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  1. ABNORMALITIES OF TEETH 牙齒的異常-環境與發育的影響 Environmental Alterations of Teeth Developmental Alterations of Teeth 王文岑 高雄醫學大學 牙醫學系

  2. ENVIRONMENTAL ALTERATIONS OF TEETH • Developmental tooth defects • Turner’s tooth • Hypoplasia caused by antineoplastic therapy • Fluorosis • Syphilitic hypoplasia • Postdevelopmental structure loss • Tooth wear • Internal and external resorption • Discolorations of teeth • Intrinsic stains • Extrinsic stains • Localized disturbances in eruption • Primary impaction • Ankylosis

  3. Enamel development • Three stages:1. Matrix formation: protein laid down 2. Mineralization: minerals deposition, majority of original prot. removed-- diffuse, opaque white, soft enamel 3. Maturation: final mineralization-- translucent, hard enamel • Amelogenesis imperfecta • Enamel hypoplasia

  4. Enamel development • No remodeling after initial formation • Timing of ameloblastic damage has a great impact on location & appearance of the defect • Development of crown : from 14th week of gestation to 12 months of age in deciduous dentition; 6 months to 15 y/o in permanent dentition • Neonatal ring on deciduous enamel and deposition with a rate of 0.023mm/day

  5. See Box 2-2 Factors associated with enamel defects Systemic- 1. Birth-related trauma: premature birth 2. Chemicals: antineoplastic C/T, fluoride, tetracycline 3. Chromosomal abnormalities: trisomy 21 4. Infections: chicken pox, CMV, syphilis 5. Inherited diseases: Vit.D-dependent rickets 6. Malnutrition: Vit. A deficiency 7. Metabolic disorders: hypoparathyroidism, maternal diabetes 8. Neurologic disorders: cerebral palsy

  6. See Box 2-2 Factors associated with enamel defects Local- 1.Local acute mechanical trauma 2. Electric burn 3. Irradiation 4. Local infection: periapical inflammatory disease

  7. Clinical and Radiographic Features Environmental enamel defects: 1.Hypoplasia:pits, grooves or large area of missing enamel 2. Diffuse opacities: variation in translucency, normal thickness, white opacity without clear boundary 3. Demarcated opacities: increased opacity, a sharp boundary with adjacent normal enamel, normal thickness

  8. Turner’s hypoplasia, Turner’s tooth • Permanent teeth • Periapical inflammatory disease of the overlying deciduous tooth, less frequently in anterior teeth • Traumatic injury- not rare -45% children sustain injury to their deciduous teeth, 23% permanent teeth development disturbed Turner’s hypoplasia secondary to previous trauma

  9. Turner’s teeth

  10. Hypoplasia caused by antineoplastic therapy • Under 12 y/o, esp. under 5y/o • Age at treatment, forms of therapy Chemotherapy- • Less alteration than radiation • Increased number of enamel hypoplasia and discolorations, slight smaller tooth size, radicular hypoplasia

  11. Radiotherapy- • 0.72 Gy related to mild defects in enamel, dentin (一般成人頭頸癌照射一次約為2Gy) • Dose, radiation field

  12. Developmental radicular hypoplasia and microdontia caused by radiotherapy

  13. Hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia, mandibular hypoplpasia, reduced in vertical development of lower 1/3 of face • Mandibular hypoplpasia may caused by Radiation →impaired root development →reduced alveolar bone growth • Cranial radiation→ altered pituitary gland function→ growth failed

  14. *Dental fluorosis • 1901, Dr. Frederick S. McKay: Colorado brown stain • 1909, Dr. F.L. Robertson in Bauxite, Arkansas • 1930, H.V. Churchill: high concentration of fluoride of Bauxite(13.7ppm) and Colorado • 1931, Dr. H. Trendley Dean: association between fluoride, dental fluorosis and prevalence of caries among children • 1.0 ppm reduced caries by 50~70% and associated with low and mild mottled enamel • 0.7~1.2 ppm water fluoridation was recommended after 1962, currently 0.7ppm is recommended due to increased dental fluorosis

  15. Dental fluorosis • Retention of the amelogeninprotein in enamel structure→ hypomineralized enamel→ permanent hypomaturation→ increased surface and subsurface porosity→ alters light reflection and create white, chalky area

  16. Dental fluorosis • Critical period for clinical dental fluorosis is the 2nd and 3rd year of life, dose dependent • Caries resistant

  17. Syphilitic hypoplasia • Congenital syphilis • Hutchinson’s incisors & mulberry molars

  18. POSTDEVELOPMENTAL LOSS OF TOOTH STRUCTURE • Begin from enamel surface (tooth wear): Attrition, abrasion, erosion, abfraction • Begin from dentin, cemental surface: internal or external resorption

  19. Attrition • Tooth to tooth contact during occlusion and mastication, some are physiologic • Accelerated by: poor quality or absent enamel, premature contact, intraoral abrasives, erosion, grinding habits • Incisal, occlusal and interproximal surfaces

  20. Abrasion • Pathologic loss of tooth structure or restoration secondary to the action of an external agent (ex. Toothbrush, hair grips, toothpicks, chewing tobacco, biting thread, dental flossing…) • Toothbrush abrasion: horizontal buccal cervical notches of exposed radicular cementum and dentin with smooth surface. • Greater on prominent teeth ( canines, premolars , and teeth adjacent to edentulous area) and side of the arch opposite to the dominant hand • Demastication- when tooth wear is accelerated by chewing an abrasive substance between opposing teeth (both attrition and abrasion)

  21. Abrasion

  22. Improper use of hair grips Abrasion Long-term use of tobacco pipe

  23. Erosion • Chemical process, exposure to acidic foods or drinks, medications (chewable Vit. C, aspirin), involuntary regurgitation (ex. esophagitis, pregnancy), voluntary regurgitation (ex. psychologic problems, bulimia) • Perimolysis- dental erosion from gastric secretion • Facial surface of maxillary anteriors affected-dietary source • Posterior teeth extensive loss of occlusal surface, and palatal surface concave dentin surrounded by an elevated enamel rim- regurgitation of gastric secretion

  24. Erosion concave dentin surrounded by an elevated enamel rim

  25. Erosion A bulimia patient

  26. Abfraction • Repeated tooth flexure caused by occlusal stresses (tensile stress) → concentrate at the cervical fulcrum → may produce disruption in the chemical bonds of enamel crystal →cracked enamel can be lost or removed by erosion or abrasion • Wedge-shaped cervical defects, deep, narrow V-shaped, not allow toothbrush to contact base; if the defect, often affect a single tooth • Almost exclusively on facial surface and more often in bruxism, higher in mandibular dentition

  27. Abfraction

  28. Treatment and prognosis of tooth wear • Resolve pain and sensitivity • Identify the cause of tooth structure loss • Protection

  29. INTERNAL & EXTERNAL RESORPTION • Internal resorption- by cells located in pulp, rare • Follows injury to pulp tissues, physical trauma or caries, continue as long as vital pulp remains, may result in communication of the pulp and PDL • External resorption-by cells in PDL, common

  30. Factors associated with external resorption

  31. Clinical and Radiographic Features Internal resorption- • Inflammatory resorption- dentin replaced by inflamed granulation tissue • Pink tooth of Mummery: internal resorption involved coronal pulp Balloonlike enlargement of the canal • Replacement, or metaplastic absorption- pulpal dentinal walls are replaced by bone or cementum-like bone

  32. Clinical and Radiographic Features External resorption- • Moth-eaten loss of tooth structure, less well-defined and variation in density in radiography • Most involved apical or midportions of root, occasionally, begin from cervical (invasive cervical resorption)

  33. Histopathologic Feature • Increased cellularity, vascularity and collagenization • Numerous multinucleated dentinoclasts • Inflammatory cells infiltration

  34. Treatment and prognosis • Internal resorption- • Removal of all soft tissue from site of resorption • Endodontic treatment before perforation in internal resorption • Placement of calcium hydroxide paste for remineralization • Surgical exposure and restoration • Extraction • External resorption- • Identification and elimination the accelerating factor

  35. ENVIRONMENTAL DISCOLORATION OF TEETH • Extrinsic- surface accumulation of exogenous pigment • Intrinsic-secondary to endogenous factors that result in discoloration of underlying dentin

  36. Extrinsic stains • Bacterial- Chromogenic bacteria, green, black-brown, orange coloration Frequently in children, labial surface of maxillary ant. in gingival third • Iron- formation of ferric sulfide • Tobacco • Food and beverage- chlorophyll • Gingival hemorrhage- Hb. breakdown to biliverdin • Restorative material – ex. Amalgam • Medications- iron, iodine, silver nitrate, chlorhexidine, stannous fluoride

  37. Intrinsic stains • Amelogenesis imperfecta • Dentinogenesis imperfecta • Dental fluorosis • Erythropoietic porphyria – • autosomatic recessive disorder of porphyrin metabolism, increased synthesis and excretion of porphyrins and their related precursors • Porphyrin deposition in teeth, reddish-brown coloration, red fluorescence when exposed to a Wood’s UV light • Present both in dentin and enamel in deciduous teeth, but only dentin affected in permanent teeth

  38. Erythropoietic porphyria Hyperbilirubinemia

  39. Intrinsic stains • Hyperbilirubinemia- bilirubin, breakdown product of RBC, jaundance (yellow-green discoloration), erythroblastosis fetalis, biliary atresia • Biliverdin deposition, green discoloration of teeth (chlorodontia) • Ochronosis-alkaptonuria, blue-black discoloration • Trauma- coronal discoloration, pulp necrosis • Localized RBC breakdown

  40. Intrinsic stains • Medications- Tetracycline (bright yellow to dark brown), chlortetracycline (gray-brown), oxytetracycline (yellow) , minocycline hydrochloride • Time of administration dose, duration • Avoid from pregnancy up to 8 yrs of age

  41. Minocycline hydrochloride • Tx for Acne • Blue-gray from incisal 3/4, to dark green or black in roots, also affect developed teeth • Skin, nail, sclera, conjunctiva, thyroid, bone discoloration in susceptible individuals Stained alveolar bone

  42. Treatment and prognosis • Extrinsic stains- polishing • Intrinsic stains- bleaching, bonded restoration, crowns

  43. LOCALIZED DISTURBANCES IN ERUPTION • PRIMARY IMPACTION-Teeth cease to eruption before emergence • ANKYLOSIS-Cease of eruption after emergence and anatomicfusion of tooth cementum or dentin with alveolar bone

  44. Impaction • 3rd molars, maxillary canines, mandibular premolars, mandibular canines, maxillary premolars, maxillary central incisors, maxillary lateral incisors, and mandibular second molars; usually angulated or diverted Factors associated with impaction: • Crowding and deficient maxillofacial development • Overlying cysts or tumors • Trauma • Reconstructive surgery • Thickened overlying bone or soft tissue • A host of systemic disorders, diseases or syndromes

  45. Classification : • Partially erupted or full bony impaction • according to angulation: Mesioangular, distoangular, vertical, horizontal or inverted • Eruption sequestrum

  46. Treatment and Prognosis Choice of treatment: • Long-term observation • Orthodontically assisted eruption • Transplantation • Surgical removal The risks associated with nonintervention: • Crowding dentition • Resorption and worsening of the periodontal status of adjacent teeth • Development of pathologic conditions, ex infections, cysts or tumors

  47. The risks associated with intervention: • Transient or permanent sensory loss • Alveolitis • Trismus • Infection • Fracture • TMJ injury • Periodontal injury • Injury to adjacent teeth

  48. ANKYLOSIS Infraocclusion, secondary retention, submergence, reimpaction, reinclusion

  49. ANKYLOSIS Clinical And Radiographic Features • Pathogenesis is unknown, may be secondary to many factors and result in PDL barrier deficiency. • May occur at any age, any tooth • Most affect 8~9yr-old children and D , E , D , E • PDL absent • Occlusal, periodontal problems, impaction of the underlying teeth Treatment and Prognosis • Variable: extraction, orthodontics, segmental osteotomy

  50. SHAPEGemination, Fusion, Concrescence Accessary cusps Dense in dente Ectopic Enamel Taurodontism Dilaceration Hypercementosis Supernumerary roots NUMBER Hypodontia Hyperdontia SIZE Microdontia Macrodontia STRUCTURE Amelogenesis imperfecta Dentinogenesis imperfecta Dentin dysplasia I & II Regional odontodysplasia DEVELOPMENTAL ALTERATIONS OF TEETH