Developmental Disturbances in Teeth PDF

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Prof. ESSAM GABALLAH

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dental disturbances developmental disorders dental anatomy dentistry

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This document details developmental disturbances in teeth, covering topics such as size variations (microdontia, macrodontia), shape variations (dense invaginatus, taurodontism), and growth disturbances (premature eruption).

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Prof. ESSAM GABALLAH Developmental disturbances in teeth I- Size of teeth: 1- Microdontia * Def. * Types:  generalized - true (pituitary dwarfism) - false (relative)  localized. 2- Macrodontia...

Prof. ESSAM GABALLAH Developmental disturbances in teeth I- Size of teeth: 1- Microdontia * Def. * Types:  generalized - true (pituitary dwarfism) - false (relative)  localized. 2- Macrodontia * Def. * Types:  generalized - true (pituitary gigantism) - false (relative)  localized (focal) - hemifacial hypertrophy II- Shape of teeth 1- Dense invaginatus. 2- Dense evaginatus 3- Taurodontism 4- Talon cysp (rubnsteintaybi S.). 5- Dilaceration. 6- Concrescence 7- Enamel pearls. 8- Supernumerary roots. 9- Germination. 10-Fusion. III- Disturbance of growth (eruption of teeth): 1- Premature e. 1 Prof. ESSAM GABALLAH 2- Delayed e. 3- Multiple unerupted teeth. 4- Embedded and impacted teeth. 5- Ankylosed deciduous teeth. IV- number of teeth: a- Anodontia * Def. * Types: acc. To: 1. Cause a. true. b. false. c. Pseudoanodontia. 2. Number of affected teeth a. Partial b. complete (total) - def. - cause. - site. - effect b- Supernumerary teeth: * Def. * Types. 1. Supplemental 2. Conical, maleformed supernumeraries. * Associated with: 1. Gardner's S. 2. Cleido cranial dysplasia. V- Defects of enamel: a- Environmental:  Factors (intensity – duration – time). 2 Prof. ESSAM GABALLAH  Type of defect (hypocalcification – hypoplasia).  Etiologic factors: 1. Local (turner's teeth). (pathogenesis – site – clinically). 2. Systemic factors - Time (birth – 6 years). - Site (anterior teeth and 6 ) (1ry teeth + tip of 6 + perm. Incisors  intra uterine defect) - Factors: 1) Childhood infectious d. 2) Nutritional defects as rickets hyperclacemia 3) Congenital $ (Hutchinsosn I. & mulberry M.) 4) Fluorosis (dose, site, factors, clinically) 5) Birth trauma. 6) Idiopathic. b- Amelogensis imperfecta (genetic): * Def. * Types : 1. hypoplastic. 2. hypocalcified. 3. hypomaturation type. * Clinically - of each type. - colour. - X-ray. - Effect. VI- defects in dentine: 1- Dentinogenesis otmperfecta (hereditary opalescent dentine) 3 Prof. ESSAM GABALLAH * Def. * Type: 1. I 2. II 3. III (brandy wine type) (shell teeth). * Clinically a. color. b. hardness. c. tooth morphology  crown(bell or tulip shape)  root c. Caries * X-ray  I and II  III * M/P. * ttt 2- Dentine dysplasia * def. * Types. I- Radicular and II- Coronal Color Caries x-ray M/P VII- D. in enamel and dentine: Regional odonto dyplasia (ghost-teeth) I- Alterations in size: a- Microdontia Def.: Teeth in the dentition are smaller than normal. Types and causes: 4 Prof. ESSAM GABALLAH 1- Generalized 2- Focal or localized * Affects all teeth * Single teeth is smaller than * May be: normal  True teeth are smaller than * The shape of this tooth is also normal e.g. pituitary dwarfism. changed.  False relative i.e teeth are of e.g. 2 which is cone or peg shape normal size (but the jaw is called peg lateral (upper 2 is the large). most common microdont This may be hereditary as the child followed by 8 then inheret, the size of the jaw from one supernumerary teeth). parent and the size of the teeth from * It is a hereditary condition the other parent. (autosomal dominent) b- Macrodontia * Def. enlarged teeth of the dentition * Types and causes 1- Generalized 2- Focal or localized * Affects all the teeth * Abnormally large tooth or group * May be: of teeth  True (absolute) as in pituitary * most commonly seen in gigantism. mandibular 3rd molars.  Relative (false)  due to * Seen also in a condition called small mandible or maxilla hemifacial hypertrophy where teeth with normal teeth. on the affected side are abnormally This result in: large compared with the unaffected a- Crowding of teeth due to ↓ side. space. b- Abnormal eruption pattern. 5 Prof. ESSAM GABALLAH II- Alterations in shape: a- Gemination Def.: The attempt to make two teeth from a single enamel organ. Clinically: may appear as: 1. Partial cleavage with the appearance of two crowns sharing the same root canal. 2. or complete cleavage or twining occure resulting in two teeth from one tooth germ. Aet: Unknown but may be due to trauma. Effect: 1- bad cosmetic appearance. 2- Crowding. b- Fusion: Def.: The joining of two developing tooth germs resulting in a single large tooth structure. Clinically: this process may 1- Involve the entire length of the teeth. 2- Or may involve the roots only where cementum and dentine are shared And root canals may be  separate  or shared. NB: To differentiate fusion from gemination we count the number of teeth i.e if the number is ↓  fusion and if ↑  germination but if the fusion occurs bet. Normal and supernumerary tooth so it is impossible to differentiate bet. The two conditions). Cause: unknown but may be trauma. c- Concrescence 6 Prof. ESSAM GABALLAH Def.: A form of fusion in which the adjacent already formed teeth are joined by cementum which may occur before or after eruption. Aet: 1. trauma. 2. over crowding. Site: Maxillary 2nd and 3rd molars. Effect: If one of the two teeth requires extraction so surgical sectioning must be done to save the other tooth. d- Dilaceration: Def.: Abnormal curving or angulation of the root. Aet: 1- Trauma during development  ie. Movement of the crown or of the crown and part of the root from the remaining developing root may  sharp angulation after the tooth complete development. 2- Hereditary factors are involved in small number of cases. Effect: 1- Difficult extraction 2- Difficult root canal filling. e- Dens invaginatus (dens in dente or teeth with in a tooth): Def.: Abnormality of teeth representing exaggeration or accentuation of the lingual pit. Aet: Genetic. Clinically: * may be  superficial crown only is affected.  deep crown and root are affected Site:  Permanent maxillary lateral incisors.  Other incisors may be affected.  May be unilateral or bilateral. 7 Prof. ESSAM GABALLAH Effect: caries and pulpitis so prophylactic filling of the pit is necessary. f- Dens evaginatus: Def.: Abnormal tubercle or cusp located in the center of the occlussal surface. Site: premolars of mongoloid race (Asians, Eskimos) (frequently bilateral). Effect: Occlusal abrasion of this cusp  pulp exposure of the accessory pulp horn extending into the cusp  periapical pathology. So  Judicious grinding to of the cusp to stimulate 2ry dentine formation and grinding of the opposing tooth to avoid abrasion and pulp exposure. g- Taurodontism (as it resembles teeth in bulls): Def.: This term is referred to teeth with elongated crowns or apically displaced furcations resulting in pulp clambers with an increased apical occlusal height. Aet: Genetic More common in Down's syndrome and Eskimos. h- Supernumerarty roots: Site:  Mostly seen in mandibular canines, premolars and molars.  Rare in mandibular incisors. Effect: Important to identify by x-ray before  extraction.  or root canal ttt. i- Enameloma "Enamel pearls" "Enamel Drops" 8 Prof. ESSAM GABALLAH Def.: small deposites of enamel frequently found on the roots of the teeth either in contineuity with the normal enamel of the crown or separate at some distance from the normal enamel. Origin: Disturbance during odontogensis which has caused a localized area of hertwig's sheath to form enamel. Site: maxillary permanent molar teeth between the roots, occasionally they are situated near the apex. Cl/P: Seen as small circumscribed masses of the same appearance as normal enamel. M/P: May consist entirely of enamel. May contain small core of dentine. May contain small amount of pulp tissue. j- Talon cusp: Def.: Structure resembling eagle's talon which projects lingually from the cingulum areas of the maxillary or mandibular permanent incisors. H/P: consists of normal enamel and dentine and horn of pulp tissue. Clinical implications: 1- There is a deep developmental groove bet. the cusp and the lingual tooth surface which may be susceptible to caries. 2- Esthetics problems. 3- Occlusal problems. So. * Restoring the groove to prevent caries. * Remove any occlusal interference (avoiding pulp exposure). * This defect is common in patients with rubinstein, Taybi syndrome: 1- Talon cusp. 2- Developmental retardation. 3- Board thumbs. 9 Prof. ESSAM GABALLAH 4- Great toes. 5- Characteristic facial features. IV- Alterations in number: a- Anodontia: Def.: Absence of teeth. Types: may be classified according to: 1- Cause  True  Pseudoanodontia: when teeth are abscent clinically because of impaction or delayed eruption. False: when teeth have been exfoliated or extracted. 2- Number of teeth affected  Partial (hypodontia) Def.: Affecting one or several teeth. Cause: Congenital Site: 1) max 2 2) 3rd molars. 3) 2nd premolars. Effect congenitally missing lateral may  mesial shift of the canine infront of the mouth beside the centrals  bad aesthetics.  complete (total) Def.: failure of the dental lamina to develop with absence of all t. Cause: congential Effect: failure of the development of the alveolar process with the ridge resemble that of elderly persons 10 Prof. ESSAM GABALLAH N.B: It is frequently associated with a condition called hereditary ectodermal dysplasia in which there is failure of development of many ectodermal structures e.g: 1- Abscent sweat glands  smooth, shing, dry skin. 2- Scanty fine hair. 3- Fingers may be defective. 4- Associated with partial or total anodontia. b- Supernumerary teeth: Def.: Are extra or supernumerary teeth in the dentition arising from excessive organized growth of the dental lamina of unknown cause. N.B: Natal teeth are supernumerary teeth appearing at the time of birth. Post permanent dentition supernumerary teeth appearing after the loss of permanent teeth (may be due to eruption of a previously impacted teeth). Types: 1- Supplemental teeth:  of normal shape.  Mostly max. centrals, max. premolars and 4th molars. 2- Conical, maleformed supernumeraries:  More common than supplemental teeth.  Mostly in max. incisor region, if bet. 1|1 called mesiodense. * It may be 1- Isolated (familial). * or associated with 2- Gardner's syndrome. 3- Cleidocranial dysplasia. Gardner's syndrome: 1- Multiple polyposis of large intestine. 2- Osteomas of bone. 11 Prof. ESSAM GABALLAH 3- Multiple epidermoid or sebaceous cysts of the skin (scalp and back). 4- Occasional occurance of Desmoid tumours. 5- Impacted supernumerary and permanent teeth. Cleidocranial dysplasia: 1- Aplasia or hypoplastic clavicles. 2- Craniofacial malfermations. 3- Supernumerary and unerupted teeth. N.B: Ankylosis: fusion of the root of the tooth to bone by loss of periodontal ligament and bone formation instead of it. V- Defects of enamel: a- Enviromental defects of enamel: * Factors affecting the extent of the enamel defect: 1- The intensity of the etiologic factor. 2- The duration of the factors presence. 3- The time at which the factor occurs during crown development. * Type of the defect:  it may be: 1- Hypoplasia (quantitative):  The enamel is pitted, grooved or very thin but hard, smooth and translucent, the pits may be arranged in raws or columns. Staining of the pits may occur.  In hereditary defects  both dentitions are affected.  In environmental  one dentition or even one tooth is affected. 2- Hypocalcification (quqlitative):  Enamel matrix is normal in quantity but mineralization is defective in newly erupted tooth the enamel is of normal 12 Prof. ESSAM GABALLAH thickness and form but weak and opaque or chaulky in appearance. It tends to become stained and relatively rapidly worn away. 3- Hypomaturation:  The enamel is of normal form on eruption but opaque, white to brownish-yellow, soft and liable to attrition but not as severely as hypocalcified type. * Etiologic factors: 1- Local (turner's teeth): Pathogenesis: Trauma and inflammation (abcess formation) can affect the amelobalsts overlying the developing crown resulting in enamel hypocalcification or hypoplasia. Site: - it affects a single tooth. - mostly seen in permanent teeth in which the overlying deciduous tooth becomes abscessed or forced into the enamel organ of the permanent tooth. Clinical: appear clinically as  areas of coronal discolouration (hypocalc.) Or  pits and irregularities (hypoplasia). 2- Systemic factors: Time: most occur during the time of development of the crowns of permanent teeth i.e after birth and before the age of 6 years (except 8/8). Site: most the defects affect anterior teeth and 1st molars. If the primary teeth are affected + tips of 1st permanent molars + permanent central incisors so the defect has occurred in utero (intra uterine) as these are the teeth undergoing enamel calcification during this period. 13 Prof. ESSAM GABALLAH Factors: 1- Childhood infectious diseases. 2- Nutritional defects as rickets. 3- Congenital $  where I.U. infection by treponema pallidum Affects  permanent incisors (Hutchinson's incisors) are tapered incisally and are notched centrally on the incisal edge.  first molars (mulberry molars) having lobulated occussal surface. 4- Fluorosis Dose  ingestion of drinking water containing fluoride more than 1 p.p.m during the time of the formation of crowns may  enamel hypoplasia or hypocification. Site: It may be endemic in areas containing high fluoride content in the drinking water. Defect affecting factors: The defect depend on duration, time, intensity (concentration). Clinically it may be: a- Mild to moderate:  ranges from white enamel spots To "mottled" brown and white discolourations. b- severe  pitted, irregular and discoloured enamel.  Although folurosis of teeth renders them caries resistant it may be of bad cosmetic appearance and may need dental restorations. 5- Birth trauma  neonatal line in 1ry teeth. 6- Idiopathic. 14 Prof. ESSAM GABALLAH b- Amelogenesis imperfecta: Def.: A group of similar – appearing hereditary disorders of enamel formation in both dentitions. Types: * According to 1- Different inheritance patterns. 2- Clinical appearance. * It is classified into: a. Hypoplastic type. b. Hypocalcified type. c. hypomaturation type (crystals are immature). (there are also numerous subtypes of these 3 major groups) Clinically: 1- Hypoplastic type:  ↓ enamel matrix ranging from pits and grooves to complete absence of enamel.  This lead to abnormal contour and abscent interproximal contact points. 2- Hypocalcified type.  Normal amount of enamel but it is soft and friable.  It fractures and wear's easily. 3- Hypomaturation enamel can be lost by chipping away from the underlying dentine.  Color: - ranges from white opaque to yellow to brown. - The teeth tend to darken with age due to exogenous staining.  X-ray 15 Prof. ESSAM GABALLAH - enamel appear reduced in bulk showing a thin layer over the occlusal and inter proximal surface. - normal pulp and dentine.  Effect - bad aesthetic - although the enamel is soft & irregular teeth are not prone to caries. V- Defects in dentine: a- Dentinogensis imperfecta: (hereditary opalescent dentine)  due to discolouration Def.: Autosomal dominant defect of dentine affecting both 1ry and permanent dentition. Types  3 types: 1. Type I: - occurs with osteogenesis imperfecta - 1ry teeth are more severely affected than permanent teeth. 2. Type II: Only dentine abnormalities with no bone disease. 3. Type III (Brandy urine type) (shell teeth) - Only dental defects. - Similar to type II with some clinical and x-ray variations. Clinically: all 3 types share the following signs: a- Color:  Unusual translucenty of the tooth with color varies from yellow brown to grey.  This abnormal color is due to abnormal underlying dentine. b- Hardness: easy fracture of enamel due to: 1- Poor support by underlying dentine. 16 Prof. ESSAM GABALLAH 2- Abscense of scalloping bet. enamel and dentine. This  rapid wear of the tooth substance.  In type III  multiple pulp exposures are seen due to thin dentine. c- Tooth morphology excessive constriction at the cemento enamel junction giving the tooth crown a bell shape (tulip shape)  Root: short and blunted. d- Caries: these teeth are not excessively susceptible to caries. X-ray Type I and II: 1- Opacification of the of the pulp due to continued deposition of dentine (precacious obliteration of the pulp). 2- Short roots. 3- Bell shaped crowns. Type III: 1- Thin dentine (so called shell teeth). 2- Large and wide root canals and pulp chambers 3- Periapical radiolucences. Microscopically: 1- The dentine have few but large and irregular dentinal tubules. 2- Pulp is completely replaced by irregular dentine overtime. 3- Dentino enamel junction is smooth. 4- Normal enamel. NB: the pat may have blue sclera (thin reflecting the colour of aquos). ttt 1- Using crowns to prevent tooth wear and improve aesthetic. 2- These teeth should not be used as abutments as roots are prone to fracture under stresses. 17 Prof. ESSAM GABALLAH b- Dentine dysplasia: Def.: autosomal dominant defect of dentine. Types: I – Radicular type II- coronal type Clinically Color Both dentitions are normal Opalscent in 1ry dentition normal in permanent dentition Caries More caries resistant than normal teeth x-ray 1- short roots * Decideous teeth similar to 2- completely obliterated type I. pulps (residual fragments of * Permanent teeth have pulp tissue appear as enlarged pulp chambers horizontal radiolucencies called "thistle tubes" and are called chevrons) filled with globules of 3- Periapical radiolucenses abnormal dentine. which may be chronic abcesses, granulomas or cysts. M/P: 1- Enamel and the immediately adjoining dentine appear normal. 2- Deeper layers of dentine show atypical tubular patterns with: a. Amorphous atubular areas. b. Irregular organization. VII- Defects in enamel and dentine: Regional odontodysplasia (ghost teeth) 18 Prof. ESSAM GABALLAH 1- Developmental disorder affecting maxillary teeth more than mandibular teeth. 2- The affected tooth is malformed. 3- Enamel is thin hypoplastic and hypocalcified. 4- Dentine is thin. 5- Large pulp chambers. 6- Early tooth loss. 19

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