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 tongue - 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
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Keratoses and related disorders of oral mucosa -color of normal mucosa depend on: vascularity,
-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
*koilocytosis*tt: surgical excision , freezing, chemical cautery.
*etiological factor: tobacco, betal liquid , other chewing 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 geneIts 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 isn’t 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):
_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 don’t 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) .
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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
like lesion, usually asymptomatic, no atrophy, no ulceration .
-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 isn’t 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 .
*oral lesion: variable lesion, most on buccal mucosa.
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Diseases of Temporomandibular joint
*developmental disorders*Inflamatory disorders*ostoearthorosis*Functional disorders*loose bodies*neoplasms*Age change in the jaws & TMJ*Triamua & disloction
1 -developmental disordersA-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 2nd decade2-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-Rare-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
opening-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)-symmetrical
-20-70% TMJ Invloved , usually asymptomatic
-When symptomatic:
*limitation of opening*stiffness*crepitus*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*it’s rare in TMJ-clinical feature:
*pain*crepitus*limitation of jaw movement*deviation on opening*many clinical cases are silent
*suggest in relation with:
a- untreated myofacial pain-dysfunction syndromb-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
bodies4-loose bodies
*Radioopaque bodies apparantly lying free within joint space (Rare in TMJ , common in major joint)
*may cuase discomfort , crepitus,limitation in movement*The main couse in TMJ are:
a-intracapsular fracturesb-fractured osteophytes in ostoearthorosis
c-synovial chonromatosis:
-disease of unknown etiology-charactrized by formation of multible nodule of
cartilage-may released in the joint space and appear as loose
bodies5-Neoplasms-primary in TMJ are Rare-Benign tumer are more frequent (chondoromas &
osteomas)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
disc-remodeling may result in anterior displacment of the
disc-there may perforation to disc in it’s posterion
attachment
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
*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 3rd of face is retrusive, severe malocclusion is common.________________________
_fiber osseous lesion :*replacement of normal bone by fibrous tissue. It cant be
_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 doesn’t 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 separated.
***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(café 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.
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 appearance .
*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 extraction.
_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 1st 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
*(Garré’s 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.
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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.
*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 limbs.
* 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.
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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. 3-3rd phase(distorted bone become fixed)
*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
non-aggressive .*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 alveolary._______________
_giant cell tumor of bone: (true neoplasm) *occur in long bone, rare in jaw.
