Patho Buccal: Intra PDF

Patho Buccal: Intra Cours 1: Intro Prendre en considération les dx dif Ex. Ulcère solitaire could also be ulcère traumatique, aphteux ou carcinome épidermoïde. Éléments à ressortir pendant l’anamnèse : P, Q, R, S, T P : palliatif – provocateur. Wh...

Patho Buccal: Intra Cours 1: Intro Prendre en considération les dx dif Ex. Ulcère solitaire could also be ulcère traumatique, aphteux ou carcinome épidermoïde. Éléments à ressortir pendant l’anamnèse : P, Q, R, S, T P : palliatif – provocateur. What causes, worsens or eases pain. Qu’est ce qui provoque la douleur? Q: qualité. Describe pain. R: region ou site. What region the pain touches. Dans quelle region resentez vous la douleur, ou plus précisement, près de quelle dent ? S: sévérité. Intensity of pain. Quelle est l’intensité de votre douleur dans un échelle de 1 à 10, si 1 est une douleur tolérable et qui ne vous dérange pas et 10, une douleur qui vous empêche de dormir la nuit et intolérable ? T: temps. Chronological description of pain. La douleur varie-elle durant la journée? Si oui, expliquez quelle moment (eg. Nuit) vous observez cette variation. LEARN MINI-ATLAS! EXAM document! You should also read “Oral and Maxillofacial Pathology” by Neville, 5th version. You should also know details of last year’s notes. He can ask us to describe a lesion. But MOST IMPORTANTLY, do a correlation between what is happening in the mouth and the pathologic report. Do this format: description, demographic, histology, differential DX, prognostic. Description of lesion example: nodule. Couleur rose pale. Sur intérieure de la muqueuse jugale. Cécile (base + large que top) ou pédiculée (top + large que base) Primary lesions: (9) Macule: plane, alteration of color (any color) Papule: slightly raised, NO liquid, variable size (< 5 mm)  Plaque: slightly raised (like papule), size > 5 mm Nodule : raised surface, larger than papule, + profondeur (sub-cutanous or sub- muquous), masse tissulaire Tuméfaction: PATHOLOGICAL increase in volume (gonflement), NO palpable mass Vésicule: raised WITH LIQUID (serum, blood, plasma), caused by formation of cavités intra-épidermiques, dimension < 5 mm Bulle: raised WITH LIQUID (serum, blood, plasma), similar to vésicule but larger at its base and + deep, diameter > 5 mm Pustule: contains pus Kératose: white-colored lesion, caused by exaggerated deposition of keratin on epithelium surface scale = squames ; exorciation = fissure Secondary lesions: (9) Érosion: superficial loss of tissue due to trauma, does NOT touch couche basale germinative, generally no scar (cicatrice) Ulcération: loss of continuity of surface epithelium, with or without scar  Fissure: depression in tissue resulting in linear loss of continuity of epithelium Pseudo-membrane: reaction from secondary mucous to necrotic agent, seen often in surface of ulceration Escarre: necrosis of tissue by thermal, chemical or gangrère Squames: accumulation of cellular fragments from couche cornée, may cover surface of erosion Desquamation: loss of superficial epithelium (détachement des squames) Croûtes: déssechement of exsudat (blood, plasma, pus) on surface of lesion Cicatrice : fibrous replacement tissue Quelques données démographiques: Âge: ▪ Gingivostomatite herpétique primaire: ENFANTS > adultes ▪ Herpes buccal récurent : ADULTES > enfants Sexe : ▪ Cancer buccal et leucoplasies : FEMMES > hommes ▪ Lichen plan : HOMMES > femmes Race : ▪ Dysplasie cémento-osseuse périapicale : NOIRS > blancs ▪ Maladie Paget et lupus érythémateux : BLANCS > noirs Sites : ▪ Cancer buccal : plancher et bord latéral > palais dur ▪ Leucoplasie chevelue : latéral > ailleurs ▪ Nodule sur joue : polype fibro-épithélial ▪ Nodule sur palais : tumeur glande salivaires mineurs Prévalence : ▪ Lichen plan > lupus érythémateux ▪ Leucoedème > noevus blanc spongieux Signes vs symptômes : ▪ Signes : something you can see, objective ▪ Symptôme : something the patient describes, subjective Cours 2: Maladies osseuses Ostéogénèse imparfaite : 5 types, HEREDITARY, may be lethal COL1A1 + COL1A2 in 90% cases ; affects MUTARATION of type 1 collagen (bone, ligament, dentine, sclère) Clinical: bone fragility, fractures +++, hearing problems, sclère bleue (CARACTERISTIC, exam?!) Less severe in DP Prevalence of class III MALOCCLUSION, crossed occlusion, béance antérieure (due to MAX hypoplasia +/- MAND hyperplasia RX: thin cortical bone, generalized OSTEOPOROSIS, bilateral TRUMATIC cysts Histopathology: immature bone w/ lack of lamellar bone formation, matrice ostéoïde REDUCED, trabeculae are thin/short/disorganized TX: symptom control (bisphosphonates) + prevention of fractures Ostéopétrose : 3 types, rare HEREDITARY metabolic disease Caracterized by bone densification; caused by defect in OSTEOCLASTE functioning or differentiation (bone does NOT resorb) Many genes identified (among some that code for RANK, RANK-L, OPG); causing disorder in the production of acids in “lacunes d’Howship” & inadequate molecular exchanges Histopathology: obliteration of medullar cavities by dense compact bone; we may either see unchanged/increase in osteoclasts or decrease. If unchanged or increased, absence of “lacunes d’Howship”. If decreased (almost absent), RANK & RANK-L anomaly.  TX: bone marrow allograft (alogrèffe moelle osseuse) for “maligne infantile” only IF adequate genetic DX & absence of neurological effect ; symptomatic treatement for all other forms. Transfusions are done to treat for anemia, and osteomyelitis should be treated Pronostic: lethal for “infantile”; other forms have better outlook Ostéopétrose maligne infantile: ▪ DX during birth/childhood ▪ Description: lack of white and red blood cells, as well as platelets (plaquettes); obliteration of medullar cavities & replacement of bone marrow (moelle osseuse) by compact bone (os compact), sclerosis of cranial foramens (which can cause nervous compressions) ▪ Results in: anemia, increased risk of infections and bleeding; increased fragility & fractures + difficulty to visualize roots + decreased vascularization (mandibule –> very high risk ostéomyélite); facial paralysis, blindness and deafness (paralysie facial, cécité et surdité) Ostéopétrose intermédiaire: ▪ Most symptoms shown around 10 yo, bone marrow stays fonctionnal (generally) ▪ Moderate anemia & extramedullary hematopoiesis (hématopoïèse extra-médullaire) Ostéopétrose adulte: ▪ 40% asymptomatic ▪ Description: cranial nerve compression, bone fractures, ostéomyélite mandibulaire ▪ Gene manifests itself on chromosome 1 Dysplasie cléido-crânienne : Gene RUNX2/Cbfa1 on 6p21 chromosome (6) The gene controls osteoblast differentiation from mesenchymal cells during membranous ossification; & chondrocyte maturation during endochondral ossification RUNX2 seems to play a role in odontoblast differentiation, formation of enamel and proliferation of dental lamina Description: rare condition with NO predominance, autosomal dominant with complete penetrance, 40% cases have NO family history, normal intelligence Clinical symptoms: pt have clavicular, cephalic, and dental anomalies; hypoplasia of clavicula is typical and usually partial, but BILATERAL: 10% have complete aplasia; pt have small size and certain characteristics: large skull, hypertelorism, pronounced frontal bossing, widened and depressed base of the nose Buccal anomalies: palatine vault is high, narrow and hollowed out (voûte palatin haute, étroite et creusée); high prevalence of palatin fissures, maxillary hypoplasia and relative mandibular prognathism Dental anomalies: extended retention of primary teeth, and delayed eruption of permanent teeth; MANY supernumerary teeth (dents surnuméraire) up to 50 teeth! Causes dentigerous cysts (kystes dentifère) TX: restore pt esthetic & function (but, in most cases asymptomatic). Extraction of primary teeth Maladie de Paget: Nom alternative: ostéite déformante Description: INCREASED bone remodeling (cause hypertrophie et désorganisation os COMPLÈTE), deformities & microfractures causes pain, 2nd most COMMON metabolic bone disease (osteoporosis is #1) Démographie: England, West Europe, britannique émigrés, 60 yo and + (frequency INCREASES with age), slightly more common in MEN. Étiologie: unknown but related to ENVIRONNEMENTAL and GENETIC factors which cause osteoclast (& potentially osteoblast) function deregulation. 10-20% have POSITIVE family history, POLYOSTIQUE > monostique Sequestome 1 (SQSTM1): most common MUTATION, codes for p62 (activates NF-κB which INCREASES osteoclast activity), 20-50% of those with positive family HISTORY, 5- 20% in other cases, most SEVERE form & YOUNG age Osteoclast precursors have VERY high AFFINITY for factors that STIMULATES bone RESORPTION: 1,25(OH)2D3 + RANKL + interleukine-6 (IL-6) Pathologie: deregulation in FORMATION & bone RESORPTION process. o Phase lytique: bone is resorbed (by numerous large osteoclasts with many o nuclei) + bone remodeling is VERY FAST o Phase mixte: resorption process accompanied by excessive bone deposition by osteoblasts. The bone formed is ANORMAL. The collagen is ANARCHIQUE. Bone vasculisation is INCREASED. o Phase sclérose: Bone deposition is PREDOMINANT. Bone is BAD quality and DISORGANIZEED. “Mosaique à l’os”. Bone is WEAK and vascularisation is REDUCED.  Clinical Symptoms: o Os affectés (most to least): iliac bone, lumbar vertebrae, femur, tibia and skull (crâne = signe xpeau) o Atteinte mâchoires = 17% (more MAXILLARY), enlargement of the middle third of the face (“tete de lion”), o Asymptomatic in MORE than 50% of patients, results in INCREASE of alkaline phosphates o Progressive INCREASE of skull circumference (densification) –> OBLITERATION of cranial foramens and nervous compressions (causes deafness and blindness) o Main symptoms: severe pain and DEFORMATIONS of long bones! Cavité buccal: o Symmetric ENLARGEMENT of alveolar ridge, lowering of the palatine vault (voute palatin) o Enlargement of alveolar ridge causes progressive INADAPTATION of denture (protheses dentaires) & DIASTEMA formation RX: o Loss of DIFFERENTIATION between SPONGY bone and CORTICAL bone; bone HYPERTROPHIA, osteolysis, generalized HYPERCEMENTOSIS o Phase lytique (diminution density): OSTEOPOROSIS (osteoporose circonscrite) + radioclaire au crane o Phase osteoblastique (augmentation density): CORTICO-MEDULLARY dedifferentiation + THICKENING outer skull; bone sclerosis « aspect de ouate de coton », generalized HYPERCEMENTOSIS and loss of lamina dura Laboratoire: o Bilan phosphocalcique NORMAL usually o Pyridinolines, Déoxypyridinolines and N-télopeptides (allows to measure remodelling) = biological markers  Histopathologie o Areas of OSTEOLYSIS adjacent to bone APPOSITION o INCREASED osteoblasts, lamellar bone is ABNORMAL (large fibres of collagen, partly calcified and misoriented). REPLACES spongy bone of the epiphyses, the cortical bone and fills the medullary cavity. Osteoclasts ++ VOLUME and nuclei (50-100!) o Bone TRABECULAE have a MOSAIC appearance, and are demarcated by reversal lines (lignes basophiles inversées) o (causes bleeding during extraction) o Advanced stages: acellular spherical masses FUSE to form large areas of sclerotic bone (causes osteomyelitis during extraction) TX: normalise biological markers, BIPHOSPHONATES (only if ACTIVE and risk of complications), adjustment or redo dentures, difficulty during extraction o Note: in severe cases, HIGH risk of osteomyelitis (ostéomyélite) during CHX Pronostic: o Low fatality o UNLIKELY risk of sarcoma: ▪ Osteosarcoma: 1%, mostly in long bones ▪ Fibrosarcoma: even lower risk ▪ Certain cases, large cell bone tumor may happen ▪ Increase in vascularization during active phases MAY cause congestive HEART failure (neurological symptoms are also possible) Chérubisme: HERIDITARY disease, BILATERAL and symmetric Autosomal dominant, variable expressivity and HIGH penetrance  Gene: SH3BP2 on chromosome 4 (4p16) Modifies osteoblastic and osteoclastic activity Touches MAXILARIES (rarely anything else) Clinical symptoms: o Starts during childhood between 2-5 yo, progresses until stabilizes at PUBERTY, appearance becomes almost normal at 30 yo o Causes maxillaries expansion (+++ common in MANDIBULE, tuberosities +++ in max) and certain aesthetic changes o Predilection site: ANGLE of mandibula and ascending RAMUS o BILATERAL and symmetric: bilateral non-painful swelling (tumefaction) that swells cheeks and stretches face (eyes downward) o “cherubin vers ciel”; speech, chewing and swallowing disorders Dental anomalies: o Agenesis of second and third MOLARS inf, absence or mvmt of primary & permanent, resorption or PREMATURE loss of primary and LATE eruption of permanent RX: o Radioclear, MULTILOCULAR, bilateral and symmetric implicating ANGLE of mandibule -> causes expansion, thinning and perforation of CORTICALES. o Advanced stages: GRANULAR aspect (“verre depoli”) o Teeth that are in lesioned sites may be impacted (incluse) or moved  Histologie : looks like granulome centrale à cellule géant (GCCG), but LESS dense stroma. Eosinophilic tissue MAY surround small blood vessels. Advanced lesions have + DENSE fibrous tissue, a LIMITED nbr of giant cells and newly formed bone trabeculae. TX : DO NOT TREAT with radiotherapy. CHX not RECOMMENDED (due to regression; only consider if very advanced). Extraction of included teeth, ortho and dentures are possible solutions. Hyperparathyroidie (HPT): Can be primary, secondary or tertiary. Primary: 85% caused by parathyroid ADENOMA. Hyperplasia or rare carcinoma of parathyroid gland cause 10%. Seen in syndromic cases, such as NEM-1/2. Caused by INCREASED serum PTH level + HYPERCALCAEMIA. Symptoms include: painful bones, renal stones, abdominal groans and psychic moans. Secondary: chronic renal failure is most COMMON cause. Vitamin D deficiency and PTH resistance are other possible causes. Decrease of phosphate excretion, hyperphosphatemia and hypocalcaemia. Stimulates secretion of PTH -> stimulates bone resorption AND increases serum CALCIUM level. Also reduces Vit D production -> reduces calcium absorption and leads to hypocalcaemia  RX: o OSTEOPOROSIS. Loss of cortical definition surrounding max sinus and mand canal. Loss of lamina dura. “Verre depoli”. Brown tumors (large cell osteolytic lesion) are sometimes observed. Laboratoire: bilan sanguine of primary -> hypercalcaemia, hypophosphatemia, INCREASED serum PTH level, increased urinary phosphate Histopathologie: REDUCTION of bone trabeculae count, INCREASED count of osteoclasts. Brown tumors ressembles GCCG, and is INDISTINGUISHABLE histologically; therefore, parathyroid gland function may be investigated. TX: o Primary hyperparathyroidism treated by CHX excision of adenoma or gland. o Secondary treated by organ transplant (restores calcitriol function and normalizes phosphate/calcium level). o Parathyroidectomy recommended if pt does NOT respond to TX Maladies osseuses d’origine diverses Ostéosclérose idiopathique: Region with dense bone, NOT associated with infection/dysplastic/neoplastic or systematic condition DX dif: ostéite condensante (has INFLAMMATORY process) Investivage for Garner syndrome IF MULTIPLE lesions Clinic: prevalence is 5%; 90% in posterior region of mandibula. No predilection for gender. Completely ASYMPTOMATIC, causes no expansion of cortical bone and tooth remains ALIVE RX:  o Radio-opaque, usually alone o Well defined & does NOT have radioclaire ligne around it o The possible differential diagnosis are: ostéite condensante, dysplasia cémento- osseuse périapicale, cémentoblastome, ostéome TX: dx from x-ray is sufficient Ostéite condensante (sclérosante): Region with dense bone, from INFLAMMATORY process (eg. Maladie pulpaire, lesion apical, atteinte paro); teeth is NOT necessarily dead (if paro) Prevalence: kids or young adults. Touches mostly premolar/molar of MANDIBULA and does NOT cause any bone expansion RX: o Radio-opaque at apex, no radioclaire contour o Affected tooth usually manifests a deep carious lesion, defective restauration, thickening of periodontal ligament or periapical inflammation DX: in cases of doubt, vitality test allows to differentiate with idiopathic osteosclerosis TX: elimination of what causes inflammation (eg. Extraction or endodontic treatment) Défaut ostéoporotique localisé de la spongieuse osseuse : Caused by hematopoietic tissue collection, resulting in radiotranslucent region Prevalence: 75% adult WOMEN. Touches posterior of MANDIBULA, especially edentulous areas Clinic: always ASYMPTOMATIC  RX: radiotranslucent region that is POORLY defined, with fine bone trabeculae. NO signs of bone expansion or sclerotic reaction in periphery Histopathologie: NORMAL collection of hematopoietic cells and bone trabeculae TX: x-ray is non diagnostical; a biopsy must be done to exclude other pathological condition Granulome centrale à cellules géantes (GCCG) : Benign intraosseous lesion Presents certain mutations : TRPV4, KRAS, FGFR1 Prevalence: WOMEN 3 :1 (3 times more likely), all ages but 60% of cases are seen in UNDER 30. Mandibula, especially anterior to 1st permanent molar, is the predilection site Careful: if BILATERAL, investigate for chérubisme! Clinical: 2 types o Non-aggressive: ▪ SLOW growth and LOW recurrence rate ▪ Mostly ASYMPTOMATIC o Aggressive: ▪ More in YOUNG pt ▪ FAST growth and HIGH recurrence rate ▪ LARGE size when discovered ▪ Symptoms: pain, paresthesia, expansion/perforation of bone cortices, extension into soft tissues, ulceration of the surface mucosa and dental resorptions RX: radioclaire lesion, uni/multilocular w SEPTAS. Granular appearance. Well defined, but NON-corticated. In maxillary, lesions are MAL defined and imitates a malignant process  Histopathologie: o Cellular proliferation in highly VASCULARIZED stroma o Population of fusiform/oval MONONUCLEAR cells and population of MULTINUCLEATED giant cells of OSTEOCLASTIC nature o Number, form, and dimension vary CONSIDERABLY from case to case o Stroma demonstrates areas of HEMORHAGE and EXTRAVASION of red blood cells, hemosiderin deposits, and trabeculae of osteoid or immature bone TX: CHX -> conservative IF non-aggressive; aggressive requires larger excision with extraction of teeth present in lesioned site Lésions fibro-osseuses bénignes: Normal bone replaced by COLLAGEN fibers ; can resemble to immature bone (ostéide), bone or tissue similar to dental cement Developmental, reactional (dysplasique) & neoplastic conditions Dysplasie fibreuse: “Défaut développement” GNAS gene, on chromosome #20 Severity depends on when lesion happens Two forms: MONOstotique vs POLYostotique Can present cutaneous and endocrinal symptoms Dysplasie fibreuse MONOstotique: o +++ frequent, 80-85% cases o No predilection by sex ; maxillaries = predilection site  o Touches: ribs (côtes), femur, tibia and maxillaries Dysplasie fibreuse POLYostotique : o 2+ bones (up to 75% of bones) ; often only ONE HALF of body o Predilection: WOMEN o Clinical: symptoms related to long bones (pain, deformities, difference of length, fractures) o Cranio-facial injury: facial asymmetry, vision issues, loss of hearing, nasal congestion, obstruction of upper lungs o Skull injury: neurological symptoms o 2 syndromes: Jaffe-Lichtenstein & McCune-Albright Jaffe-Lichtenstein syndrome (polyostotique): o Cutaneous pigmentation (taches café au lait) ; affects TRUNK (tronc) and THIGHS unilateraly, but can also touch buccal mucous McCune-Albright syndrome (polyostotique): o Cutaneous pigmentation (taches café au lait) + ENDROCINAL disorders (early puberty in girls, hyperthyroidism, diabetes or pituitary adenoma) o Dental anomalies: oligodontia, tooth movements, taurodontism, enamel disorders and prolonged PERSISTANCE of primaries Cranio-facial area: MONOSTOTIQUE form is most common, with predilection at POSTERIOR of MAXILLARY; symptoms start at childhood or teenager; slow EXPANSION (buccal + lingual) of arcade with movement of teeth ; teeth remain VITAL RX: o Initial: lesions begin radio-claire (similar to cyst) and become mix  o Final: bone DENSIFICATION (radio-opaque), “pelure d’orange ou verre dépoli” (EXAM !!), poorly defined contour o Cortical EXPANSION (without breach), loss of lamina dura, OBLITERATION of sinus o May move mandibular canal upwards: key tale SIGN of fibrous dysplasia Histopathologie: o well-VASCULARIZED connective tissue stroma w/ woven bone trabeculae (CHINESE characters), variable # of osteoCLASTS o NO caspule (not surrounded by osteoblasts), fuses with regular bone o Trabaculae: irregular, curvilinear, imature TX: o Growth is MAXIMAL in childhood and teenage years, STABILIZES with bone MATURITY o Conservative TX, ideally DELAY until END of growth o If deformities are minon = no TX o If major = “ostéotomies modelantes” AFTER growth end ; if in active phase, 20- 50% risk of recurrence o May cause: hemorrhagic cystic lesions (kyste osseux anévrysmal) or GCCG. Risk of sarcoma transformation is VERY low (seen in radiotherapy) o EXAM!!! NEVER EVER DO RADIOTHERAPY o DX dif: ostéite et ostéomyélite (cortical breach + sequestres) Dysplasies cémento-osseuses: MOST frequent LFOB (lesions fibro-osseuses benign) of maxillaries ABNORMAL et DISORGANIZED bone production with NO risk of malignant transformation DX dif: epithelial dysplasia (risk MALIGNANCY) 3 conditions: periapical, focal, familial floride o Periapical: ▪ +++ frequency in BLACK WOMEN, 30-50 yo (70% of cases) ▪ WOMEN: Men ratio = 10-14:1 ▪ Predilection: ANT of MAND ▪ Asymptomatic, all teeth are VITAL (EXAM!!!) ▪ Periodontal ligament stays INTACT w/ NO bone expansion ▪ Stade OSTEOBLASTIQUE = MIXTE lesion ; radio-opaque centre in radioclaire lesion ▪ Stade MATURATION = +++ radio-opaque with thin radioclaire contour ▪ Histopathology: maturation –> amas os lamellaire + spherules denses, peu vascularisé o Focale: ▪ WOMEN, 20-50 yo = 90% patients ▪ BLACKS +++, but also seen in whites (contrary to periapical) ▪ Predilection: POST of MAND ▪ Possible expansion, but RARE ▪ DX dif: fibrome cémento-ossifiante (EXPANSION!) ▪ 3 stages: radio-claire, mixte, radio-opaque with WELL-defined irregular periphery ▪ ++ zone édentée, but also apex  ▪ No TX o Floride : ▪ BILATERAL + MULTIFOCAL ▪ WOMEN, BLACK, average aged ▪ Predilection : POST of maxillaries ▪ DX dif : maladie Paget (IF +++ EXPANSION) ▪ Maturation phase may : GENERALIZED effect on alveolar bone ▪ Radioclaire lesions (kystes traumatique) can develop in radio-opaque regions ▪ Maturation: radio-opaque lesion surronded by radio-CLAIRE line ▪ Clinical : most DANGEROUS –> bone is sclerotic, little vascularization susceptible to OSTEOMYELITE ▪ Pt must have EXCELLENT HYGIENE + regular visits ▪ Active infection: ANTIBIOTICS, not effective thought (may need excision of bone) Cémentome gigantiforme familiale: HERIDITAIRY AD, very RARE, WHITES (EXAM!!!) Benign neoplasm of maxillary: 1. Fibrome cémento-ossifiante: Benign neoplasm Demography: WOMEN 5:1, WHITE > African > others Predilection: premolar-molar of MAND (EXAM!!) RX: o Well DEFINED, UNILOCULAR, radio-claire/mixte o Usually has thin radio-claire line o Teeth are moved/resorbed  o Expansion osseuse concentrique POSSIBLE o Curvature of INF border of MAND = characteristic of MAND lesions Histopathologie: VASCULARIZED fibrous CAPSULE , large single fragment tumor (easily removed) or many large fragments ; OSTEOBLASTIC rimming (surrounding), immature bone trabeculae, little hemorrhage TX: enucleation, excellent prognosis, NO risk of malignancy or recurrence 2. Chondrome: Tumor of CARTILLAGE, only in maxillaries DX dif: chondrosarcoma bien différencié (EXAM !!) Predilection : ANT of MAX + condyle TX : AGGRESIVE, complete ablation, condylotomy (if touches condyle) 3. Ostéome: Composed of MATURE, lamellar (compact) and SPONGIOUS bone Predilection : head & neck and maxillo-facial region Slow, asymptomatic growth, possible facial ASYMETRY RX: dense, radio-OPAQUE Multiple osteoma: Gardner syndrome: o APC gene, chromosome 5, AD o 1/3 cases = NEW mutation o Osteoma localized on angle of mandibula = VERY characteristic o +++ dents SURNUMERAIRES INCLUSES, odontomes, kystes dentifères o Polypes intestinaux (13-25 yo) = close to 100% risk malignancy!! (early dx allows resection of colon and saves lives) o Extra-oral: epidermic cysts, cutaneous fibroma, desmoid tumors  Ostéome ostéide: o LESS than 2 cm o Very RARE in maxillaries o Nocturnal pain helped by aspirin, tumor secretes prostaglandin o RX: radio-claire (or radio-opaque centre), well-defined, osteosclerotic contour Osteoblastoma: o Maxillaries = 10% cases o WOMEN, POST of MAND o 85% cases in YOUNG pt ( epith cell degeneration & inflammation -> higher OSMOTIC pressure -> draws more liquid & higher ORTHOSTATIC pressure -> resorbs structures + symmetric GROWTH of cyst SLOW growth (allows sclerotic reaction) RX: radioclaire, WELL-defined cortex & contour, symmetric, unilocular (usually) Exam: lumière kystique, épithélium revêtement et paroi tissu conjonctif Microscopic exam allows differentiate between types of cysts (eg. developmental vs inflammatory) NOTE! Difference between radicular cyst, residual cyst and inflamed dentigerous cyst CANNOT be made histologically  Odontogeneses cysts origin: Malassez epithelial debris, Serres debris or reduced enamel epithelium Kystes Odontogène: 1. Inflammatory a) Kystes radiculaire: From Malassez epithelial debris coming from necrotic pulp (chronic inflammation) Forms periapical granuloma Inflammation from pulp causes PROLIFERATION of Malassez debris -> forms islands of epith -> lose vascularization & degenerates w/ LIQUIDE over time -> forms multiple microcavities -> microcavity fusion causes cyst Inflammatory factors play a role: interleukines + protaglandines 50-75% cases in MAXILLARIES (MOST frequent) 30-50 yo, rarely in primary Predilection: MAX > mand, ANT Non-vital Usually ASYMPTOMATIC, unless very large (causes bone expansion) RX: attached to tooth root, may have thin radio-opaque contour, loss of lamina dura continuity, may resorb tooth DX dif: granulome périapical (histopathology, same TX) Histopathologie:  o Epithelium = Pluristratified, non-keratinized, pavimenteux (can become hyperplasic with formation of anastomosing arcades) o Contour = Dense conjunctive tissue w/ chronic inflammatory cells (lymphocytes + plasmocytes) (if aigue = polynucléaires) o Cyst: brown liquid w/ debris o Other: mucus cells + ciliated cylindric epith, zones of hemorrhage + macrophages that phagocyte hemosiderin, foam cells (macrophages spuneux) that phagocyte lipids, dystrophic calcifications, cholesterol cristals, Rushton body (corps easonophile fines/lineaire/épigle in 10% kystes radiculaires) b) Latero-radicular cyst: Touches LAT root of NON-vitale tooth Stimulates Malassez debris to form cyst DX dif: kyste lat paro *dent vital Histopathology: same as radicular periapical cyst c) Residual cyst: Cystic transformation of RESIDUAL granuloma or incomplete elimination of ABANDONED periapical cyst May be LARGE size, but LESS inflammation (since source is removed) TX: EXTRACTION of tooth + curettage OR ROOT CANAL i. Ablation chirurgical -> histopathology to identify if cyst or tumor ii. No recurrence d) Buccal bifurcation cyst (kyste bifurcation buccal): (KB) BUCCAL surface, 1st MANDIBULAR molar 5-11 yo kids, 1/3 BILATERAL RX: radioclaire buccal lesion on 1st mandibular molar (occlusal), apex of molar is deviated to lingual cortical, crown deviated to buccal TX: CHX ablation of lesion w/out extraction i. Alternative treatment -> daily saline-peroxide rinse  e) Paradental Cyst: Distal of 3rd mandibular molar that is sous-muqueuse or partiellement incluse & multiple episodes of pericoronitis Histopathology: cannot be distinguished from inflamed dentigerous cyst 2. Developmental Origin a) Dentigerous cysts Most COMMON developmental cyst Associated to dent incluse (develops around crown), attaches on enamo-cementous jct Develops following separation & accumulation of liquid between reduced epith of enamel and surface of tooth Touches: 3rd MAND molars, SUP canines, 3rd MAX molars; youth (20-30 yo) Usually asymptomatic, but large lesions may cause painless bone EXPANSION RX: associated to crown, tooth maybe moved to max sinus or ascending branch mandibula, may cause resorption to adjacent structures, can happen lateral to crown Histopathology: LOOSE conjunctive tissue w/o inflammation (may have inactive Malassez debris), PLURISTRATIFIED pavimentous epith (2-4 layers). If infected, will be + DENSE w/ mix of inflammatory factors (++ lymphoplasmacytic); epith will also be hyperplasic w/ elongation of retes pegs DX dif: o Dental follicle  o Ameloblastoma o Ameloblastic fibroma (youth) o Adenomatoid odontogenic tumor TX: enucleation of cyst + extraction of tooth** (IF third molars!) o Marsupialisation may be used to reduce large volume cysts (prevent fractures) o If canine, enucleation + ortho to restore occlusion o May cause ameloblastoma or muco/epidermoid carcinoma b) Eruption cyst Accumulation of clear fluid, during eruption of tooth dp or DP, may bleed if occlusion trauma (eruption hematoma) TX: none, rare cases excision to speed eruption c) Odontogenic keratokyste (KKO) From dental lamina debris (Serres) Different from other cysts: AGGRESSIVE, high-risk recurrence, distinct histology, different growth Does NOT grow by osmotic pressure, but rather by epithelial cell PROLIFERATION! Mutation on PTCH1 (chromosome 9) in all syndromic cases and 80% non-syndromic 3-11% odontogenic cysts, seen in 10-40 yo Predilection: mandibula (+++ vs max) in 60-80% cases, 3rd MAND molar + ascending mandibula branch May also touch PM or inc.  If big, VERY RARE non-painful expansion RX: may be uni or multilocular, cyst invaginates roots, 20-40% associated to dent incluse If MULTIPLE keratokystes, investigate Gorlin syndrome or multiple nevoid basal cell carcinomas Histopathology: THIN fibrous conjunctive tissue w/ microcysts, 6-8 layers of pavimentous (ondulated) and parakeratinized laminate, basal cells are hyperchromatic & in palisade, absence of rete peges between conjunctive tissue & epith, epith separates easily (makes enucleation difficult) TX: CHX (cyst ablation) + vigourous curettage (ostectomie), modified Carnoy solution to REDUCE recurrence (30%), marsupialisation if too big; RX long term follow-up + can transform in ameloblastoma or epidermoid carcinoma Gorlin syndrome: ▪ AD, 5% pt with MULTIPLE kerotocysts ▪ Young ++, HIGH potential recurrence, ▪ Histology: MORE microcysts  ▪ Signs: bone, cutaneous, neurological ▪ Bone: bifid ribs, mild mandibular prognatism, hypertolerism, broad nose base, flat face, frontal bossing ▪ Cutaneous: nevoid basal cell carcinomas (no sun exposure), palmoplantar hyperkeratosis ▪ Neurological: calcification falx cerebri, medulloblastoma, ovarian fibroid Primordial cyst: DNE -> odontogenic keratocyst d) Orthokeratinizing odontogenic cyst: 2/3 of cases = dentigerous cyst in RADIO/HISTO Predilection: young ++, POST of mand Very low recurrence, non-aggressive Histology: pavimentous and ORTHOkeratinized epith (NOT hyperchromatic/palisade) e) Lateral periodontal/gingival cyst (DX dif: kyste lat-radiculaire inflammatoire) (KLP) Lateral periodontal = rare, lat of root on VITAL tooth, 30-60 yo mostly MEN Origins from dental lamina (Serres) Periodontal predilection: mand premolar-molar (75%), max sup incisor Gingival predilection: 40-50 yo, canine-PM INF + inc-canine-PM SUP, tumefaction w/ liquid on BUCCAL (rarely other)  RX: lat surface, forme poire ou goutte d’eau (round), slight DIVERGION of roots ; gingival = no change bcz soft tissue Histopathology : conjunctive tissue w/o inflammation, THIN epith (layers of cuboidal cells) ; areas focal thickening, formed by clear cells (++ glycogen), “epithelial plaques” TX: periodontal cyst -> enucleation + preserve tooth vitality ; gingival cyst treated by surgical excision DX dif: lat-radicular inflammatory cyst, odontogenic keratocyst, other (ameloblastoma, odontogenic fibroma) f) Botryoid cyst MULTILOCULAR form of lat periodontal cyst “Bourgeons nodulaires” like « grappe de raisins » Multiple cystic cavities in fibrous tissue Epith/TX similar to lat periodontal cyst – but HIGH recurrence g) New born’s gingival cyst Proliferation of dental lamina (Serres), WHITE NODULES on alveolar ridge Predilection: MAX Histology: many keratine “squames” + thin layer (1) PARAkeratinized multistratified squamous epith h) Calcifying odontogenic cyst (Gorlin, KOC) Controverted 80% cases cyst, 20% have odontomas ; 2 forms: central + peripheric 20-40 yo, ANT of mandibula/max, causes EXPANSION (non-painful) RX: unilocular, well-defined (30-50% have opaque calcifications), 30% dent incluse DX dif: odontogène épithéliale calcifiante, fibro-odontome améloblastique, odontome Histology : presence of GHOST cells (pale, eosinophilic, no nuclei, calcifications), basal layer is CUBOIDAL/CYLINDRIC in PALISSADE shape w/ hyperchromatic nuclei. Superficial layer has cells with “longs prolongements cytoplasmic”, similar to reticulum étoilé TX : CHX + follow-ups (recurrence very low)  i) Glandular odontogenic cyst (KGO) Origin: Serres debris Adults 40yo+, ANT mandibula, large size (multilocular >> uni), can PERFORATE corticals ! TX : recurrence -> 25-30% -> aggresive CHX + follow-up Histologie: cuboidal w/ c. ciliés + mucus cells, TC has NO inflammation Non-Odontogenic Cysts: 1) Nasopalatine duct cyst + cyst incisive papilla (kyste canal nasopalatine, KNP) Seen in nasopalatine duct (incisor canal), ANT of palate Most COMMON non-odontogenic cyst (nasopalatine) Develops from epith debris PROLIFERATION of nasopalatine canal Seen in soft tissue at exit of foramen incisive (cyst of incisive papilla) Clinic: o Incisive papilla: blue-colored swelling on papilla, usually asymptomatic o Nasopalatine duct: MEN 30-50 yo, usually asymptomatic but may cause TUMEFACTION of ANT palate RX: o Between roots of SUP central INC, variable shapes (pear, heart, etc), usually SCLEROTIC border o If < 6 mm, normal foramen. If > 6 mm, suspect nasopalatine cyst.  Histopathology: o Depends on position of cyst in canal. If near nasal cavity, PSEUDOSTRATIFIED. If inflammation or near buccal cavity, PLURISTATRIFIED PAVIMENTOUS. Most commonly has multiple types of epith. o Must contain following: blood vessels, nerves and mucous glands (normal) TX: enucleation or radiographic follow-up (many nerves in cyst = parathésie risk) 2) Nasolabial cyst Cyst of soft tissue –> mucous fold between upper lip and nose wing (aile nez) Cystic degeneration of epith debris that form naso-lacrymal canal Predilection: WOMEN 30-40 yo, causes inflammation in soft tissus in canine region RX: none (soft tissue) Histopathology: pseudostratified columnar epithelium with several GOBLET cells TX: enucleation 3) Palatal cysts of newborn Nodules of keratin, white yellowish seen in palate, often in median raphe region. Epith debris from minor salivary glands form cyst No treatment (empties itself)  4) Globulomaxillary lesions (DNE) ALMOST all develop from odontogenic epithelium in upper lateral incisor and canine. In 50%, lesion compatible to odontogenic cyst with inflammatory origin (radiculaire or lat-radiculaire). Other cases, lateral periodontal cyst OR odontogenic TUMOR RX: radioclaire causing diversion between roots of canine and LAT SUP inc. Vitality allows to differentiate nature (whether inflammatory or no) 5) Median palatine (posterior) cyst Considered variant -> post nasopalatine cyst To dx actual cyst = EXPANSION on palate, post to incisive papilla 6) Median mandibular cyst MAND median line Represent odontogenic cysts (glandular odontogenic, odontogenic keratocyte, lat periodontal, PA) Pseudocysts of maxillaries: NO EPITHELIUM 1) Aneurysmal bone cyst (ABC) Most frequent in long bones, but also in maxillaries Cause: vascularization DISORDER of bones -> primary cause or secondary to pre- existing bone lesion (arteriovenous malformation, fibrous dysplasia, GCCG) Predilection: long bones + vertebrae. Maxillaries only 2% (post of MANDIBULA ++ common). LESS than 30 yo!  Clinic: RAPID PAINFUL swelling of mandibula, tooth are moved or resorbed RX: uni/MULTI locular w thining of CORTEX (may perforate) Histopathology: vascular spaces do NOT have endothelial cells (blood w/out epith). 20% may identify lesion such as GCCG or fibro-osseux TX: curettage or enucleation +/- cryotherapy 2) Traumatic cyst Synonyms: hemorrhagic, solitary (EXAM!!) Empty intraosseous cavity Original theory: trauma -> hematoma (bone bleeding) -> hematoma disintegration creates cyst (DNE non-trauma cases) Predilection: long bones. Post of MANDIBULA for cases in maxillaries. YOUNG 10-20 yo (very rare < 5 yo OR > 35 yo). Teeth stay VITAL. RX: larger cysts go between roots of adjacent teeth = apparence lobulée or festonée –> similar to KERATOCYTE and MUST INVESTIGATE (EXAM!) Histopathology: thin conjunctive tissue, bone shows signs of remodelling TX: CHX essential for DX. If causes bleeding during CHX, confirms hematoma DX and helps bone regen. 3) Stafne bone cavity Depression in LINGUAL cortex of mandibula, in molar region where sub-mandibular salivary gland is found. Predilection: POST mand, between molars and mandibula angle, SUPERIOR to mandibular canal  Developmental anomaly (even tho found in adults), RX similar to cyst. Cavity is static (no evolution) No TX (DX made from clinical + RX) Kystes des tissus mous: 1) Cervical lymphoepithelial cyst Developmental, asymptomatic, + young, fluctuating/moving mass Location: LAT of neck, ANT to SCM muscle Similar lesions -> parotid/sub-mandibular glandes in HIV pts; intra-oral form exists Histopathology: PLURIstratified, pavimenteux, PARAkeratinized; TC w/ +++ LYMPHATIC tissue/follicules TX: biopsy by aspiration required usually, EXCISION 2) Intraoral lymphoepithelial cyst RARE Develops on lymphatic tissue in mouth -> Waldeyer lymphatic ring, ventral surface tongue, floor of mouth, soft palate YELLOW-WHITEISH, slightly raised, asymptomatic, young adults ++ Histopathology: ++ “squames keratin”, same as cervical type TX: recurrence VERY RARE, excision, excellent prognosis 3) Dermoid cyst (from inclusion of multipotent epith c. floor of mouth) Developmental, cystic form of teratoma tumor Predilection: floor of mouth, young adults +++  Clinical: depends on location (above or below mylohyoidien), mass is mobile/soft due to ++ keratin & sebum o Above = intraoral tumefaction MOVES tongue UPWARDS + BACKWARDS o Below = neck tumefaction on median line giving double chin appearance Histopathology: PLURIstratrified, pavimenteux, ORTHOkeratinized; cyst wall (paroi) contains SEBACOUS glands, sweat glands (SUDORIPARES) and pilosebaceous follicles (PILO-SÉBACÉS) TX: excision, good prognosis 4) Epidermoid cyst Similar to dermoid, but different pathogenesis (from hair follicles, one of MOST common cysts on skin/face) + cyst wall does NOT contain EPIDERMAL ANNEXES Most simple form of teratoma in buccal cavity Similar to epiderma of skin Histopathology: same, w/o epidermal annexes. Granular layer is preeminent. « Lumière kystique » filled w/ DESQUAMATED KERATIN TX: excision, good pg 5) Thyroglossal tract cyst Cyst forms on thyroglossal canal (when epith persists), fluctuating/mobile mass MOST common developmental cyst of NECK, found on thyroid gland (median line) Predilection: ABOVE hyoid bone, young +++ (less 20 yo) Histopathology: pluristratified, pavimenteux or CILIATED COLUMNAR, cyst wall contains thyroid tissue Associated cancer: papillary adenocarcinoma of thyroid gland TX: excision, conservative tx has HIGHER recurrence, ensure that other functional thyroid tissue are present before CHX Other cysts: 1) Mucocèle et grenouillette Does NOT have epith, results from MUCUS extravasation following rupture of canal from salivary gland 2) Kyste de rétention muqueux Salivary origin cyst caused by SALAVARY GLAND BLOCKAGE 3) Kyste cilié du maxillaire Caused by CHX intervention in MAX sinus (Calwell-Luc operation) or following difficult EXTRACTION in MAX. Can reach significant size, most COMMON in JAPAN Tumeurs odontogènes d’origine ÉPITHELIALE: From epithelial OR ectomesenchyme elements EXCLUSIVE to maxillaries (lame dentaire) Location: interior of bones OR periphery (gum or edentulous alveolar ridge) Eg. o Ameloblastoma resembles soft tissues in enamel organ o Myxome odontogène ressembles dental PAPILA o Fibrome améloblastique/odontoma ressembles enamel organ, young pulp, hard tissues of tooth To know: o Biological behaviour varies greatly; some are hamartomas ( or benign neoplasms, while very are malignant o Advanced lesions associated to cortical expansion  o Malignant forms may present intraoral tumefaction, cortical swelling, often pain! o Classification is based on biological behaviour (benign or malignant) AND interaction between epithelial and ectomesenchymal elements (EXAM!) 1) Ameloblastoma: benign epith tumor True neoplasm of enamel organ, locally AGRESIVE May invade structures LOCALLY, and recurrence is common if conservative TX MOST frequent odontogeneses tumor after odontoma 3 types: conventionelle (solide OR multikystique), unikystique, périphérique ; DESMOPLASTIC is histologicaly variant (RX similar to LFOB) TX/prognosis varies based on situation Some forms = malignant Forms: o Conventionelle: ▪ Age: 30-60 yo (rare < 20 yo) ▪ No SEX predilection ▪ Predilection: 85% MAND, specifically molar, mandibule angle and branche montante; when MAX = molars, can INVADE sinus max + base of skull (causes DEATH!) ▪ Asymptomatic usually, advanced cases present tumefaction (non- painful) that may PERFORATE corticals ▪ RX: radioclaire, uni or multi (+++ common)-locular « Bulle de savon, grappe de raisins, nid-d’abeilles » Teeth may be moved, often resorbs ADJ roots  Usually DENT INCLUSE -> 3rd molars Tumor invades spongy bone trabeculae w/o resorbing it (lesions appear smaller) ▪ (Tomodensitometry + MRI can detect true size) ▪ DX dif: myxome odontogène, kératokyste odontogène, GCCG, hémangiome, kyste osseux anévrysmal ▪ Histologie: 2 types -> folliculaire OR plexiforme Folliculaire o « Îlots epith odontogène » o Basal cells are HYPERCHROMATIC, palisade w/ inversed polarisation o Cells (in centre) inside epith are spaced + polyédrique, similar to reticulum étoilé, OFTEN have cystic degen o TC is vascularized & present b/w epith islands Plexiforme: o ANASTOMOSING trabeculae of epith cells in VASCULARIZED stroma o Periphery cells are HYPERCHROMATIC, palisade w/ inversed polarisation o Cells (in centre) are FEW and similar to star reticulum o LOOSE stroma, well-vascularized w/ sign of DEGEN (+ RARE than folliculaire)  Other variants (+++ rare) o “Métaplasie malpighienne” = améloblastome acanthomateux (similar to epidermoid carcinoma OR squamous odontogenic tumor) o Granular degeneration = améloblastome granulaire (aggresif) o Améloblastome desmoplastique = ANT of max/mand, b/w 30-50 yo, MIXTE (similar to fibro-osseux lesions), poorly defined contour, cystic degen is rare ▪ TX: curettage -> 50-90% recurrence -> wide excision w/ healthy margins (1.5-2 cm) OR bloc excision (advanced lesions) o These TX have 15% recurrence o MAX lesions are ++ aggressive (less dense vs mand, harder to excision due to proximity to vital structures) o Unicystic: ▪ NOT aggressive, YOUNGER pt vs conventional ameloblastoma (23 yo avg) ▪ Predilection: 90% in POST of MAND (often 3rd impacted molar) ▪ RX: cystic presentation (radioclaire) ▪ DX dif: dentigerous, odontogenous keratokyste ▪ Histologie: 2 types Luminal: o Cystic lesion has epith w/ ameloblast appearance o Nodules of tumoral plexiform ameloblastoma seen in lumière, no proliferation in TC  Mural (+ aggressive, + recurrence) o “Îlots” of follicular/plexiform ameloblastoma in TC, MAY have proliferation in lumière ▪ TX: ENUCLEATION + aggressive curettage (ONLY for MURAL & IF +++ infiltration –> 10-20% recurrece) o Périphérique: ▪ Very RARE, origins from gingival epith or odongenous debris ▪ GINGIVAL growth, non-painful/ulcerous (similar to polype fibro-epith) ▪ Predilection: MAND > max, POST ▪ ABSENCE of bone damage ▪ Superficial erosion may be seen in corticals ▪ Histology similar to conventional amelobastoma ▪ “Métaplasie malpighienne” OFTEN PRESENT ▪ TX: excision (CHX), 25% recurrence o Malin: ▪ Very RARE, can send METASTASIS in lungs ▪ Histology: conventional ameloblastoma –> NO signs MALIGNANCY o Carcinome améloblastique : ▪ Histology: follicular/plexiform ameloblastoma w/ signs MALIGNANCY (cellular pleomorphism, hyperchromatism, ++ MITOSIS/necrosis) ▪ VERY aggressive, RAPID perforation of bone plates + tumoral EXTENSION in soft tissue ▪ RX (resembles malignant): POORLY defined, INFILTRATION of surrounding structures  ▪ Predilection: 60% MAND, in POST, 30% recurrence/metastasis 2) Épithéliale calcifiante (Pindborg, 1%) Origins from STRATUM INTERMEDIUM cells of enamel organ Predilection: 20-60 yo (40 yo avg), PM-MOL of MAND, 50% dent incluse Initial: asymptomatic; final: slow & progressive tumefaction of bone plates RX: MULTILOCULAR (unless initial phase), radioclaire (unless +++ calcifications) o Note: if calcifications are present, they are localized on crown of impacted tooth Can cause cortical EXPANSION or resorption of roots Histology: proliferation of polyedric epith cells (HYPERchromatic nuclei + prominent intercellular junctions), arranged in cords or islands, in collagenized stroma. Caracteristic –> globules of amyloid substance, amorphous hyaline appearance + concentric calcifications in amyloid substance (anneau de Lisgang; can give mixte appearance) TX: excision w/ little bit of healthy tissue, 15% recurrence 3) Squameuse (malpighienne) Benin tumor, origins from epith debris in periodontal ligament, touches ALL AGES (40 yo avg) Predilection: slightly + in MAND, asymptomatic, may cause GINGIVAL growth w/ dental mobility/pain RX: radioclaire (somewhat triangular), advanced lesions MAY be multilocular  Histology: o “îlots d’épithélium malpighien” in fibrous stroma, cells are flattened/cubic (different that ameloblastic cells) o May be keratinized or have microkystes DX dif: ameloblastome acanthomateux OR epidermoid carcinoma TX: excision or curettage, extraction of teeth may be necessary to completely remove tumor 4) Adenomatoide (TOA): 3-7% Benin, NOT aggressive (some consider as hamartoma) -> but sometimes, progressive growth reaches important size Predilection: YOUNG women (2:1) -> 60% under 20 yo (10-19 yo), 90% before 30 yo, ANT of MAX, 70% dent incluse (SUP canine) Usually asymptomatic, may cause non-painful expansion RX: radioclaire, uniloculaire w/ cystic appearance, 60% present calcifications (« flocons de neige »), may diverge roots o 2 forms : folliculaire = similar to dentigerous cyst ; extra-folliculaire = NOT associated to dent incluse DX dif: dentigerous cyst (however, TOA may have calcifications and lesions may extend past JEC to the root) Histology: o Encapsulated, proliferation of fusiformes, cuboidal & cylindric epith cells o Cuboidal/cylindric cells w/ inversed polarisation form glandular/canalicular structure o Calcifications are present, may represent formation of enamel  TX: excision (easily removed due to capsule), extremely rare recurrence Tumeurs odontogènes d’origine ECTOMÉSENCHYMATEUSE: 1) Myxome odontogène Benin, NON-encapsulated, locally infiltrating -> mesenchymal origin of dental papilla 3rd most common after odontoma & ameloblastoma Predilection: 25-30 yo, MAND > max (angle of mandibula) Asymptomatic, but may cause expansion OR cortical perforation RX: uni/multi-locular, « bulle de savon », caracteristic -> thin linear trabeculations (intersection forms angle droit) DX dif : ameloblastome, fibrome odontogène central, GCCG, kyste osseux anévrysmal Histopathologie: o White, gelantin-like (macroscopic) o Star cells, spaced w/ cytoplasmic extensions o Stroma is LOOSE, abundant mucoid aspect (matrix w/ acidic mucopolysaccharides -> hyaluronic acid/chondroitin sulfate) o Varies in COLLAGEN level ; if abundant = fibromyxome TX: small lesions = curettage; advanced = excision w/ healthy tissue o MAX lesions are MORE aggressive o Recurrence = 25% -> 5 year follow-up 2) Fibrome odontogène Rare, fibroblastic origin (various qts of inactive odontogenous epith) 2017/2023 OMS classification -> omits difference b/w poor and rich form epith cells 2 forms: central & peripheric o Central = ALL ages (40 yo avg), WOMEN, PM-MOL of MAND o Peripheric = less common, FIRM/IMMOBILE growth on BUCCAL of gums (++ MAND) RX: central form -> small lesions unilocular (large = MULTI), expansion WITHOUT cortical perforation, tooth mobility may be seen Histologie: o NON-encapsulated, fibrous cellular TC o Variable qt of “ilots”/inactive odontogenic epith trabeculae o Epith may be ABSENT or VERY present o Calcifying structure (similar to dentine) TX: excision + VIGOUROUS curettage o Central = ablation of ADJ teeth sometimes o Peripheric = curettage until perioste (50% recurrence w/o) 3) Cementoblastoma (1%) True neoplasm of cementum, may cause B or L cortical expansion Predilection (EXAM!!!): 75% under 30 yo, 80% PM-mol MAND -> ½ cases 1st MAND mol Rarely dp Caracteristic = pain in VITAL, non-carious tooth  RX: Radio-OPAQUE w/ thin radioclaire line DX dif: hypercémentose, ostéite condensante, ostéome ostéoide, ostéoblastome Histopathologie : o Calcified tissue, formed by “travées” of cellular cementum or by large cementicles o Irregular basophilic lines (similar to Paget disease) o Surrounded by NON-calcified matrix, active zones surrounded by cementoblasts/osteoclastic large cells TX: extraction Tumeurs odontogènes d’origine mixtes : 1) Fibrome améloblastique Simultaneous prolif of ODONTOGENIC epith & mesenchymal tissue (w/ stared and ovoid cells in loose strom) in dental papilla Predilection: 75% < 20 yo, 75% dent incluse, slightly more in MEN/MAND (molar/angle) RX: unilocular, but large = multilocular, but does NOT invade cortical Histologie: o Cells may ANASTOMOSE, or in ISLANDS (similar to enamel organ w/ cylindric peripheric c. in PALISSADE around reticulum étoilé o Travées are LONG and THIN -> two layers cuboidal/cylindric with cells similar to reticulum étoilé in center o TC hyalinated o NO calcification 2) Fibrosarcome améloblastic: MALIGNANT, mesenchymal portion presents malignancy (nuclear hyperchromatism, pleomorphism, ++ MITOSIS) 45% are RECURRENCE from fibrome améloblastique Rapid GROWTH w/ tumefaction, pain, ulceration & tooth mvmt TX: radical TX, very rare metastasis 3) Odontome: most frequent! BENINE, formed during teeth formation Considered as hamartoma -> pseudotumoral malformation w/ excessive growth or abnormal arrangement of c. normally present Central, rare cases peripheric (gums) Two forms: composé + complexe o Composé = most frequent, multiple tiny teeth formation surrounded by sac folliculaire in ANT of MAX, persistence of non-calcified enamel matrix o Complexe = NO denticule formation, irregular mass dental hard tissue (disorganized DENTINE) and pulp, molar region mand/max, calcified enamel matrix found in empty spaced from decalcified enamel o Fibro-odontome améloblastique = initial phase of odontoma, 50% mutation BRAF V600E (EXAM!!), since 2017 -> NOT distinct entity, < 10 yo in POST of MAND, histologically similar to fibrome améloblastique Predilection: teenagers + YOUNG adults (< 20 yo) Asymptomatic, may take place of missing tooth, RARELY may cause expansion  RX: radio-opaque w/ thin radioclaire line, + dense cortical, may be b/w roots o If discovered before tooth formation -> radioclaire TX: ablation 4) Tumeur à cellules fantômes: NOT important Locally INVASIVE, prolif of odontogenic epith c. in COLLAGENIZED stroma Phantom cells + dysplasic dentine is present