Developmental oro facial disturbances part 1

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Developmental oro facial disturbances part 1

  1. 1. DEVELOPMENTAL ORO-FACIALDISTURBANCES PART IDr. Ali TahirB.D.S, R.D.S,M.Phil Oral Pathology
  2. 2. ORAL PATHOLOGY It is the speciality of dentistry and pathology that deals with the nature, identification and management of Dr. Ali Tahir diseases affecting the oral & maxillofacial regions It is a science that investigates the causes, processes & effects of these diseases The practice of oral pathology includes research, diagnosis of disease using clinical, radiographic, microscopic biochemical or other necessary examinations & investigations
  3. 3. DISTURBANCES IN SIZE Microdontia When one or more teeth are smaller than normal Dr. Ali Tahir Generalized  True generalized: When all teeth are uniformly smaller than normal Cause: Pituitary Dwarfism, Down’s syndrome  Relative generalized: When mandible or maxilla are somewhat larger (Macrognathia) but teeth are of normal size Localized  When one tooth is involved  Maxillary lateral incisors are the most common
  4. 4. Dr. Ali TahirMICRODONTIA
  5. 5. DISTURBANCES IN SIZE Macrodontia When one or more teeth are larger than normal Dr. Ali TahirGeneralized True Generalized: When all teeth are uniformly larger Relative Generalized: When maxilla/mandible is smaller in size (Micrognathia) but teeth are of normal sizeRegional It is localized e.g; Hemifacial hypertrophy (unilateral), segmental odontomaxillary dysplasia Rhizomegaly :  When only roots are larger than normal
  6. 6. Dr. Ali TahirMACRODONTIA
  7. 7. DISTURBANCES IN NUMBER Anodontia Congenital absence of all teeth Dr. Ali Tahir Associated with Hereditary Ectodermal Dysplasia Hypodontia Congenital absence of one or more teeth Third molars, maxillary lateral incisors are most commonly absent teeth consecutively
  8. 8. Dr. Ali Tahir
  9. 9. DISTURBANCES IN NUMBERSupernumerary TeethTeeth in excess of normal number Dr. Ali Tahir More common in maxilla (90%) Examples Maxilla  Mesiodens  Paramolars  Lateral incisors Mandible  Premolars  paramolars Multiple supernumerary teeth are seen in Cliedocranial dysplasia and gardner sydrome
  10. 10. SUPERNUMERARY TEETH Dr. Ali Tahir
  11. 11. DISTURBANCES IN ERUPTIONPremature Eruption Natal Teeth: Dr. Ali Tahir  Erupted decidous teeth present at time of birth Neonatal:  Deciduous teeth that erupt in first 30 days of life Premature eruption of entire permanent dentition should suspect the possibility of hyperthyroidism
  12. 12. Dr. Ali TahirNATAL TEETH
  13. 13. DISTURBANCES IN ERUPTIONDelayed Eruption Eruption later than the normal age of eruption Dr. Ali Tahir Usually idiopathic Or associated with systemic conditions such as rickets, cliedocranial dysplasia, cretinism Gingival fibromatosis
  14. 14. DISTURBANCES IN ERUPTIONImpacted teethTeeth with eruption that is impeded by a Dr. Ali Tahir physical barrier Causes:  Dental crowding  Supernumerary teeth  Odontogenic cysts  Odontogenic tumors (odontomas) Most common are mandibular and maxillary third molars followed by maxillary cuspids
  15. 15. IMPACTED TEETH Classified according to their orientation as  Mesioangular Dr. Ali Tahir  Distoangular  Horizontal  Vertical According to their stage of eruption  Completely impacted (within bone)  Partially impacted (partly in soft tissue)
  16. 16. IMPACTED TEETHPartially impacted teeth that communicate with the oral Dr. Ali Tahir cavity are more prone to pericoronitis Complications  Root resorption of adjacent normal tooth  Infection & pain  Dentigerous cyst  External resorption of impacted tooth
  17. 17. IMPACTED TEETH Dr. Ali Tahir
  18. 18. DISTURBANCES IN ERUPTIONEruption Sequestrum A small spicule of calcified tissue that is extruded Dr. Ali Tahir through the alveolar mucosa that overlies an erupting molar
  19. 19. DISTURBANCES IN SHAPEDilaceration A sharp bend or Dr. Ali Tahir angulation involving the root of the toothCauses: Trauma during tooth formation Continued root formation during a curved or tortuous path of eruption
  20. 20. DISTURBANCES IN SHAPETaurodontism A molar with an Dr. Ali Tahir elongated crown and apically placed furcation of roots resulting in an enlarged rectangular pulp chamber. Occurs because of late invagination of Hertwig’s Epithelial Root Sheath
  21. 21. DISTURBANCES IN SHAPEDens Invaginatus Developmental Dr. Ali Tahir anomaly characterized by a deep enamel lined pit that extends for varying depths into the underlying dentin displacing the pulp chamber
  22. 22. DENS IN DENT AND SUPERNUMERARYCUSPSupernumerary cusps Dr. Ali Tahir Teeth containing additional cusp Example: Cusp of caribili, Talon cusp
  23. 23. DISTURBANCES IN SHAPEDens Evaginatus Characterized by Dr. Ali Tahir cusp like supernumerary enamel protrusion on occlusal or lingual surface of crown
  24. 24. Gemination Single rooted tooth with Dr. Ali Tahir unusual wide, partly divided crown or two separate crowns. Cause: Because of partial division of a single tooth gem Teeth count is normal
  25. 25. DISTURBANCES IN SHAPEFusion Abnormally shaped Dr. Ali Tahir tooth with wide crown or a normal crown with additional root(s) Cause: Results from the union of two tooth germs
  26. 26. DISTURBANCES IN SHAPEConcrescence Union of the roots of Dr. Ali Tahir two or more normal teeth by confluence of their cementum. Cause: Trauma, Inter- septal bone loss
  27. 27. DISTURBANCES IN SHAPEHypercementosis One or more teeth with excessive deposition of Dr. Ali Tahir cementum of roots Causes: Increase/Decreased occlusal forces, Paget’s disease, hyperpituitarism, chronic inflammation
  28. 28. Cervical Enamel Projections Dr. Ali Tahir Apical extension of coronal enamel beyond the smooth cervical margin
  29. 29.  Hemispheric structures that may consist Dr. Ali Tahir entirely of enamel or may contain underlying dentin & pulp Mostly present in roots of maxillary or mandibular molars
  30. 30. DISTURBANCES IN STRUCTURE OF ENAMEL Acquired Environmental factors Dr. Ali Tahir  Bacterial (syphilis), viral infections  Inflammation  Nutritional deficiencies  Chemical injuries  Trauma Genetic  Amelogenesis Imperfecta
  31. 31. ACQUIRED DISTURBANCESFocal enamel hypoplasia Localized enamel hypoplasia involving one or two Dr. Ali Tahir teeth  Example: Turner tooth, results from localized inflammation or trauma during tooth development Enamel has pitting areas or deformed with yellowish or brownish discoloration
  32. 32. ACQUIRED DISTURBANCESGeneralized Enamel Hypoplasia Systemic or Environmental factors inhibit functioning ameloblasts. Dr. Ali Tahir Enamel has horizontal lines of small pits or grooves Example:  Hutchinson’s incisors and mulberry molars due to congenital syphilis  Neonatal line  Flourosis Can also be seen in hypocalcemia (Vit. D deficiency), measles, chicken pox, scarlet fever, Vit A & C deficiency
  33. 33. GENERALIZED ENAMEL HYPOPLASIA Dr. Ali Tahir
  34. 34. ACQUIRED DISTURBANCESFlourosis (Flouride mottling) Minimal Flourosis: Dr. Ali Tahir Smooth enamel surface with white flecks Mild Flourosis: Smooth enamel surface with white opaque areas Moderate to severe: Pitting and brownish discoloration Severe: Enamel is softer and weaker than normal, resulting in excessive wearTeeth are largely resistant to caries
  35. 35. Dr. Ali Tahir
  36. 36. HEREDITARY DISTURBANCESAmelogenesis Imperfecta A heterogeneous group of genetic disorders Dr. Ali Tahir exhibiting faulty enamel formation (affects both primary & permanent dentition)Normal enamel formation:1. Enamel matrix formation2. Mineralization of enamel3. Enamel maturation (secondary mineralization)Accordingly three types of AI is identified
  37. 37. TYPESClinical Features: Hypoplastic (focal or generalized)  Decreased enamel formation by disturbance in function of ameloblasts Dr. Ali Tahir  Enamel is thinner than normal  Radiodensity is greater than that of dentin Hypocalcified  Defect in mineralization of enamel  Enamel is off normal thickness but softer than normal  Can be easily removed with a blunt instrument  Radiodensity is lesser than that of dentin Haypomaturation  Focal or generalized areas of immature enamel crystallites  Enamel of normal thickness, but less harder and is radiolucent e.g. snow capped teeth
  38. 38. WITKOP/SAUK CLASSIFICATION Hypoplastic  Pitted, autosomal dominant  Local, autosomal dominant Dr. Ali Tahir  Smooth, autosomal dominant  Rough, autosomal dominant  Rough, autosomal recessive  Smooth, X-linked Hypocalcified  Autosomal dominant  Autosomal recessive Hypomaturation  Autosomal dominant (with taurodontism)  X-linked recessive  Pigmented, autosomal recessive  Snow-capped teeth
  39. 39. Dr. Ali Tahir
  40. 40. DISTURBANCES IN STRUCTURE OF DENTINAcquired Turner tooth Regional odontodysplasia Dr. Ali TahirGenetic Dentinogenesis Imperfecta  Type I  Type II  Type III Dentin Dysplasia  Type I  Type II Familial hypophosphatemia (Vit. D resistant rickets)
  41. 41. DENTINOGENESIS IMPERFECTAA hereditary (autosomal dominant) defect consisting of opalescent teeth composed of irregularly formed & undermineralized dentin that obliterates the pulp chambers & canals Dr. Ali TahirTypes: Type 1  Associated with osteogenesis imperfecta.  Characterized by bluish tint to sclera Type 2  Hereditary opalescent dentin  Most common type Type 3  Also called brandywine type  Clinically the same as type 1 & II  Multiple pulpal exposures of decidous dentition
  42. 42. DENTINOGENESIS IMPERFECTAClinical Features Both dentitions are affected Oplaescent teeth with bluish grey to brownish Dr. Ali Tahir or yellowish discoloration Abnormally soft dentin, enamel easily chipped off Despite the exposure of dentin, teeth are not prone to cariesHistopathology The mantle dentin is normal whereas remaining dentin is severely dysplastic Amorphous matrix with globular & inter-globular areas of mineralization Irregularly widely spaced disoriented dentinal tubules
  43. 43. Dr. Ali Tahir
  44. 44. RADIOGRAPHICALLY Type I & II  Bulb shaped crowns Dr. Ali Tahir  Constricted cemento-enamel junction  Thin roots  Varying degrees of obliteration of pulp chamber & canals Type III  Same features or may show extremely large pulp chambers surrounded by thin shell of dentin
  45. 45. DENTIN DYSPLASIAA hereditary defect in dentin formation where root dentin is abnormal & gnarled, roots are Dr. Ali Tahir shortened & tapered Also called Rootless teeth Autosomal dominant Two types  Type I (radicular)  Type II (coronal)
  46. 46. DENTIN DYSPLASIATypes:1) Radicular Dentin Dysplaisa: Dr. Ali Tahir  Brownish or bluish translucency in cervical region  More common than type II  All teeth in both dentitions are affected  Teeth often show increased mobility & exfoliate prematurelyHistopathology:  Enamel and mantle dentin is normal  Remaining coronal and root dentin consists of nodular masses composed of tubular dentin and osteo-dentin  Slit-like pulp remnants may be seen between nodular masses  Gives an appearance of ‘lava flowing around boulders’
  47. 47. Dr. Ali Tahir
  48. 48. RADIOGRAPHICAL FEATURES Short blunt roots, may be absent entirely Dr. Ali Tahir Mandibular molars have W-shaped roots Dentition may show obliteration of pulp chambers & canals Crescent shaped remnants of pulp may be seen
  49. 49. Dr. Ali Tahir
  50. 50. DENTIN DYSPLASIA TYPE II (CORONAL) Both dentitions affected Deciduous teeth with bluish-grey, brownish or yellowish discoloration Dr. Ali Tahir Same translucent, opalescent appearance as in DI Permanent teeth have normal clinical appearanceHistopathology: Deciduous teeth  Normal zone of mantle dentin that changes abruptly into dense amorphous dentin with irregular arrangement of tubules. Permanent teeth  Globular and inter-globular areas of dentin in pulpal third of dentin with atubular root dentin  Has pulp stones in pulp chamber  Narrow pulp canals
  51. 51. RADIOGRAPHIC FEATURES Deciduous teeth show obliteration of pulp chambers & canals as Dr. Ali Tahir seen in DD type I & DI Roots are normal Pulp chambers of permanent teeth are enlarged Thistle-tube or flame shaped pulp chamber Pulpal calcifications in coronal pulp chamber
  52. 52. REGIONAL ODONTODYSPLASIA (GHOSTTEETH)Defective formation of enamel and dentin with abnormal pulp and follicle calcifications with Dr. Ali Tahir surrounding soft tissue hyperplaisa along- with accumulations of spherical calcifications and odontogenic rests
  53. 53. CLINICAL FEATURES More common in maxilla Affects several adjacent teeth in the same quadrant Dr. Ali Tahir Mostly in permanent dentition Deformed teeth with soft, leathery surface Discolored, yellowish brownHistopathology Dysplastic, globular and interglobular dentin Widened predentin layer Enlarged pulp chamber with pulp stones
  54. 54. RADIOGRAPHIC FEATURES Ghost teeth Decreased Dr. Ali Tahir radiodensity Enamel & dentin are very thin Large pulp chambers Pulp stones
  55. 55. Dr. Ali Tahir
  56. 56. DISTURBANCES IN STRUCTURE OFCEMENTUMHypophosphatasia Disorder of bone mineralization caused by Dr. Ali Tahir deficiency in alkaline phosphatase in serum and tissues Autosomal recessive/dominant Delayed formation and eruption of dentition Premature loss of primary teeth Spontaneous loss of permanent teethRadiographically Enlarged pulp chambers & pulp canalsHistopathology Absence or marked reduction of cementum
  57. 57. HYPOPHOSPHATASIA Dr. Ali Tahir

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