BDS 10002 Disorders of hard tissues 2_44e5e79b3c15af17663918067c86982b (2).pdf

BDS10002 Disorders of Hard Tissue Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological features of...

BDS10002 Disorders of Hard Tissue Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological features of common hard tissue defects, in particular: amelogenesis imperfecta, dentinogenesis imperfect, fluorosis and resorption. Initiation stage proliferation stage Eruption stage Histo & morphodifferentiation stage Number Size Apposition & calcification Eruption stage Shape Normal Tooth development ID Structure Structure of teeth Enamel Hereditar y genetic Felfamily Dentin Acquired memberwiththis onlyproblem Hereditary Environmental or Acquired Affects both permanent & deciduous teeth Affects only one dentition usually permanent duringits development because the deciduous forms during intrauterine life Affects all teeth A single tooth or a group of teeth may be affected Affects either enamel or dentin Affects both enamel & dentin Produces vertical defects Produces horizontal defects hereditary acquired Disturbances in Enamel Hereditary [Amelogenesis imperfecta] Acquired O Cala c on maturation aprotein minerals Amelogenesis Imperfecta enamel formation imperfection Hereditary It is a group of conditions caused by defects in the genes that encode Enamel matrix proteins OR Proteins or enzymes essential for mineralization of enamel matrix x Mutations in the genes for 1 ameloblastin , 2 enamelin 3 tuftelin, 4 AMELX genes encoding amelogenin x Amelogenesis Imperfecta Classification is complex and based on: a) Pattern of inheritance [autosomal or sex linked, dominant or recessive] b) Type of defect c) Appearance Types: 1) H. enamel hypoplasia problem in matrix formation 2) H. enamel hypocalcification (hypomineralisation) 3) Hypomaturation (Both types may co-exist) Amelogenesis imperfecta [hypoplasia] Normal The defect is mainly quantitative due to decrease in the amount of organic matrix formed. O color texture pitting roughness vertical a er I Amelogenesis imperfecta [hypoplasia] Normal surface g Amelogenesis imperfecta [hypoplasia] The remaining enamel is hard, smooth, reflect light and translucent. Teeth tend to be small in size with loss of contact points. Enamel is frequently stained brown.. Amelogenesis imperfecta [hypoplasia] Enamel is friable, fracture and the teeth show attrition. total loss of enamel Amelogenesis Imperfecta [hypocalcification] verytorough chalky white a I due calcification The amount or thickness of enamel matrix formed is normal and the defect is due to failure in normal mineralization. Enamel lacks its surface luster or gloss and the color of the teeth varies from white opaque to yellow brown. Teeth tend to darken with age owing to exogenous staining. Amelogenesis Imperfecta [hypomaturation] hypoplasia B hypo calcification Amelogenesis Imperfecta Hypoplasia Hereditary Hypocalcification Amelogenesis Imperfecta Hypoplasia minerals Hypocalcification Quantitative Qualitative Deficient matrix Normal matrix Normal mineralization Defective mineralization Thin enamel- vertical pitted grooves- aplasia Normal enamel thickness Normal hardness Soft enamel Smooth in unpitted areas Rough Translucent- shiny Opaque- dull Normal radiopacity Decreased radiopacity indistinguishable from dentin Remember!!!!! Disturbances in enamel Hereditary Amelogenesis imperfecta Affects only one dentition usually permanent a single tooth or a group of teeth may be affected Affects both enamel & dentin Produces horizontal defects Acquired  Local [trauma, infection & irradiation]  Systemic factors Dentin formation is less sensitive to insult!!!!! Acquired Enamel Hypoplasia Acquired defects of enamel are usually confined to the permanent dentition, The deciduous dentition escapes since metabolic disturbances and infections severe enough to affect the structure of developing teeth will usually give rise to abortion. Factors associated with enamel defects: Local factors Systemic factors Local factors Trauma Traumatic injures to deciduous teeth (usually incisors) may pass deeply into their sockets resulting in their roots impinging upon the developing tooth germs of their permanent successors. Local factors Trauma radiotherapy I cancerpatients Infection Turner’s hypoplasia Infection: Osteomyelitis Periapical infection of a deciduous tooth, (usually molars), may reach the underlying developing tooth germ of the succeeding premolar. Sever infections such as osteomyelitis of the mandible during the time of tooth development Turner’s hypoplasia Acquired enamel hypoplasia of a single tooth (may be 2 teeth) due to local factor (trauma or infection) radiotherapy T.at Turner’s hypoplasia Acquired enamel hypoplasia of a single tooth (may be 2 teeth) due to local factor (trauma or infection) Systemic Factors associated with enamel defects: Nutritional deficiency: vitamins A & D, calcium Infections: scarlet fever, chicken pox, measles, syphilis Hormonal disturbances: hypothyroidism Birth related trauma enamel hypoplasia Systemic Factors associated with enamel defects: Ingestion of chemicals: dental fluorosis, tetracycline & cytotoxic drugs Associated with general diseases: cleido cranial dysplasia, ectodermal dysplasia, Down’s syndrome Dental Fluorosis [Mottled Enamel]  Ingestion of drinking water containing fluoride at levels greater than 1.5 part per million during the time of tooth formation may result in enamel hypoplasia or hypocalcification. yemenB Saudi  Dental fluorosis affects mainly the permanent teeth. Deciduous teeth are rarely affected because they are formed in intrauterine life and excess fluorides are taken by the maternal skeleton. Pathogenesis: Increased fluoride levels interfere with ameloblastic function, which adversely affects both enamel matrix formation and calcification. Dental Fluorosis [Mottled Enamel] A fluoride content duringpregnancy excessive fluoride from me mother adds fluoride to the child to the bones without the teeth Teeth is protected cquereddetects permanentdevelopingteeth can be affectedduringthe T fluoride content Dental Fluorosis [Mottled Enamel] Clinically: Enamel mottling may be graded as follow: Very mild: Small white opaque areas involving >25% of the surface area of the tooth. Mild: White opaque areas involving 50% of the surface area of the tooth. Moderate: The whole enamel may be affected with white chalky areas or yellowish or brown staining. Severe: The enamel is grossly defective, pitted, opaque, stained brown or black, brittle and easily chipped away from the tooth surface. Dental Fluorosis [Mottled Enamel] 72590 Whitechalky 2590 50 pitied opaque brow Dental Fluorosis [Mottled Enamel] Histological features The amelodentinal junction is irregular with accentuated scalloping. The prisms are seen to pursue an irregular course. Normal The prisms and interprismatic substance appear to be defectively calcified [The stain is localized in the interprismatic substance]. accentuation as for the binding of enamel B dentin 99 accentuation I dental fluorosis severe Developmental disturbances in Dentin formation Hereditary Dentinogenesis imperfecta Dentinal dysplasia B permanent deciduous both enamel B dentin vertical Environmental (due to local or systemic factors) Dentine formation is less sensitive to insult!!!!! environmental causes does not affect 3 tooth color Dentinogenesis Imperfecta [Hereditary Brown Opalescent Dentin] dark grey D translucencywith ashine This is an inherited disorder of dentin formation that either occurs normal enamel In association with osteogenesis imperfecta due to mutation in genes COL1A1 and COL1A2 that results in deficiency in type 1 collagen As an only defect due to mutations in dentin sialoprotein, a dentin matrix protein, rather than collagen genes. Now diagnosed as osteogenesis imperfecta and not considered as dentinogenesis immperfecta anymore Brandy wine type, shell teeth, pink tooth is now considered as a severe form of dentinigenesis imperfecta Osteogenesis Imperfecta Comprises a group of hereditary disorders characterized by impairment of collagen maturation, which forms a major portion of bone Dentinogenesis Imperfecta Clinically  Both deciduous and permanent dentitions  The teeth are opalescent with the color ranging from bluish-gray to brown to yellowish.  The crowns of the teeth may be of normal, or slightly smaller than normal size, with a constricted neck [bulbous appearance]. Dentinogenesis Imperfecta Clinically  enamel is structurally normal, rapidly lost due to: a-poor support by abnormal soft dentin b-loss of scalloping of amelodentinal junction.  The roots are short and stunted. amelogenesis imperfecta dentinogenesis imperfecta Dentinogenesis Imperfecta Radiographic features  Small bulbous crowns.  Partial or total obliteration of the pulp. can't be seen  The roots are short and blunted and may be fractured. Normal Dentinogenesis Imperfecta Histological features  Normal enamel.  DEJ is straight rather than scalloped.  Dentinal tubules are fewer in number, widely spaced, larger in diameter than normal, irregular and may pursue a tortuous course. Odontoblast processes I Normal Dentinogenesis Imperfecta Histological features The pulp shows the following: Numerous pulp stones. Obliteration of pulp chamber and root canal by poorly formed dentine. Pulps are obliterated by pulp stones Shell Teeth or Brandywine Type [severe form of Dentinogenesis Imperfecta]  Discovered in Brandywine isolate in state of Maryland, USA.  This is a very rare abnormality, the dentin is quite thin and forming a shell around the wide pulp.  Early pulp exposure is common sequel of caries affecting these teeth. pulpexposure widepulp Shell Teeth or Brandywine Type [severe form of Dentinogenesis Imperfecta] Radiographic features Thin dentin shell and wide pulp but not obliterated Extremely short roots Shell Teeth or Brandywine Type [severe form of Dentinogenesis Imperfecta] Histological features  Normal enamel. thin dentin  The dentinal tubules are dilated, reduced in number or abruptly disappeared.  The pulp: is very wide, and consists of coarse fibrous connective tissue Dentinogenesis Imperfecta severe normal thin denn Radiographic findings Histological features dentin gifts expose Dentinogenesis Imperfecta Radiographic findings Histological features Partial or total obliteration of the pulp. The roots are short and blunted and may be fractured. Thin dentin shell and wide pulp but not obliterated Extremely short roots Normal enamel. DEJ is straight rather than scalloped. Dentinal tubules are fewer in number, widely spaced, larger in diameter than normal, irregular and may pursue a tortuous course. Numerous pulp stones. Obliteration of pulp chamber and root canal by poorly formed dentine. The pulp: is very wide, and consists of coarse fibrous connective tissue Resorption Definition A condition associated with either a physiologic or a pathologic process resulting in loss of dentin, cementum or bone. Resorption Internal Replacement or metaplastic inflammatory External Internal resorption very rare This is a rare condition in which a progressive resorptive process occurs in the pulp chamber or root canals Pathogenesis of inflammatory type Precipitating factors (infection, 1 trauma) Vascular changes 2 in the pulp & inflammation Formation of 3 odontoclast like giant cells Resorption of 4 internal wall of pulp Examination & Diagnosis: Visual examination Teeth usually show a pink spot [if it occurs in the crown cervical zone is most commonly affected] Signs & symptoms Mostly asymptomatic Discovered by radiographic examination Examination & Diagnosis: Radiographically Area of internal resorption show balloon like dilatation of the canal Treatment Root canal treatment should be done immediately to avoid perforation of the tooth Internal resorption trauma infection Pathogenesis of metaplastic type Precipitating 1 factors Formation of 2 odontoclast like giant cells Resorption of internal wall 3 of pulp Replacement of resorbed part with bone or 4 cementum like material External resorption very common Pathologic resorption is frequently seen, and will result in premature loss of the affected teeth if untreated Causes Traumatic injuries Orthodontic tooth movement, Chronic infections of the pulp or periodontal structures Re-implantation of teeth Cysts Tumors perapical External resorption Radiographically Appears as a moth- eaten loss of tooth structure (radiolucency) Most commonly involves the apical & mid portions of the root Key points  Defects in tooth structure are hereditary or acquired (environmental)  Defects in tooth structure will result in poor esthetics of teeth  Enamel formation is more sensitive to insults than dentin formation  Turner’s hypoplasia is an acquired enamel hypoplasia of a single tooth (may be 2 teeth) due to local factor (trauma or infection)  Shell tooth is now considered as a severe form of dentinigenesis imperfecta  Tooth resorption is either internal (rare condition) or external (common condition) Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological features of common hard tissue defects, in particular: amelogenesis imperfecta, dentinogenesis imperfect, fluorosis and resorption. Reading material: Students are advised to review any relevant teaching provided in the first year. In addition they are advised to read relevant sections of the following texts: Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp107-118 Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 23-44 Thank you