogenic sarcomas In some patients, lesions occur as exophytic hard
nodules on the attached gingiva, appearing as soft tissue epulides.

OSTEOGENIC SARCOMA
• large areas of radiopacity within a diffuse, nondefined radiolucent background
• widening of the periodontal membrane in adjacent teeth.

OSTEOGENIC SARCOMA
• An occlusal radiograph usually reveals a sunburst pattern of radiopacity radiating from
the periosteum

OSTEOGENIC SARCOMA
• HISTOPATHOLOGY
• Four intraosseous variants and one juxtacortical histologic variant of osteogenic
sarcoma exist.
• Osteogenic sarcoma lesions must contain normal or abnormal osteoid or bone.

The osteoblastic
type
equal distribution of
the pleomorphic and
hyperchromatic
sarcomatous cell
component and the
hypercellular
trabecular bone
The
chondroblastic
type
Contains deposits
of hypercellular
cartilage and
abnormal osteoid
and bone.
Fibroblastic
osteogenic
sarcoma
is composed of
sarcomatous
shaped cells with
little malignant
osteoid.
Completely
radiolucent on
radiographs.
Telangiectatic
lesions
reduced hard tissue
component and a
greatly increased
number of
blood vessels and
giant cells.

OSTEOGENIC SARCOMA
• Juxtacortical (parosteal) lesions are located above the periosteum
• and are low-grade osteoblastic lesions containing large separate areas of malignant
cartilage.
• Lesions are usually nodular and may only contact the cortical bone in focal areas.

CHONDROSARCOMA
• Chondrosarcomas are malignant bone tumors in which the malignant cells produce
abnormal cartilage exclusively and no osteoid or bone.
• Primary chondrosarcomas (arising directly from bone cells as malignant neoplasms)
• Secondary chondrosarcomas (arising in a preexisting benign cartilaginous lesion such
as enchondroma or osteochondroma)

CHONDROSARCOMA
• Lesions have been associated
with
Paget disease
Ollier disease
(multiple enchondromatosis)
Maffucci syndrome
(multiple enchondromatosis,
hemangiomas, and fibromas)
Association with

CHONDROSARCOMA
• Age 30- to 40-year-old age group
• Location anterior maxilla, where preexisting nasal cartilage is present,
• the premolar areas of the mandible, the site of the embryonically derived Meckel
cartilage.
• Lesions are expansile masses that produce distortion of the areas.
• Pain and paresthesia may occur
• nasal obstruction and breathing difficulties occur.

CHONDROSARCOMA
• an expansile “motheaten” radiolucent area with indistinct boundaries
containing flecks or blotchy radiopacities throughout.
• Widening of the periodontal membrane of associated teeth

CHONDROSARCOMA
• HISTOPATHOLOGY
• They may be well-differentiated and resemble a benign cartilaginous lesion or they
may be anaplastic, composed of spindled cells with little evidence of cartilage
formation.
• Most lesions exhibit a combination of abnormal cartilage surrounded by neoplastic
cells.
• Lesions are graded I to III, depending on the amount and maturity of the cartilage
the proportion and anaplasticity of the connective tissue cells.
• In grades II and III, areas of myxoid tissue and cystic degeneration are present.

EWING SARCOMA
• The lesions consist of densely packed, small, darkly stained round cells without
prominent nucleoli or distinct cell borders.
• Ewing sarcoma is a highly malignant bone tumor thought to arise from primitive
neuroectodermal cells.
• Ewing sarcoma comprises 10% of the malignant bone tumors.
• Most common in the femur and pelvic bones, with only 1% of lesions affecting the
jaws.

EWING SARCOMA
the presence of
the t(11; 22)(q24;
q12) translocation
creates the
EWS/FLI1 fusion
gene
expression of a
chimeric protein

EWING SARCOMA
Age younger
patients, usually
children and
adolescents
In the jaws, patients
may experience
loosening teeth and,
in later stages, focal
ulceration.
Slight to
moderate fever
Leukocytosis
In the area of
involvement,
pain is
concurrent with
rapid swelling.
Increased
sedimentation
rates
Location The
mandible is
affected more
often than the
maxilla, cranial
base, and skull.

EWING SARCOMA
• RADIOGRAPHIC
FEATURES
“moth-eaten”
Appearance of involved bone
“onionskin” reaction
The periosteum often has a
lamellar layering

EWING SARCOMA
• HISTOPATHOLOGY
• Individual cells may be of two types:
• Both cell types are undifferentiated cells
• darkly staining
nuclei and a visibly
delineated
cytoplasm
small and round
• a finely granular
nucleus
• and a faint ill-
defined cytoplasm
larger

EWING SARCOMA
Silver nitrate
staining
• septa surrounding lobules of cells
PAS stains and
ultrastructural
studies
• characteristic glycogen granules in neoplastic cells
Immunomarkers
• to rule out other tissues of origin and establish the
presence of vimentin-positive intermediate filaments.

REFERENCES
• Contemporary Oral and Maxillofacial Pathology

Bone Lesions Oral Pathology

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