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Keratoses and related disorders of oral mucosa

- color of normal mucosa depend on: vascularity,

melanin, epithelial thickness and keratenization.
*non-keratinized mucosa: labial & buccal mucosa, FOM,
ventral of the tongue.
* keratinized mucosa: gingival, hard palat, dorsum of the
- white lesion: abnormal increase in keratenization.
- krtatosis: normal increase in keratin
- we use scarping or wiping test.
-classification of white lesion:
*hereditary: OEN, lueko edema
*infective: candisosis, syphilis, hairy lueko plakia
*idiopathic: luekoplakia
*dermatological: lichen planus, LE
*neoplastic: carcinoma in situ, SCC
-orthokeratoses: anucleated, granular cell layer is
- parakeratoses: pyknotic nucleus , granular cell layer
isnt evident.
-atrophy: dec epithelial thickness
- atypia: change cell type(in a level of cell)
- dysplasia: change cell type (in a level of tissue)
white sponge nevus (WSN) :

*hereditary keratoses
* benign , not premalignant
*caused mutation in gene coding (3,14) and can be
caused by abnormal desquamation
*shaggy, folded, not well defined lesion
*cannot be scarped of
* can affect any part of mucosa on any age.
*hyper keratoses , acnthosis , edema, no inflammation ,
no etypia or dysplasia.

* racial pigmentation, variant of normal
*caused by local irritation , smoking, and dark people
*bilateral, milky appearance, folded appearance
*contain glycogen.
*hereditary keratoses
**** Here ***

Mechanical trauma frictional keratosis:
* a cute trauma: plester , ulceration
* a chronic: hyperkeratosis
*ex: sharp tooth, orthodontic tt
*resolve when irritation removed within 10 days-2weeks

Chemical trauma:
*ex: aspirin
* sloughing, ulceration,

Thermal trauma:
*palatal lesion
* more in smoker (pipe smoker)
*nicotinic stomatitis : reversible , not premalignant

*white patch cannot be characterize clinically or
histologically as any other lesion.
*diagnosis arrived by exclusion
*cannot be wiped off
* can be premalignant or not depend on histological
* affect by ethnicity.
*predominant in males and older people and more in
FOM.(previous study)
* F:M equal, increased in younger people.
*homogenous lesion: flat, uniform, crack, only white in
*Non-homogeneous: irregular, speckled or verroucous ,
it worse prognosis
*erythroplakia: red in color or maybe red and white
* feature indicate malignant change:
Fixation, induration, ulceration, lymphadenopathy, bone
* it is idiopathic, and multifactorial.
*predisposing factor : tobacco, alcohol, candida (fungal
infection) or candidal leukoplakia.
*veruses: 1- human papilloma virus (HPV)
2- epestin barr virus (EBV)
*oral epithelial atrophy: its incidence increase by :
Iron deficiency, submucos fibrosis, tertiary syphilis,
*tumor suppressor gene: mutation in p53 on
chromosome 17p.
*sanguinaria-associated leukoplakia: type of flower
cause gingivitis, and malignant transfusion is determined.
* leukoplakia is widely varied in degree of keratoses,
thickness of epithelium,
* not all leukoplakia is dysplastic
*important note:
Leukoplakia is clinically diagnosed and not depend on
any histopathological feature.
*smoking consider as predisposing factor:
1-presence of chevron peaks in keratin (V-shaped
2-melanin incontinence
*Dysplasia maybe mild(grade-I) not extend beyond the
lower third of epithelium, moderate(grade-II) in the
middle third of epithelium, severe(grade-III) upper third
of epithelium
* feature of epithelial dysplasia:
1-abnormal mitosis . 2- basal cell hyperplasia. 3- drop-
shape rate ledge. 4-distripute polarity(lose of cellular
orientation. 5-increase in nuclear rate. 6-nuclear
hyperchromatism. 7-promenent and enlarged nucleoli .
8- irregular epithelial stratification. 9- nuclear and
cellular polymorphism. 10-dyskerarosis. 11- lose or
reduction of intracellular adhesion.
*malignant transfusion is more in: FOM, ventral of
tongue, lingual of lower aspect of mucosa.
*risk assessment depend on: size, site, clinical
appearance, degree of epithelial dysplasia.

Oral epithelial tumor:
- benign tumor: sequamous cell papilloma
- malignant tumor: sequamous cell carcinoma,basal cell
carcinoma , melanoma.
- human papilloma virus (HPV): at least 16 type isolated
for oral cavity, low risk associated with benign lesion,
look like normal mucosa, it typically infect keratenocytes
in skin and mucosa.
* koilocytes: virally infected epithelial cell with HPV
and have many cellular change.

- HPV associated lesion:
1-sequamous cell papilloma:
*benign tumor, single lesion, may be pedunculated or
sessile, appear like warty or cauliflower with white pink
growth depend on amount of keratin.
*histopatholigically: its papillary finger like projection of
epithelial cell. No malignant transfusion.
* tt: conservative excision .
2- veruca valgaris (common warts):
*pedunculated or sessile , single or multipile.
*most often white in color (hyperkeratosis)
*most often orthokeratinization
*tt: surgical excision , freezing, chemical cautery.
3- condyloma accuminatum (venereal wart)
Commonly seen in anoginetal region, but can be seen
orally, multiple soft pink(keratinization isnt a feature) ,
can be pedunculated or sessile.
*pappilary lesion , its a manifestation for HIV ,
* prominent acnthosis, hyperplastic and elongation of
rate ridge.
* koilocytosis.
4-hecks disease (focal epithelial hyperplasia) {rare
*multiple epithelial elevated plaque, more on lower lip
and buccal mucosa.
*histologicaly: hyperkeratosis, acnthosis.
*hyperplastic rateridge fuse with each other.

Sequamous cell carcinoma: (SCC)
*the commenest oral malignancy.
tobacco, betal liquid , other chewing : etiological factor *
habits, alcohol, diet and nutrition (iron, vitamin A) ,
dental factor( poor oral hygiene, faulty dental
restoration), occupational risk (outdoor worker.. SCC
of lip border : it more in lower lip and more in men) ,
virus ( HSV, HPV, EPV), immuonosupression (ex:HIV
increase risk of lip cancerr), chronic infection like
candidal infection and syphilis.

_ oncogenes and tumor-suppressor gene
Its growth promoting proto-oncogenes and growth
inhibiting tuomer suppressor gene. During
carcinogenesis , proto oncogenes may undergo mutation
or-and become active. Also tumor suppressor gene may
mutinied . as a result cell growth increased.
_early lesion of SCC:
*white patches, small mass , no ulceration or erythema,
red patches (erythroplakia), in active ulcer.
_ advanced or late lesion:
*rough nodular, broad base, pain may be a feature ,
Mobility of teeth, altered sensation, metastasis spread.
well differentiated tumor (low grade):
*intra-cellular bridge is recognizable, keratin pearl,
nuclear and cellular polymorphism isnt prominent , few
mitotic figure.
Moderate differentiated tumor:
*still readly identify, more polymorphism , less
keratinization, a abundant and atypical mitotic figure.
Poorly differentiated tumor(high grade):
*keretinization absent , prominent polymorphism, a
abundant and atypical mitotic figure, stained brown cell
(epithelial cell positive for cytokeratin), difficult to
differentiate epithelial cell.
*most SCC are locally destructive. And all of them show
invasion, indurations and fixation. It has many pattern of
invasion(infiltration of adjacent cell):
- sheet or broad group.
- small, narrow, isolated, individual malignant cell. (poor
* it has variable pattern of metastasis to the lymph node:
- increase with the size of primary tumor
- when it spread to the neck it may be: intra-capsular or
extra-capsular. It result in fixation and poor prognosis.
Verrucous carcinoma: _
*thick white warty plaque, most common in man buccal
sulcus, mainly affect elderly people, prognosis is good
when it isnt metastasis. It well differentiated (low grade)

_ carcinoma in situ:
*severe epithelial dysplasia, basement mem is intact,
No invasion of lamina properia, its pre-malignant lesion
.progress to invasive carcinoma,
_ premalignant lesion: leukoplakia, erythroplakia,
candidal leukoplakia, carcinoma in situ.
_ premalignant condition: oral submucos fibrosis, LP,
acitinic keratosis.
_ basal cell carcinoma (rodent ulcur):
*coomon neoplasm of skin, affect old people who
exposed to UV light, vermilion border especially upper
lip. If it multiple in young people who dont expose to
UV light nevoid basal cell carcinoma syndrome.
_melanocytic nevi and melanoma:
*neoro-ectodermal origin,
*moles(acquired melanocytic): common nevus of head
and neck skin. Considered as hamartomatous lesion.
Malignant change rarely occur, more in hard palate and
buccal mucosa, it locate histopatholigically : intra
dermal, junctional, compound nevus.

*malignant melanoma: caused mainly by excessive
exposed to UV light, clinical appearance (asymmetry,
border irregularity, color variation, diameter more than
6mm) , its rare orally (brown, black color).

Dermatological causes of white patches:
_Lichen plannus (LP):
* the commonest dermatological patches (chronic
mucotanous disease), more common in female.
* skin lesion: locate in any site especially flexure surface
of wrist. Scalpel affect may lead to alopecia. Appear
clinically as strea, papule(solid elevation , no fluid) ,
annular, bulbous, linear .
May cause wide spread rash, after they go they leave
pigmented scar.
* oral lesion: may occur alone or with skin lesion. 90%
occur on buccal mucosa, mostly bilateral lesion, it may
be :
- Non-erosive lesion: reticular, papular, annular, plaque
like lesion, usually asymptomatic, no atrophy, no
- erosive (atrophic) lesion: shallow ulceration, diffuse red
lesion (resample erythroplakia), superficial red glazed
ulcer. Usually symptomatic.
* LP cause desequamative gingivitis.
* LP may be orthokeratoses or parakeratoses, and
acnthosis result in sow teeth pattern. It has T-lymphocyte
infiltrate, and basal cell degradation may cause
subepithelial bullia lead to lake cohesion bt epithelium
and lamina properia.
*LP is almost benign lesion (very small proportion of
malignant transfusion), the causes isnt fully understood,
in most cases it is idiopathic.
*it can be associated with systemic disease.
_ Lichenoid reaction:
* appear similar to LP, caused by: hypersensitivity
reaction to drug or amalgam.
*its usually unilateral but LP is bilateral.
_Lupus erythematous (LE):
*chronic mucocutanous disease affect skin and oral
mucosa, more common in female. It mainly 2 forms:

1- chronic discoid lupus erythematous (DLE):
*skin lesion:localized red patches heal with scar,
symmetrical lesion around nose and cheek (butterfly
rash), follicular plugging of hair follicle lead to hair loss.
*oral lesion: most common on buccal mucosa, its
orthokeratinized or parakeratinized , keratin plugging,
liquifiactive degeneration of basal cell.

2- systemic lupus erythromeatous (SLE):
*skin lesion: maculopapular (skin rashes) , butterfly
*oral lesion: variable lesion, most on buccal mucosa.


Diseases of Temporomandibular joint

*developmental disorders
*Inflamatory disorders
*Functional disorders
*loose bodies
*Age change in the jaws & TMJ
*Triamua & disloction

1- developmental disorders
A-Condaylar Aplasia :
-Extremly rare
-Unilateral or bilateral
-associated with other facial anomalies
B-condaylar hupoplasia
-Congenital(unknown) or acquired
{truma,radiation,infection (from middle ear)
-Uni or bilateral
-Earlier damage = more severe facial deformity
-Rare, self limiting
-Genirally Unilateral (Deviation to opposite side)
-become apparent in 2
2-Inflamatory Disorders
A- Trumatic arthraitis
-Damage to joint following acute truma may lead to
trumatic artharitis or hemoarthorosis
-resolve if tissue not severly damaged, otherwise scar
tissue formation will lead to ankylosis
B-Infevtive arthritis
-May reach TMJ By:
*direct spread from adjacent focus (middle ear,
surrounding celluitis)
*Hematogenous spread from distant focus
*Facial truma
-Staphylococcus aureus most common isolate
-Signs of acute infection : Pain, trismus,daviation on
-may result in fibrous or bony ankylosis
C-Rheumatoid Arthritis
-Non organ , autoimmune disease
-commonly in early adult life
-Female > Male
-systimic distribution in wich joint involvment is the
main feature,others ( Anemia , weight loss ,
subcutaneous nodules)
-10% Sjgron syndrom may show
-smaller joint more affected (in hand)
-20-70% TMJ Invloved , usually asymptomatic
-When symptomatic:
*limitation of opening
*referred pain
*tendernes on biting
*severe disability is unusual

-Seroligical findings:
*Rheumatoid factor present in 85%
*Elevated ESR becouse of hypergammaglobulinemia.
3- ostoearthorosis
-degenerative disease affect weight bearing joints
-in the TMJ it differs from other joints :
*not a weight bearing joint
*articular surface is coverd with fibrousus tissue rether
than hyaline cartilage
*its rare in TMJ
-clinical feature :
*limitation of jaw movement
*deviation on opening
*many clinical cases are silent
*suggest in relation with:
a- untreated myofacial pain-dysfunction syndrom
b-loss of molar support
c-disc displacment

*spontenous resolution is common

Radiographic change:
*variable and not pathognomic
*focal or difuse bone loss on condyle
*flatting and reduction in bony size
*reduction in joint space
*if large may fracture and presentedon RG as loose
4-loose bodies
*Radioopaque bodies apparantly lying free within joint
space (Rare in TMJ , common in major joint)
*may cuase discomfort , crepitus,limitation in
*The main couse in TMJ are:
a-intracapsular fractures
b-fractured osteophytes in ostoearthorosis
c-synovial chonromatosis:
-disease of unknown etiology
-charactrized by formation of multible nodule of
-may released in the joint space and appear as loose
-primary in TMJ are Rare
-Benign tumer are more frequent (chondoromas &
6-Age change in the jaws & TMJ
-Atrophy of alveolar bone is mainly related to tooth loss
-increase with age & accelerat by osteoporosis
-loss in Facial hight uppward and downward
-in TMJ difficult to distinguish changes
-main change due to remodeling of articular surface and
-remodeling may result in anterior displacment of the
-there may perforation to disc in its posterion
7-trismus & dislocation

-trismus: limitation of mouth opening
-temporary tismus is more common
-may couse by intra or extra articular factor
*Couses of trismus
A- Intra articular factor
*trumatic arthritis
*infective arthritis
*Rheumatoid arthritis
*intracaspular fracture
*fibrous or bony ankylosis

B- Extra articular factor
*adjecent infection , inflamation & abscess
*extraxcapsular fracture
*overgrowth of coronoid process
*fibrosis from burns or radiation
*hematoma/fibrosis of medial ptyrigoid
*myofacial pain-dyscomfort syndrom
*drug associated dyskinasia & psychotic

-displacment of condyle out of glonoid fossa
-Couses of unstable joints
a-abnormal nuromascular activity
b-weaknes of capsule and lateral ligament
c-Anatomical factor
-Rarely, its Hapitual or recurrent


Bone disorders:
Inherited and developmental disorders of bone:
_ Osteogenesis imperfecta: (hereditary disorder)
*sclera usually appear blue, and may lead to deafness,
and it cause joint hypermobility, it usually associated
with dentenogenesis imperfecta .
*It has 4 types:
- type1(classical type) with or without dentenogemesis
- type II(prenatal type)
- type III (progressively deforming) with dentenogenesis
- type IV : similar to type1 but more severe.
_osteopetrosis: (stone bone)
*extensive density of bone and obliteration of bone
marrow, mandible >maxilla, delay eruption of teeth,
complication of teeth extraction.
*2 patterns:
1- malignant type: autosomal recessive progressive,
occur early in life, death before puberty
2- benign type: autosomal dominant, les severe, late in
* there is lack of distinction bt cortical and medullary
bone on RG, also, the root of teeth invisible.
* histologically there is persistence of woven bone and
lack of lamellar bone .
_ cleidocranial dysplasia:
*it affect mainly skull, jaws, clavicle, dental anomalies
also common. The fontaneless and other suture still open,
partial or complete loss of clavicle, retained of deciduous
teeth, delayed or non-erupt permanent teeth, with
multiple impaction, cyst, supernumerary teeth.
_ achondroplasia:
*common form of dwarfism, associated with
endochondrial ossification, head and trunk had a normal
size but the limps extremely short, middle 3
of face is
retrusive, severe malocclusion is common.
_ fiber osseous lesion:
*replacement of normal bone by fibrous tissue. It cant be
distinguished histologically alone. It divided into :
1- osseous dysplasia: fibrous dysplasia, cemento-osseous
2- benign-fibro-osseous neoplasm: ossifying fibroma or
cemento-ossifying fibroma.
_ fibrous dysplasia of bone:
*** monostotic fibrous dysplasia: (common) , one bone
involved, maxilla>mandible, majority pt is young and
children, gradually painless increasing swilling lead to
facial asymmetry, canine fossa obliterated, the lesion
doesnt cross the mid line of maxilla, in mandible it
affect molar and premolar area, teeth may fail to erupt, In
RG U notice radiolucent initially (like cyst), also U will
find ground- glass (orange peal stippling) feature, with
ill-defined border,teeth may displaced and root may
***polystotic fibrous dysplasia: (less common), more in
females, affect several bone, serum alkaline phosphate
may increase, it usually diagnosed in childhood, it
associated with skin pigmentation(caf lue melanotic
spot), oral pigmentation. There will be replacement of
bone tissue by fibrous tissue(progressive remodeling of
woven bone) , U will find aneurismal bone cyst,
pathogen is complex , its not inherited its developmental.
_ Bone disorders:
*localize to jaws involve teeth bearing area, it include:
periapical cemental dysplasia, focal cemento-osseous
dysplasia, floride cemento osseous dysplasia(gigantiform
dysplasia), female > male, and more in mandible, its
multiple or small lesion(<1cm): if it in the apical portion
of mandibular incisorperiapical cemantal dysplasia,
If it involve one or more quadrant on one or both jaws
florid cemanto osseous dysplasia .
_ ossifying fibroma (cemento-ossifying fibroma):
* encapsulated benign neoplasm, consist of fibrous
tissue containing varying amount of bony trabeculea, and
round classified bodies. Appear as slowly enlarged and
progressive swilling lead to sino-nasal complex, more in
female, in RG it radiolucent or radiopaque or mixed.
Histologically called psammomatoid ossifying fibroma
(sand like)
_ cherubism: autosomal dominant inherited disease.
*more in male, appear with facial deformity (fullness of
cheek and jaws producing a typical chubby face) ,
painless bilateral swilling of the jaw bt 2-4 yr age,
involve mandible alone or with maxilla, it need cosmetic
surgery, eye apper upturned to heaven. Cherubic
* premature loss of deciduous teeth , failure development
of many permanent teeth.


Bone healing
_ healing of an extraction socket:
*socket immediately fill with clot, which form
granulation tissue, (6 weeks after extraction) , U eill
notice that the height of alveolar bone reduced after
remodeling, socket is obliterate 20-30 weeks after
_ osseointegrated implants:
*healing of bone around endosseous implant(intimate
interface bt bone and implant), need several month to
heal, implant also, penetrate soft tissue (similar to
dentogingival function), collagen bundles run parallel to
the long axis of implant. (epithelium doesn't run epically
along post surface). Plaque accumulation lead to
inflammation around the implant and the microbes which
found on it similar to natural teeth.

Inflammatory disease of bone:
_dry socket (alveolar osteitis) : severe pain 2 days after
extraction, healing extremely slow bcz clot fail to form.
_ focal sclerosing osteitis: squelea of periapical
inflammation, result from low grade irritation, usually
asymptomatic , common in the 1
permanent molar,
_ osteomyelities : depend on severity of irritation and
host defense. It affect jaws as a result of: trauma,
radiation injury, pagets disease, osteopetrosis, major
vessels disease and many systemic factor which impaired
host defense.
_suppurative osteomylities: acute or chronic(>1month),
caused by dental infection mainly by staphylococcal or
local trauma (anaerobes predominate), more in mandible,
may due to thrombosis of mandibular a. lead to extensive
necrosis. In maxilla the circulation is rich.
Necrosis lead to fill marrow space with pus, and the
suppurative infection extend to adjacent space,stripping
of persteoum compromises blood supply lead to future
necrosis. Some time it need surgical removing to
enhance healing.
* if it acute it will cause: pain, swilling, trismus, pyrexia,
paresthesia of lip, mobility of teeth.
* if it chronic it will cause: swilling, pain, discharge pus.
*in RG there will be sufficient bone resorption in 10-14
days, sequestra may be seen.
_ chronic sclerosing osteomylities: localized lesions are
identical to focal sclerosing osteitis. some previously
reported diffuse types probably represent infected florid
cemento-osseous dysplasia. However, diffuse sclerosing
lesions of the mandible as a complication of spread from
contiguous focus of low-grade infection/inflammation
such as periapical granuloma have been reported.
_ Chronic Osteomyelitis with Proliferative Periostitis
*(Garrs Osteomyelitis, Periostitis Ossificans), Seen
almost exclusively in mandible in childrenand young
adults. result from spread of low grade chronic apical
inflammation through cortex, Bony hard swelling on
outer surface of mandibleRadigraphs show focal
subperiosteal overgrowth of bone with smooth surface on
outer cortical plate.The subperiosteal mass consists of
irregular trabeculae of actively forming woven bone with
scattered chronic inflammatory cells in fibrous
marrow.Periosteal new bone formation (periosteal
reaction) /onion-peel appearance.
_ Chronic PeriostitisAssociated with Hyaline Bodies
(Pulse Granuloma, Vegetable Granuloma):
*An unusual from of chronic periostitis in the jaws.
Histologically associated with hyaline ring-shaped
bodies with foreign body reaction. Hyaline material is
thought to represent vegetable material, especially pulses
which may gain access to tissues via surgery, open root
canal or trauma. Similar hyaline bodies are occasionally
seen with apical granulomas and capsules of odontogenic
cysts, thought to be due to impaction of food debris
down a root canal.
_Radiation Injury and Osteoradionecrosis
Radiotherapy for oral malignancy affects the vascularity
of bone. It causes proliferation of intima of blood vessels
(endarteritis obliterans). This can cause serious
consequences in the mandible due to its readily
compromised blood supply. The non-vital bone which
results from reduction in blood supply is sterile and
asymptomatic. It is, however, very susceptible to
infection and trauma e.g. from a denture. Extensive
osteomyelitis with painful necrosis of bone, often
associated with sloughing of overlying oral and
sometimes facial soft tissues may occur, even years after
radiotherapy. Modern methods of radiotherapy have
greatly reduced its incidence.
_ Bisphosphonate-Induced Osteonecrosis of the Jaws:
*Bisphosphonates: They are used in the prevention and
treatment of osteoporosis, Paget's disease of bone, bone
metastasis, multiple myeloma, primary
hyperparathyroidism, osteogenesis imperfecta, and other
conditions that feature bone fragility. Defined as an area
of exposed bone in the maxillofacial region that did not
heal within 8 wk after identification by a health care
provider, in a patient who was receiving or had been
exposed to a bisphosphonate and had not had radiation
therapy to the craniofacial region.Risk appears to be
greater with use of intravenous forms than oral forms.
Mandible > maxilla, Prevention & Management All sites
of potential jaw infection should be eliminated before
bisphosphonate therapy is initiated to reduce the
necessity of subsequent dentoalveolar surgery.
Conservative debridement of necrotic bone, pain control,
infection management, use of antimicrobial oral rinses,
and withdrawal of bisphosphonates are preferable to
aggressive surgical measures for treating this condition.


Metabolic and Endocrine Disorders of Bone
_ Osteoporosis:
*Bone loss gradually predominates over apposition in
adult life. It results either when bone loss is excessive, or
when apposition is reduced. Female >male, Osteoporotic
bone is of normal composition but is reduced in quantity.
The jaws may be involved. In edentulous patients, it may
leave the mandible as a thin fragile strip of bone which
can be easily fractured. It has been suggested that
osteoporosis is a risk factor in chronic periodontitis, but
evidence is still little.
_Primary Hyperparathyroidism:
* excessive hormone secretion results in: 1.
Hypercalcemia. 2. Hypercalciuria. 3. Metastatic
calcification in urinary tract, blood vessel walls and
*Severe cases may variably be associated with:
1. Bone pain. 2. Bone cysts (osteitis fibrosa cystica). 3.
Pathological fractures. 4. Brown tumors. 5. Renal colics
due to stones. 6. Mental changes including depression,
emotional liability, poor mentation, and memory defects.
7. Increased incidence of peptic ulcer. 8. Chronic
pancreatitis. 9. Hypertension.
*histologically there is Increased osteoclastic activity
throughout the skeleton. Occasionally, focal areas of
bone resorption result in formation of lesions called
brown tumors (giant cell lesion). Biochemical changes
have to be demonstrated to confirm diagnosis.

_ Secondary Hyperparathyroidism:
* Occurs in response to:chronic hypocalcemia most
frequently due to chronic renal failure or in association
with rickets and osteomalacia. Involvement of the jaws
has been reported.
_ Rickets and Osteomalacia:
* Classically, rickets and its adult counterpart,
osteomalacia are due to deficiency of, or resistance to the
action of vitamin D. Deficiency may be due to lack of
exposure to sunlight or dietary causes. Radiographic
changes are similar to osteoporosis, but in contrast, there
is failure if mineralization of osteoid and cartilage.
* Children with rickets suffer from skeletal defects
including: 1. Flattening of skull with frontal bossing and
conspicuous suture lines. 2. Chest shows the classic
rachitic rosary, a grossly beaded appearance of
costochondral junctions resulting from enlargement of
costal cartilage. 3. An outer curvature of the sternum
(pigeon breast deformity). 4. Deformities of spine and
* Dental abnormalities in rickets include: 1. Delayed
eruption. 2. Enamel hypoplasia. 3. Increased width of
predentin. 4. Large amounts of interglobular dentin.
_ Acromegaly :
*Caused by prolonged and excessive secretion of growth
hormone usually due to an adenoma of anterior lobe of
pituitary developing after epiphyses have closed.
*There is renewed growth of bones of the jaws, hands,
and feet with overgrowth of some soft tissues, including
the lips and nose. Reactivation of condylar growth center
of mandible causes enlargement, protrusion, and spacing
of teeth.

Bone disorders:
_ pagets bone disease:
*etiology: usually unknown, it associated with genetic
predisposition (ch 18q). it has 3 phase:
1- osteolytic phase. 2- mixed(osteolytic and
osteogenasis) phase. 3-3
phase(distorted bone become
* it involve single or small number of bone, common in
weight bearing bone. Maxilla>mandible. Lead to
enlargement of skull and facial bone.
* in dentate pt: there will be malocclusion, spacing teeth
and retrocline incisor.
* edentulous pt: difficulty in wearing denture.
* in RG: start with osteoporosis, then develop to patchy
osteosclerosis, then cotton-wool appearance.
*it lead to ankyolosis of teeth.
*diagnosis of pagets depend on blood chemistry, serum
alkaline phosphate levels is often increase.
*tt: bisphosphinate and calcitonin.

Giant cell lesion of bone:

_ central giant cell granuloma: (not neoplastic)
*more in female and old, only in the jaw , more in
mandible, mostly in ant. Part of the jaw.
*asymptomatic swilling of bone, may be aggressive or
*appeare as radiolucent lesion on RG.(expantion of
cortical palate)
*unilocular or multi locular.
*it should be diagnosed by biochemical investigation of
parathyroid hormone.
*histologically U will find a large number of giant cell.
*tt: simple enculation and curettage.
Peripheral giant cell granuloma: _
* identical to central giant cell granuloma, but it occur
extra alveolary (withen soft tissue) rather than intra
_ giant cell tumor of bone: (true neoplasm)
* occur in long bone, rare in jaw.
*Higher reoccurrence rate.
*May metastasize (10%)
_ exostosis (torus palatinos, mandibularis )

*non-neoplastic lesion.
* rare in childhood, slow growth.
* it may a developmental lesion, or it response to
stimulus, may follow surgery.
* torus palatinus: in midline of maxilla, in adult, slowly
increase in size
* torus mandibularis: common in premolar area, bilateral
*torus may need surgical removing for denture wear.
* it is a benign lesion but not benign tumor.
_ dense bone island:
* idiopathic osteosclerosis, (localized)
* asymptomatic
* RG: will defined sclerotic area
* no clinical significance except: it help us to distinguish
them from otherbsclerotic mass.

bone tumor:
- primary tumor of bone is rare in jaws.
Classification of bone tumors of bone:
1- bone forming tumor: *benign(osteoma,
osteoplastoma), *malignant (osteosarcoma)
2- cartilage forming tumor: *benign (chondroma),
*malignant (chondrosarcoma)
3- marrow tumor: myeloma
4- fibrous tumor: benign (ossifying, fibroma)
5-tumor like lesion in bone: langerhan cell histocytosis,
Hemangioma of bone.
6- metastatic tumor.

_ osteoma:
*benign slowly growing tumor, central or subperiosteal.
* more in mandible, usually solitary.
*gardner syndrome = multiple osteomas
* multiple supernumerary teeth, impacted teeth,
*histoligically: compact vs calaneculous type.
_ osteoplastoma:
*it ressisimple to cementoplastoma but it isnt related to
teeth root.
_ osteosarcoma:
*common primary malignant tumor in jaws.
*swilling, pain (toothache),parasthesia, displaced teeth,
*types: intermedullary lesion(centrally), juxtacortical
lesion (peripherally).
*RG: radiolucent, radiopaque, mixed. Ill-defined border.
Sunray appearance.
*histologically: abnormal ostoid,
*mandibular lesion has better prognoses.
*tt: radical surgery.
_ chondrosarcoma:
*more common than chondroma, but slower growth rate.
*maxilla > mandible
* RG: radiolucent, radiopaque, mixed. Ill-defined border
*histo: abnormal cartilage (chondroplastoma)
* mandibular lesion has better prognoses.
*tt: radical surgery
_ multiple myeloma:
* malignant tumor of plasma cell.
Types: multiple(myelomatoses) common, solitary
(plasmacytoma). Jaws lesion may solitary or multiple.
*Multiple myeloma affect any bone, jaw lesion may the
initial manifestation of the disease.
* RG: Punched out appearance.
*histo: myloma cells (malignant plasma cell)
*tt: chemotherapy

_ langerhans cell histiocytosis:

- unifocal eosinophilic granuloma.more in male and in
skull and jaw , more in mandible
- multifocal eosinophilic granuloma. more in male and in
skull and jaw , more in mandible
- disseminated histiocytosis: multi organ disease, high

* clinically: loss of teeth, periapical lesion, gingival
ulceration or enlargement.
*RG: osteolytic lesion, radiolucent periapical lesion.
*histo: pale stained cell, variable number of eosenophils.
*tt: curettage, radiotherapy.
_ hemangeoma of bone:
* more in mandible
* RG: multiple honey comp appearance.
* aspiration fresh blood
_ metastatic tumor:
* more common in bone than soft tissue
* more common in mandible
*metastatize to jaws common from carcinomas of breast,
bronchus, kidney, prostate and lung.
* asymptomatic
* metastatic tumoe is osteolytic but breast and prostate
carcinoma is osteolytic.
* metastasize is common to gingiva or alveolar mucosa
then to tongue.