Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Eruption & shedding


Published on

  • my pleasure..
    Are you sure you want to  Yes  No
    Your message goes here
  • very useful in my report! thanks
    Are you sure you want to  Yes  No
    Your message goes here

Eruption & shedding

  1. 1. Presented by :Piyush VermaMds 2 nd yearDepartment of Pedodonticsand preventive dentistry27 – 09 - 20121
  2. 2. Contents Introduction Eruption Pre eruptive tooth movement Eruptive tooth movement Theories of tooth eruption Post eruptive tooth movement Shedding of teeth Pattern of shedding Tooth resorption and repair Conclusion References2
  3. 3. Introduction The timely initiation and eruption of teeth into theoral cavity is very important for healthy dentition .It is the process by which tooth moves within theJaw bone comes into the oral cavity and comes up tothe occlusal contact and maintains its clinical position.3
  4. 4. EruptionEruption refers to the axial or occlusal movement of thetooth from its developmental position within the jaw toits functional position in the occlusal plane. Physiological tooth movements consists of thefollowing:Pre eruptive tooth movementEruptive tooth movementPost eruptive tooth movement4
  5. 5. 5Primary dentition: - 2to 6 years of agePermanent dentition:> 12 yearsDIPHYODONT
  6. 6. Phases of tooth eruption Preeruptive phase: made by the deciduous and permanent toothgerms within tissues of the jaw before they begin to erupt. Eruptive phase: Starts with initiation of root formation andmade by teeth to move from its position within bone of the jawto its functional position in occlusion. Has an intraosseous andextraosseous compartments. Posteruptive phase: Takes place after the teeth are functioningto maintain the position of the erupted tooth in occlusion whilethe jaws are continuing to grow and compensate for occlusaland proximal tooth wear.6
  7. 7. Made by the deciduous and permanent tooth germs within tissuesof the jaw before they begin to erupt.tooth germs grow rapidlycrowdedrelieved by lengthening of jawsdeciduous second molar tooth germs move backwardanterior tooth germ moves forwardPre eruptive tooth movement7
  8. 8. Permanent anterior tooth germsdevelop lingual to the primaryanterior teeth and later asprimary teeth erupt, thepermanent crowns lie at theapical 3rd of primary roots.Premolars tooth germs arefinally positioned between thedivergent roots of deciduousmolars.8
  9. 9. Histologic features Remodeling of the bony wall of crypt by selectivedeposition and resorption of bone by osteoblasts andosteoclasts. Normal skeletal morphogenesis might be involved indetermining tooth position9
  10. 10. Eruptive tooth movement The axial or occlusal movement of the tooth from itsdevelopmental position within the jaw to its final functionalposition in the occlusal plane. The actual eruption of the tooth when it breaks through thegum is only one stage of eruption.10
  11. 11. Histology Degeneration of connective tissuesimmediately overlying the erupting teeth. Eruption pathway – altered tissue areaoverlying the teeth. Macrophages destroy cells and fibers bysecreting hydrolytic enzymes. Gubernacular cord: The connective tissueoverlying a successional tooth that connectswith the lamina propria of the oral mucosa bymeans of a strand of fibrous connective tissuethat contains remnants of dental lamina11
  12. 12. 12 Gubernacular canal: Holesnoted in a dry skull notedlingual to primary teeth injaws that represent openingsof gubernacular cord .
  13. 13. 13
  14. 14. • As the tooth moves occlusally it creates space underneath the tooth toaccommodate root formation• Fibroblasts around the root apex form collagen that attach to the newly formedcementum• Bone trabeculae fill in the space left behind as the tooth erupts in the pattern of aladder which gets denser as the tooth erupts• After tooth reaches functional occlusion periodontal fibers attach to the apicalcementum and extend into the adjacent alveolar bone14
  15. 15. Stages of tooth eruptionEssentials of Oral Histology and Embryology. James Avery, 2nd edition 15
  16. 16. The rate of tooth eruption depends on the type ofmovement16• 1 to 10µm/dayINTRAOOSEOUSPHASE• 75 μm/dayEXTRAOSSEOUSPHASE
  17. 17. are those movements made by the tooth after it has reached its functional position inthe occlusal plane.They may be divided in three categories:Post Eruptive Tooth Movements17Accomodation forgrowthCompensation forocclusal wearAccomodation forinterproximal wear
  18. 18.  ACCOMMODATION FOR GROWTH - Mostlyoccurs between 14 and 18 years by formation of newbone at the alveolar crest and base of socket to keeppace with increasing height of jaws. COMPENSATION FOR OCCLUSAL WEAR -Compensation primarily occurs by continuousdeposition of cementum around the apex of the tooth.However, this deposition occurs only after toothmoves. ACCOMMODATION FOR INTERPROXIMALWEAR - Compensated by mesial or approximal drift.18
  19. 19. FACTORS CONTROLLING MESIAL DRIFT:(a) Contraction of the transseptal fibers: As the proximal toothsurfaces of adjacent teeth become worn from functional toothmovement, the transseptal fibers of the periodontal ligamentbecome shorter (due to contraction) and thereby maintain toothcontact .(b) Adaptability of bone tissue: The side of pressure on PDL fiberscauses bone resorption, whereas pull on the fibers causes boneapposition. Therefore, as the contact areas of the crownswear, the teeth tend to move mesially, thereby maintaining thecontact.19
  20. 20. (c) Anterior compartment of occlusal force: An anteriorlydirected force is generated when teeth are clenched, dueto the mesial inclination of most teeth and the forward-directed force generated from inter-cuspal forces.Eliminating opposing teeth results in elimination ofbiting forces, causing a slowing down of the mesialmigration(d) Pressure from soft tissues: Buccal mucosa and tonguepush teeth mesially20
  21. 21. Theories of resorption Root formation ( tomes 1872 ) Bone remodeling ( brash 1928 ) Dental follicle ( marks and cahill 1984) Periodontal ligament ( thomas 1967 ) Hydrostatic pressure ( sutton and graze 1985 ) Pulpal pressure ( v . Korff 1935 ) Cellular theory ( eidmann 1923) Molecular theory ( marks et al )21
  22. 22.  Active eruption Passive eruption Genetic factors Local factors ( steggerda and hill 1942)22
  23. 23. Root Formation : Root formation would appear to be the obvious cause of tootheruption since it causes an overall increase in the length of thetooth along with the crown moving occlusally. Clinical observation, experimental studies and histologicanalysis argue strongly against such a conclusion as rootlessteeth do erupt some teeth erupt more than the total length of the roots and theteeth still erupt after completion of root formation.23
  24. 24. Bone remodelingThe growth pattern of the maxilla and the mandible moves teethby selective deposition and resorption of bone.Major proof is when a tooth is removed without disturbing itsfollicle tooth germ, an eruptive pathway still forms within boneas osteoclasts widen the gubernacular canal. If the dental follicle is also removed no eruption path develops. It establishes absolute requirement for a dental follicle toachieve bony remodeling and tooth eruption.24
  25. 25. Dental Follicle Studies have shown that the reduced dental epitheliuminitiates a cascade of intercellular signals that recruitosteoclasts to the follicle. By providing a signal and chemoattractant forosteoclasts, it is possible that the dental follicle can initiatebone remodeling which goes with tooth eruption. Teetheruption is delayed or absent in and human diseases thatcause a defect in osteoclast differentiation.25
  26. 26.  Experiments done by Cahill & Marks says that viable dentalfollicle is required for the eruption. Further studies by them has shown that tooth eruption is aseries of metabolic events in alveolar bone characterized bybone resorption and formation on opposite sides of thedental follicle and the tooth does not contribute to thisprocess.26
  27. 27. Periodontal ligament Available evidences strongly indicate that the force for eruptivetooth movement lies in PDL. the PDL and dental follicle from where it forms are implicatedin the process of tooth eruption linked to contractility offibroblasts. PDL fibroblasts are able to provide a force sufficient to movethe tooth and certainly the proper structural elements exist totranslate such force into eruptive tooth movement.27
  28. 28. Cellular and molecular basis of tooth eruptionCellular basisprior to onset of eruptioninflux of mononuclear cells into coronalportion of dental folliclecellular eventsinflux of mononuclear cells28
  29. 29. Required for formation of osteoclastsResorb bone for the eruption pathwayDental follicle is interposed between the alveolar bone and tooth, it is an ideal location to regulate the cellular events of eruptionand receive signals from the tooth.29
  30. 30. Molecular basis Eruption moleculesthe molecules that initiate eruption , their localization and theregulation of the cellular events of eruption all must fit within thecontext that each tooth erupts independentlyDetermination of the molecules that may be required for eruptionbegan with the isolation of – EGF (epidermal growth factor ) TGF α (transforming growth factor ) Colony stimulating factor 130
  31. 31.  TGF α , EGF ↑ in incisor eruption colony stimulating ↑ in molar eruptionfactor 131
  32. 32.  Nakchbandi IA et al (june 2000) experiments in vivo have established that tooth eruption fails inthe absence of parathyroid hormone (PTH)-related protein(PTHrP) action in the microenvironment of the tooth becauseof the failure of osteoclastic bone resorption on the coronaltooth surface to form an eruption pathway.32
  33. 33. Localization of eruption molecules: Studies have demonstrated that the eruption genes and theirproducts are localized primarily in either the dental follicle orstellate reticulum. The tissue required for eruption , the dental follicle producesthe majority of the potential eruption molecules. The remainder of the molecules reside in the stellate reticulumadjacent to the dental follicle.E.g IL – 1 – resides in dental follicleDF -95 resides in stellate reticulum33
  34. 34.  Pulp theory It suggests that the tooth is moved lingually by the pressurefrom the pulp the explosive effect of pulpal bulge is producedby the osmotic pressure of the briskly proliferating anddifferentiating mesenchymal cells. Alveolar bone deposition Deposition of bone beneath the tooth during eruption isunlikely to be the cause rather than consequence of the tootherupting.34
  35. 35.  The classic experimental model for studying eruptionis the rat’s incisor , where continuous eruption occurswithout any additional bone being formed at the baseof tooth. However, it is quite likely that bone growth is partlyresponsible for the pre eruptive phase during whichgrowth of the entire alveolus and remodeling aroundthe tooth crypt helps to move it into place for theeruptive phase.35
  36. 36.  Active eruptionbodily movement of tooth from its siteof development to its functional position in the oralcavity. Passive eruptionApparent lengthening of the crown due toloss of attachment or recession of gingiva.36
  37. 37.  Genetic and environmental factorsThe environment, prenatal and maternal factors, socialfactors, climate etc. may influence the timing of tooth eruptionbut the determinants of this timing are still thought to be moregenetic than environmental.Lewis and Garn (1960) and Garn et al. (1965) theorized that toothformation is genetically determined and in an analysis ofmonozygotic twin pairings found strong correlations of toothformation37
  38. 38.  Local factorsLocal alterations frequently form a physical barrier to normaltooth eruption. In the gingiva, fibromatous or hyperplasticalterations may hamper the eruption of the underlying tooth .In the bone, supernumeraries, odontogenous or non-odontogenous tumours, cysts or cleft anomalies may interferewith proper eruption.38
  39. 39.  Tooth eruption in children with growth deficit.Barberia Leache E et alfound that children whose delayed growth is accompanied by alow genetic height or growth hormone deficit presentedretardation in dentition and retardation in bone age. J Int Assoc Dent Child. 1988 Dec;19(2):29-3539
  40. 40. Shedding of teeth Physiologic process resulting in the complete elimination of thedeciduous dentition.Pattern of sheddingResult of progressive resorption of roots of deciduous teeth andits supporting tissues.Pressure generated by the erupting permanent tooth guides thepattern of deciduous tooth resorption.Initially , pressure is against the root surface of the deciduoustooth and resorption occurs on the lingual surface.40
  41. 41.  Later these developing tooth germs occupy a position directlyapical to the deciduous tooth. In mandibular incisors the apical positioning of the tooth germsdoes not occur and permanent tooth erupts lingually.41
  42. 42. Resorption of deciduous molars Resorption of the roots of deciduous molars first begin on theirinner surfaces because the early developing bicuspids are foundbetween them. With continued growth of the jaws and occlusal movement ofthe deciduous molars, the successional tooth germs lie apical tothe deciduous molars. When the bicuspids begin to erupt , resorption of the deciduousmolars is again initiated and continues until the roots arecompletely lost and the tooth is shed.42
  43. 43.  Resorption occurs on the surface of cementum and dentine . Resorption involves a loss of the organic as well as the mineralconstituent of the matrix . during resorption the process of disorganization relative to themineral and the organic components occurs more or lessconcomitantly. Resorption of cementum and dentine of deciduous teeth ischaracterized by the presence of osteoclasts.43
  44. 44.  Root resorption seems to be initiated and regulated by thestellate reticulum and dental follicle of the underlyingpermanent tooth via the secretion of stimulatory molecules i. e.cytokines and transcription factors . The primary root resorption process is regulated in a mannersimilar to the bone remodeling , involving the same receptorligand system known as RANK/ RANKL( receptor activator of nuclear factor – kappa B / RANK ligand)44
  45. 45. PRIMARY ROOT RESORPTION WITHPERMANENT SUCCESSOR The pressure of erupting tooth is believed to play a contributoryrole in setting of resorption but the presence of permanentsuccessor is not a prerequisite for this process to occur. Root resorption of primary teeth starts at the site of root that isclosest to the permanent successor. E.g in anterior teethcompleted crown of permanent successor is found lingual toapical third of root of primary predecessor:Resorption of lingual surface of apical third of primary toothroot.Resorption of labial surface.Resorption proceeds horizontally in incisal direction untilprimary tooth sheds & permanent tooth erupts.45
  46. 46. PRIMARY ROOT RESORPTION WITHOUTPERMANENT SUCCESSOR The root is protected from resorption by presence ofnarrow PDL cell layers which are composed of:Collagen fibersFibroblastsCementoblasts Degradation of PDL precede root resorption & removal ofcollagen fibers of PDL is considered main step in initiationof this process. As face grows & muscles of mastication enlarge, forces thatare applied on the deciduous teeth become heavier thanprimary tooth periodontal ligament can withstand.46
  47. 47. Histology of shedding Odontoclasts are resorbing cells derived from monocyte –macrophage lineage. Giant multinuclear cells with 4 – 20 nuclei. Resorption occurs at the ruffled border which greatly increasesthe surface area of the odontoclast in contact with bone. Found on surfaces of the roots in relation to advancingpermanent tooth. Single rooted teeth shed before root resorption is completed.Distribution of odontoclasts during tooth resorption47
  48. 48.  Odontoclasts are not found in pulp chamber of these teeth. In molars , the roots are completely resorbed and crown ispartially resorbed. Odontoblasts layer is replaced by odontoclasts. Sometimes all the dentine is removed and the vascular tissue isseen beneath the translucent cap of enamel.48
  49. 49. 5 monthsAt birth 1 year2 years 3.5 years 4.5 yearsShedding of mandibular incisorFigure Source: Dr. Sandra Meyers 49
  50. 50. Tooth resorption and repair Resorption is not a continuous process but have also periods ofrepair. Resorption predominates repair. Repair is achieved by cells resembling cementoblasts. Final repair tissue resembles cellular cementum but is lessmineralized.50
  51. 51. Mechanism of resorption and shedding Pressure from the erupting successional tooth and appearanceof odontoclasts at the site of pressure. Membrane of ruffled borders act as proton pump → addinghydrogen ions to extracellular region → acidification →mineral dissolution. Increased forces of mastication with increase in jaw sizeleading to trauma to PDL → degeneration of PDL51
  52. 52.  Resorb bone for the eruption pathway Dental follicle is interposed between the alveolar boneand tooth , it is an ideal location to regulate thecellular events of eruption and receive signals from thetooth52
  53. 53. 7 years-functional occlusion attainedbut root apex is still not fully formed15 years – incisal wearFigure Source: Dr. Sandra Meyers53
  54. 54. Sequence and chronology of tooth eruptionSource:
  55. 55.  According to Hillson (1996), eruption times can bebroken into three phases: Phase One includes the emergence of permanent firstmolars and incisors (5 to 8 years of age); Phase Two consists of the emergence of thecanines, premolars, and second molars (9.5 to 12.5years); Phase Three consists of the emergence of the thirdmolars (late teens to early twenties)55
  56. 56. Chronology of Human Permanent Dentition56
  57. 57. The six/four rule for primary tooth emergenceFour teeth emerge for each 6 months of age1. 6 months: 4 teeth (lower centrals & upper centrals)2. 12 months: 8 teeth (1. + upper laterals & lower laterals)3. 18 months: 12 teeth (2. + upper 1st molars & lower 1st molars)4. 24 months: 16 teeth (3. + upper canines & lower canines)5. 30 months: 20 teeth (4. + lower 2nd molars & upper 2nd molars)1. By 5 months in utero, all crowns started calcification2. By 1 year old, all crowns completed formation3. By 2.5 years, all primary teeth erupted4. By 4 years old, all primary teeth completed root formation57
  58. 58. The rules of “Fours” for permanent toothdevelopment (3rd molars not included)At birth, four 1st molars have initiated calcificationAt 4 years of age, all crowns have initiated calcificationAt 8 years, all crowns are completedAt 12 years, all crowns emergeAt 16 years, all roots are complete58
  59. 59. Rules of “sixes” in dental development6 weeks old in utero: beginning of dental development6 months old: emergence of the first primary tooth6 years old: emergence of first permanent tooth59
  60. 60. Problems of Primary Tooth EruptionNatal and Neonatal Teeth60
  61. 61.  Eruption cyst- follicular enlargement occurring just before eruption.- blue-black color due to presence of blood- no specific treatment if uninfected61
  62. 62. Submerged primary teeth62
  63. 63.  Failure of eruption of first and second permanent molarsCamila Palma et alCONCLUSIONS 1. In this series, the failure of eruption of permanent molars was theconsequence of impactions and primary retentions. 2. Unfavorable prognosis is associated with advanced age and with molarsin the last stages of root formation. 3. Root dilaceration is a major factor limiting eruption and an indicator ofpoor prognosis. 4. The degree of non-eruption and the inclination axis are not key factors inprognosis. 5. Posterior dento-alveolar discrepancy is associated with impaction ofsecond molars. J Clin Pediatr Dent 27(3): 239-246, 200363
  64. 64.  Congenital hypothyroidism/ Cretinism- due to hypo function of thyroid gland- primary tooth eruption is delayed till 2years.- large head, protruding tongue- as soon as it is detected, treated withthyroxin.64
  65. 65.  (Rushton, 1937; Jensen and Kreiborg, 1990,1993 The defects seen in the dentitions of patients affected withCleidocranial dysplasia have been thought to arise from adisruption in the bone remodeling process. In addition to anincreased density in the maxilla and mandible, multiplesupernumerary teeth are present that show a marked delay orarrest in eruption65
  66. 66.  Impactiondue to failure in eruptionmechanismmaxillary canine, 3rd molars– commonest form66
  67. 67.  (Sauk, 1988; Gorlin et al., 1990; Jones, 1997). Eruption failure and delayed eruption are conditionsthat do not naturally involve ankylosis and areassociated with craniofacialdysostosis, hypothyroidism, hypopituitarism, andseveral genetic and medical syndromes.67
  68. 68.  Ectopic eruptiondescribes a path of eruption thatcauses root resorption of aportion or all of the adjacentprimary teeth.mandibular lateral incisor –commonestmaxillary 1st molar and canine.68
  69. 69. 69
  70. 70. Conclusion For the clinicians to treat dental problems knowledgeof proper eruption and shedding time is veryimportant . A variety of developmental defects that are evidentafter eruption and shedding of the primary andpermanent teeth can be related to local and systemicfactors.70
  71. 71. ReferencesTextbook of oral histology by Ten cate,7 th edition; 268– 289Orban‘s textbook of oral histology and embryology –(10 th edition); 372 - 386Textbook of oral development and histology by JamesAvery 3. rd. edition : 92-105.71
  72. 72. Thank you72