Developmental Disturbances Of Oral And Para Oral Structures Important Question And Answers

1. Developmental Disturbances Of Oral And Para Oral Structures

Question.1. Write notes on xerostomia.Write short notes on xerostomia.

Answer. Xerostomia or dryness of mouth is not a disease but a symptom of diffrent diseases.

Xerostomia produces serious negative effcts on patient’s life affcting the dietary habits, nutritional status, speech,taste and increase susceptibility to dental caries.

Etiology

The causes of xerostomia are classified into two categories:
1. Temporary causes
2. Permanent causes

Temporary Causes

• Psychological: Anxiety and depression are well recognized as causes of reduced salivary flow.
• Duct calculi: Blockages of a duct of major salivary gland mainly sub mandibular produces dryness of affcted side.
• Sialoadenitis: Inflmmation of salivary glands can cause reduced secretions.
• Drug therapy: A wide variety of drugs, i.e. anticholinergic,tricyclic antidepressants, bronchodilators and histamines may cause xerostomia.

Read And Learn More: Oral Pathology Question And Answers

Permanent Causes

• Salivary gland aplasia: The congenital absence of salivary glands leads to xerostomia.
• Sjogrens syndrome: This is the combination of dry mouth,dry eyes and often rheumatoid arthritis.
• Radiotherapy: The distressing cause of xerostomia is therapeutic radiography for head and neck tumors.

Clinical Features

• Unilateral dryness with pain or discomfort and swelling in affcted gland.
• Drying and burning sensations are present but mucosa appears normal.
• Due to lack of saliva mucosa will appear dry, atrophic and more often pale and translucent.
• Soreness, burning, and pain of mucous membrane and tongue are common symptoms.

Treatment

It is advisable to promote salivary stimulation by using sugar free chewing gum which is affected and convenient.

 

Question.2. Write notes on microdontia.

Answer. Microdontia is the term used to describe the teeth which are smaller than the normal.

There are three types of microdontia:

1. True generalized microdontia
2. Relative generalized microdontia
3. Microdontia involving the single tooth

1. True generalized microdontia: In true generalized microdontia all the teeth are smaller than the normal.
Its occurrence is reported in the cases of pituitary dwarfism. The teeth are well formed and are small.

2. Relative generalized microdontia: In relative generalized microdontia the normal or slightly smaller than normal teeth are present in the jaws that are somewhat larger than the normal and there is an illusion of true microdontia.

3. Microdontia involving the single tooth: It is a common condition which more commonly affects maxillary lateral incisor and third molar. Lateral incisor becomes peg-shaped.

 

Question.3. Write notes on geographic tongue.
Or
Write short note on benign migratory glossitis.

Or
Write short note on geographic tongue.

Answer. Geographic tongue is a multifocal, patchy irregular area of depapillation of tongue characterized by frequent remissions and recurrences.

Clinical Features

• It is seen in children as well as in adults.
• Geographic tongue clinically presents multiple, irregular,well demarcated, patchy erythematous areas on dorsum of tongue with desquamation of fiiform papilla.
• Although fiiform papilla are absent in desquamated zone,the fungiform papillae remain present which appear as few red dots projecting on the surface.
• Geographic tongue is a painless, asymptomatic condition,however on few occasions it may produce soreness or burning sensations.
• Remissions of initial lesions always followed by fresh recurrent lesions which involves new areas of tongue surface.

Histopathology

• The condition show hyperparakeratinization of covering epithelium of the tongue with loss of filiform papillae.
• Intercellular edema and accumulation of neutral polymorphs is often seen in layers of epithelium.
• Mild inflammatory cell infiltration is present in underlying connective tissue.

 

Question.4. Write short note on dilaceration.

Answer. Dilaceration refers to an angulation or a sharp bend or a curve in the root and crown of the formed tooth.

It occurs due to the mechanical trauma to calcified portion of partially formed teeth which lead to the displacement of calcified portion in different direction.

• The curve or the bend may occur anywhere along the length of the root, sometimes at the cervical portion, at other times midway along the root or even just at the apex of the root depending on the amount of root formed when injury occurs.
• Dilacerated teeth cause problems at the time of extraction if operator is unaware of condition, so preoperative roentgenograms before any surgical procedure are carried out.

 

Question.5. Write short note on Dens Invaginatus.
Or
Write short note on Dens in dente.

Answer. Oehlers describe dens invaginatus.

• Dens in dente or dens invaginatus is the deep surface invagination of crown or root which is lined by the enamel.
• Dens invaginatus is a developmental variation which is thought to arise as the result of invagination in the surface of tooth crown before calcifiation has occurred.
• The causes of the condition are increased localized external pressure, focal growth, retardation and focal growth stimulation in certain areas of tooth bud.
• The permanent maxillary lateral incisors are the teeth most commonly involved.

Types

• Coronal dens invaginatus
• Radicular dens invaginatus

Coronal Dens invaginatus

• This is seen more frequently as compared to radicular dens invaginatus.
• In their decreasing order, teeth affected by this anomaly are permanent lateral incisors, central incisors, premolars, canines and molars.
• This is commonly seen in maxillary teeth.
• Variation in the depth of invagination is seen from slight enlargement of cingulum pit to deep infolding which extend to apex.
• Coronal dens invaginatus is of three types viz:
  • Type I: Exhibit invagination which is confied to the crown.
  • Type II: Extends below CEJ and ends in a blind sac that may or may not communicate with adjacent dental pulp.
  • Type III: It extends through the root and perforates in apical or lateral radicular area without any immediate communication with the pulp.
• Occasionally invagination can be rather large and resemble a tooth inside a tooth that’s why it is known as dens in dente.
• In some of the other cases invagination can be dilated and disturb the formation of tooth which lead to anomalous development of tooth known as dilated odontome.
• Roentgenographically, it is recognized as a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth.

Radicular Dens Invaginatus

• This condition is rare.
• This condition arises secondary to proliferation of
  Hertwig’s epithelial root sheath, with formation of strip of enamel that extends along surface of root.
• Roentgenographically, affected tooth shows enlargement of root. On close examination, there is presence of dilated invagination which is lined by the enamel with opening of invagination situated along lateral aspect of root.

Treatment

• Type I invagination, opening should be restored after the eruption to prevent development of caries and pulpal inflammation.
• In large invagination content of lumen and carious dentine is removed and then calcium hydroxide base may be placed.
• Type III invaginations require endodontic therapy.

 

Question.6. Write a note on anodontia.

Answer. Anodontia is defied as the condition in which there is congenital absence of teeth in oral cavity.

Etiology Of Anodontia

The causes of anodontia are:

• Hereditary factor
• Environmental factor
• Familial factor
• Syndrome associated
• Radiation injury to the developing tooth germ.

Anodontia is of two types:
1. Complete anodontia: There is congenital absence of all the teeth.
2. Partial anodontia: Congenital absence of one or few teeth.

• Anodontia can also be divided into following types:
• • True anodontia: It occurs due to failure of development or formation of tooth in jaw bone.
  • Pseudoanodontia: It refers to the condition in which teeth are present within the jaw bone but are not clinically visible in the mouth, as they have not erupted, e.g. impacted teeth.
  • False anodontia: It is the condition in which teeth are missing in the oral cavity because of their previous extraction.

Complete anodontia

• It is the condition in which there is neither any deciduous tooth nor any permanent tooth present in the oral cavity.
• It is usually seen in association with hereditary ectodermal dysplasia. A complete anodontia is a common feature of hereditary ectodermal dysplasia however in many cases cuspids are present in this disease.
• Complete anodontia occurs among children those who have received high doses of radiation to the jaws as infants for therapeutic extraction.

Partial Anodontia

• It is a common phenomenon and is characterized by congenital absence of one or few teeth.
• In partial anodontia any tooth can be congenitally missing.
• Third molars are most frequently observed congenitally missing teeth.
• Mandibular first molar and the mandibular lateral incisor are least likely to be missing.

 

Question.7. Write note on amelogenesis imperfecta.

Answer. Amelogenesis imperfecta is also known as hereditary enamel dysplasia or hereditary brown enamel.

• Amelogenesis imperfecta is a heterogeneous group of hereditary disorders of enamel formation affcting both deciduous or permanent teeth.
• Disease involves only the ectodermal part of the tooth, i.e. enamel.
• It is of three types:

1. Hypoplastic type
2. Hypocalcifid type
3. Hypomature type

1. Hypoplastic type: In this the enamel thickness is usually far below the normal since disease affects the stage of matrix formation.
In this stage the teeth exhibit complete absence of enamel from crown surface or there may be a very thin layer
of enamel in some focal areas.

2. Hypocalcifiation type: This is due to disturbance in the process of early mineralization of enamel.
In this stage the enamel is soft and can easily be removed with blunt instrument.

3. Hypomaturation type: This occurs due to interruption in the process of maturation of enamel. Here the enamel is of normal thickness but it does not have normal hardness and is translucent. The enamel can be pierced with an explorer tip with fim pressure.

Clinical Features

• Color of teeth is mostly chalky white but sometimes it can be yellow or even dark brown.
• Contact points in proximal surfaces are mostly open while the occlusal surfaces and incisal edges are severely abraded.
• Enamel may have a cheesy consistency which is easily removable from tooth surface.
• Amelogenesis imperfecta does not increase the susceptibility of teeth to dental caries.
• In amelogenesis imperfecta the enamel is of near normal hardness and has some white opaque flcks at incisal areas of teeth. These types of teeth are known as snow capped teeth.

Treatment

There is no definite treatment of amelogenesis imperfecta.
Composite veneering can be done to improve esthetics of teeth.

 

Question.8.Write note on motted enamel.

Answer. Mottled enamel is a type of hypoplasia due to floride and was fist described by GV Black and Frederick S Mckay.

Etiology

It is caused due to ingestion of floride containing water during the time of tooth formation which may result in motted enamel.

Pathogenesis

Mottled enamel is due to the disturbance of ameloblasts during formative stage of tooth development.

There is histological evidence of cell development which is likely that the cell product, enamel matrix is defective or deficient. With higher level of floride, there is interference with calcification process of matrix.

Clinical Features

• There is white flcking or spottng of enamel.
• Mild changes are manifested by white opaque areas including tooth areas.
• Moderate and severe changes showing pittng and brownish staining of teeth.
• Corroded appearance of teeth.
• Those teeth which are moderately or severely affcted may show a tendency of wear and even fracture of enamel.

Treatment

Mottled enamel frequently becomes stained an unsightly brown color.
For cosmetic reasons it has become the practice to bleach the affected teeth with hydrogen peroxide.

 

Question.9.Enumerate various anomalies of teeth affecting number, size and shape. Describe one condition from each.

Answer.

Enumeration Of Anomalies Affecting Number Of Teeth

• Anodontia
• Hypodontia
• Hyperdontia, i.e. natal teeth, neonatal teeth, premature eruption.

Enumeration Of Anomalies Affecting Shape Of Teeth

• Gemination
• Twinning
• Fusion
• Concrescence
• Dilaceration
• Talon cusp
• Dens invaginatus
• Dens evaginatus
• Taurodontism
• Hypercementosis
• Enamel pearl
• Mulberry molar
• Globodontia
• Hutchinson’s incisor

Enumeration Of Anomalies Affecting Size Of Teeth

• Microdontia
• Macrodontia

 

Question.10. Enumerate the developmental anomalies associated with the teeth. Describe factors associated with acquired enamel hypoplasia.

Answer.Anomalies Affecting Hard Tissues of Oral Cavity

The anomalies which affct the hard tissues of oral cavity are:

• Amelogenesis imperfecta or hereditary enamel dysplasia or hereditary brown enamel or hereditary opalescent teeth.
• Environmental enamel hypoplasia
• Dentinogenesis imperfecta
• Dentin dysplasia.
• Regional odontodysplasia or odontodysplasia or odontogenic dysplasia, odontogenesis imperfecta or ghost teeth
• Dentin hypocalcifiation

Factors associated with acquired enamel hypoplasia

There are two types of factors which are associated with
acquired enamel hypoplasia:

1. Local factor
2. Environmental/systemic factor
1. Local factors: The local factors are infection, trauma, radiotherapy and idiopathic factors.

• When local infection or trauma causes damage to ameloblasts cells during odontogenesis, it may result in defect in enamel formation in isolated permanent tooth and this is known as focal enamel hypoplasia.
  The focal enamel hypoplasia is caused due to periapical spread of infection from a carious deciduous tooth or trauma to the deciduous tooth, the tooth affected in this process is commonly known as turner’s tooth.

2. Environmental or systemic factors: The systemic or environmental disturbances in the functioning of ameloblasts at specifi period of time during odontogenesis often manifest as horizontal line of small pits or grooves or enamel surfaces. This line on tooth surface indicates zone of enamel hypoplasia and corresponds to time of development and duration of insult. The factors in following stages:

• Prenatal period: The prenatal infections are rubella,syphilis.
  • There is presence of internal disease
  • There are excess floride ions
• Neonatal period: During this period enamel hypoplasia is caused due to:
  • Hemolytic disease of newborn
  • Birth injury
  • Premature delivery
  • Prolong labor
  • Low birth weight
• Postnatal period: During this period enamel hypoplasia is due to:
  • Sever childhood infection.
  • Prolong fever due to infectious disease in childhood
  • Nutritional deficiency
  • Hypocalcaemia
  • Rickets
  • Celiac disease.

 

Question.11. Write notes on gemination and fusion.

Answer. Gemination

• Gemination is a developmental anomaly which refers to partial development of two teeth from single tooth bud following incomplete division.
• The structure is usually one with two completely or incompletely separated crowns that have a single root and a root canal.
• The condition is seen in both deciduous and permanent dentition.
• It appears to exhibit hereditary tendency.

Fusion

• Fusion is defined as union of two adjacent normal tooth germs at level of dentin during development.
• One of the most important criteria for fusion is that fused tooth must exhibit conflent dentin.
• Both permanent and deciduous dentition are affcting in case of fusion, although it is more common in deciduous teeth.
• Fusion can be complete or incomplete and its extent will depend on stage of odontogenesis at which fusion takes place.
• The incisor teeth are more frequently affcted in both the dentitions during the condition.

 

Question.12. Write notes on taurodontism.
Or
Write short note on taurodontism.

Answer. Taurodontism is a dental anomaly in which the body of tooth is enlarged at the expense of the roots. Actually, taurodontism meAns the bull shape appearance of the tooth.

Clinical Features

• Affcted tooth in taurodontism has elongated pulp chamber with the rudimentary root formation.
• Tooth becomes rectangular in shape with minimum constriction at the cervical area.
  Taurodontism commonly affects multirooted permanent molar teeth and sometimes the premolar teeth.
• The bifurcation or trifurcation may be a few millimeters above the apices of the roots.
• Patient with hypodontia may have taurodontism.

Treatment

No specific treatment is required.

 

Question.13. Write short note on supernumerary teeth.

Answer. Presence of any extra tooth in dental arch in addition to normal series of teeth is known as supernumerary teeth.

Classification

According to the morphology

• Conical: This small peg shaped conical tooth is supernumerary tooth.
• Tuberculate: This type of supernumerary tooth
  possesses more than one cusp or tubercle. It is of barrel shaped and may be invaginated.
• Supplemental: It refers to the duplication of the teeth in normal series. The most common tooth is permanent maxillary lateral incisor.
• Odontome: This represents the hamartomatous malformation.

According to location

• Mesiodens: They are located between two upper central incisor.
• Distomolars: They are located on the distal aspect of regular molar teeth in dental arch.
• Paramolar: They are located either in buccal or lingual aspect of normal molars.
• Extra-lateral incisors: They are more common in maxillary arch.

Clinical Features

• Supernumerary teeth cause crowding or malocclusion and give rise to cosmetic problem.
• These extra teeth are responsible for the increase caries incidence and periodontal problem.
• Multiple supernumerary teeth can occur in association with the conditions like Gardener’s syndrome.
• Dentigerous cyst may sometimes develop from an impacted supernumerary tooth.

Treatment

• Supernumerary teeth should be extracted.
• Impacted supernumerary teeth should also be removed surgically since they can interfere with normal tooth alignment.

 

Question.14. Write short note on dentinogenesis imperfecta.

Answer. Dentinogenesis imperfect is an inherited disorder of dentin formation that affects deciduous and permanent dentition.

Classifiation

Sheild’s Classification

• Dentinogenesis imperfecta Type I: Dentinogenesis imperfecta without osteogenesis imperfecta.
• Dentinogenesis imperfecta Type II: Dentinogenesis imperfecta with osteogenesis imperfect
• Dentinogenesis imperfecta Type III: It is a racial isolate in Maryland and is known as Brandywine type.

Extensive studies have shown that dentinogenesis imperfect is clearly a disorder from osteogenesis imperfect, so the following revised classification is given:

• Dentinogenesis imperfecta1: Dentinogenesis imperfect a without osteogenesis imperfecta (opalescent dentine). This corresponds to dentinogenesis imperfect
  Type II of Sheild’s classification.
• Dentinogenesis imperfect 2: Brandywine type dentinogenesis imperfect: This corresponds to dentinogenesis imperfect Type II of Sheild’s Classification.

There is no substitute in present classification for the category which is designated as Dentinogenesis imperfect Type I of Sheild’s classification.

Etiology

Gene affected is present on chromosome 4 and it codes for DSPP (Dentine sialoprotein and phosphoprotein)

Clinical Features

• On eruption the teeth exhibit a normal contour and have opalescent amber like appearance.
• Few days after the eruption the teeth may achieve the normal color. Finally the teeth become gray or brownish in color with bluish reflction from enamel.
• In some cases the affcted teeth may exhibit hypomineralized areas on surface of enamel.
• Teeth are not particularly sensitive even when most of the surface enamel is lost.
• The dentin is soft and easily penetrable in dentinogenesis imperfecta, these teeth are not caries prone.

Histopathology

• Histopathologically the enamel appears normal in Dentinogenesis imperfecta. Mantle dentin is also nearly normal.
• Dentinal tubules are less in number per square unit area of dentin as compared to normal dentin. The tubules are often distorted, irregular in shape, widely spaced and larger in size.
• Pulp chamber and root canal are often obliterated by the abnormal dentin deposition.
• DEJ appears smooth or flttned instead of being scalloped.
• Large area of a tubular dentin is present.

 

Question.15. Write note on median rhomboid glossitis.
Or
Write short note on median rhomboid glossitis.
Or
Write short answer on median rhomboid glossitis.

Answer. It is an asymptomatic, elongated, erythematous patch of atrophic mucosa on mid­dorsal surface of tongue.

Clinical Features

• Condition is seen mostly in the young adults.
• It is most common among the males.
• Lesion is located immediately anterior to the foramen cecum and circumvallate papillae in midline of dorsum of tongue.
• It starts as narrow, mildly erythematous area located along the median fisure of the tongue.
• Fully developed lesion of the median rhomboid glossitis appears diamond or lozenge shaped area devoid of papilla.
• Color of lesion varies from pale pink to bright red.
• It is usually asymptomatic but occasionally causes slight soreness or burning sensation.

Histopathology

• Parakeratosis of surface epithelium
• Loss of papilla
• Thinning of supra papillary epithelium
• Presence of acanthosis with elongation of rete ridges.
• Superficial layer of epithelium shows neutrophilic infiltration and there is presence of candida hyphae.
• Underlying connective tissue is vascular and is infiltrated by chronic inflammatory cells.
• The epithelium may show features of dysplasia.

 

Question.16. Write note on lingual thyroid.

Answer. Accessory accumulation of functional thyroid gland tissue within the body of tongue is called lingual thyroid.

Clinical Features

• It is seen in females more commonly.
• In tongue thyroid tissue appears as nodular exophytic mass measuring 2 to 3 cm in diameter and is located to foramen cecum.
• It can be present as smooth cystic swelling.
• Symptoms may vary which include change of voice,bleeding, pain, dysphagia, dyspnea and feeling of tightness in throat.

Histopathology

• Normal mature thyroid tissue, although embryonic or fetal thyroid gland tissue may also be seen.
• Thyroid nodules may exhibit colloid degeneration or goiter.
• Microscopic examination of human tongue removes at autopsy reveals remnant of thyroid tissue within tongue.

Treatment

• Surgical excision should be done.

 

Question.17. Enumerate the developmental anomalies of tongue and describe any two.

Answer.

Enumeration Of Developmental Anomalies Of Tongue

• Aglossia
• Microglossia
• Macroglossia
• Ankyloglossia or tongue tie
• Cleft tongue
• Fissured tongue
• Median rhomboid glossitis
  Geographic tongue
• Hairy tongue
• Lingual thyroid nodule
• Lingual varices

 

Question.18. Write short note on dentin dysplasia.
Or
Write notes on dentin dysplasia.

Answer. It is the autosomal dominant inherited disorder characterized by the defective dentin formation and abnormal pulp morphology.

• The condition is also known as “rootless teeth”.
• It is classified into two types
  • Type I: Radicular dentin dysplasia
  • Type II: Coronal dentin dysplasia

Type i: radicular Dentin Dysplasia

It represents a peculiar disturbance in the development of radicular dentin.

Clinical Features

• It affcts both deciduous and permanent dentition.
• Root of teeth is defective and the crown portion of teeth is normal both structurally and morphologically.
• In some cases the crown of teeth reveals slight bluish or brownish tendency.
• Because of presence of functionally unstable short roots,the affcted teeth exhibit mobility.

Histopathology

• Enamel and mantle dentin are normal.
• Remaining coronal and radicular dentin appear fused nodular mass comprising of tubular dentin and osteo dentin.
• Histological appearance of such defective mass of dentinal tissue often reveals what is called as “series of sand dunes” or “lava flwing around boulders”.
• Normal and abnormal dentin is well demarcated and later reveals an abnormal distribution and orientation of dentinal tubules with whorled appearance.

Treatment

No specifi treatment.

Type ii: Coronal Dentin Dysplasia

It is an inherited disorder of dentin, which affcts the coronal dentin.

Clinical Features

• Both deciduous and permanent teeth are affcted.
• Permanent teeth are of normal color whereas deciduous teeth are amber gray color.

Histopathology

• Pulp chambers in permanent teeth are abnormally large
  and have a flme shaped.
• Pulp chamber contains many denticles.
• Root canal may be partially obliterated in apical third region.

 

Question.19. Write short note on concrescence.

Answer. Concrescence is defied as union of roots of two or more adjoining teeth due to deposition of cementum.

It is the type of fusion which is limited only to the roots of teeth and it occurs after the root formation of involved teeth is completed.

Etiology

• Traumatic injury
• Crowding of teeth
• Hypercementosis

Important Features

• Concrescence represents an acquired defect and it can occur in both erupted or unerupted.
• In concrescence beside cementum union or fusion does not occur between the enamel, dentin or pulp of involved teeth.
• Permanent maxillary molar are usually affcted by this anomaly.
• Concrescence can occur between normal molar and a supernumerary molar.
• Condition is seen in those areas of dental arch where roots of neighboring teeth lie close to one another.

Question.20. Write short note on Fordyce’s granules.

Answer. It is a developmental anomaly characterized by heterotrophic collection of sebaceous glands at various sites in oral cavity.

Pathogenesis

It is suggested that occurrence of sebaceous gland in the mouth may result from inclusion in the oral cavity of ectoderm having some of the potentialities of skin in the course of development of the maxillary and mandibular process during embryonic life.

Clinical Features

• They appear as yellow spots either separated from each other and remain in groups.
• They are seen bilaterally on the mucosa of cheeks opposite to molar tooth, on the inner surfaces of lips, retromolar area.
• They are also seen in the esophagus, female genitalia,male genitalia, nipples, palm and soles, parotid gland,larynx and orbit.

Histological Features

• They are unassociated with the hair follicles.
• Glands are superfiial and may consist of only few or more tubules, all grouped around one or more ducts which open in the mucosa.
• Ducts may show keratin plugging.

Treatment
No treatment is required.

 

Question.21.Defie anomaly. Describe in detail developmental anomalies of the tongue.
Or
Enumerate and describe the developmental disturbances affcting tongue.
Or
Describe in detail developmental disturbances affcting tongue.
Or
Give an account of developmental anomalies of tongue.

Answer. Anomaly is defied as the irregularity or deviation compared to the normal structure.

Enumeration Of Developmental Anomalies Of Tongue

• Aglossia
• Microglossia
• Macroglossia
• Ankyloglossia or tongue tie
• Cleft tongue
• Fissured tongue
• Median rhomboid glossitis
• Geographic tongue
• Hairy tongue
• Lingual thyroid nodule
• Lingual varices

Aglossia

It is characterized by the complete absence of tongue

Microglossia

This is in reality a microglossia with extreme glossoptosis. In such cases a rudimentary small tongue is observed.

Due to the lack of muscular stimulus between alveolar arches they do not develop transversely and mandible does not grow in anterior direction.

Macroglossia

Macroglossia is an uncommon condition characterized by enlargement of tongue.

Type Of Macroglossia

There are two broad categories under the heading of Macroglossia, i.e.

True Macroglossia

Pseudomacroglossia

Causes

• Congenital and hereditary:
  • Vascular malformations
  • Lymphangioma
  • Hemangioma
  • Hemihyperplasia
  • Cretinism
  • Beckwith-Wiedemann syndrome
  • Down syndrome
  • Mucopolysaccharidosis
  • Neurofiromatosis
• Acquired:
  • Edentulous patients
  • Amyloidosis
  • Myxedema
  • Acromegaly
  • Angioedema
  • Carcinoma and other tumors

Clinical Features

• It most commonly occur in children.
• In infants it is manifested by noisy breathing, drooling and diffilty in eating.
• Macroglossia result in lisping speech.
• Pressure of tongue against mandible and teeth produces lateral crenated border of tongue.
• Presence of open bite and mandibular prognathism is seen.
• Children with macroglossia often develop tongue thrusting habits, which may lead to malocclusion, open bite and diastema formation, etc.
• Macroglossia developing in adult people (as in acromegaly or in tumors, etc.) may produce spacing of teeth and distortion of the mandibular arch.
• Blockage of the pharyngeal airway due to macroglossia may result in a condition called obstruction sleep apnea.

Ankyloglossia

It is also known as tongue tie

Ankyloglossia is the condition which arises when the inferior frenulum attches to the bottm of tongue and subsequently restricts free movements of the tongue.

Clinical Features

• Males are affcted more commonly than females
• It can cause feeding problems in infants
• It causes speech defects specially articulation of the sounds l, r, t, d, n, th, sh and z
• It leads to persistent gap between the mandibular incisors.

Treatment

Frenulectomy is the treatment of choice.

Cleft tongue

• It is a rare condition which arises due to lack of merging of lateral lingual swellings of this organ.
• A partial cleft tongue is more commonly seen.
• Partial cleft occurs because of incomplete merging and failure of groove obliteration by underlying mesenchymal proliferation.

Fissured tongue

It is also known as scrotal tongue.

Clinical Features

• More common among males.
• No clinical symptom is seen in fisured tongue but collection of food debris and microorganisms in the fisures or grooves sometimes cause discomfort.
• Fissures or grooves often radiate freely in central groove on the dorsal surface in oblique direction.
• Large and deep fisures may be inter-connected and they separate the dorsum of the tongue into multiple lobules.

Histological Features

• There will be loss of fiiform papillae from the surface mucosa.
• Neutrophilic microabscess formation within the epithelium.
• Hyperplasia of the retepegs and increased thickness of the lamina propria.
• Mixed inflmmatory cell infitration in the connective tissue stroma.

Treatment

No treatment is required.

Hairy Tongue

• Hairy tongue is an unusual condition, which occurs due to hypertrophy of the fiiform papilla of tongue along with loss of normal desquamation process.
• Abnormal hair­like growth of the papilla eventually leads to formation of a pigmented, thick, mattd layer on the tongue surface often heavily coated with bacteria and fungi.

Etiology

• Poor oral hygiene
• Fungal infections
• Prolonged use of antibiotics
• Heavy smoking
• Excessive use of antiseptic mouth washes
• Chronic illness
• Lack of tooth brushing and consumption of soft foods with litte or no roughage.

Pathogenesis

• Normally the keratinized surface layers of the tongue papillae are continuously desquamated through friction of the tongue with food, rough surface of the palate and the upper anterior teeth.
  Following desquamation,tongue papillae are replaced by newer epithelial cells from below.
• Lack of tongue movements due to local or systemic disease disturbs the regular desquamation process of the tongue papilla; especially the fiiform papillae, which lengthens considerably and produces a hairy appearance on the tongue surface.
• Such hypertrophied papillae are often coated with microorganisms and become discolored.

Clinical Features

• Hairy tongue commonly affcts the mid dorsum of the tongue.
• Hypertrophy of the fiiform papillae produces a thick matted layer on the dorsal surface.
• Hypertrophied fiiform papillae may grow up to half a centimeter long, which often brushes the soft palate and produces gagging sensations.
• There can be irritation to the tongue due to accumulation of food debris and microorganisms.

Treatment

• Removal of etiological factor.
• Proper cleaning of tongue.

 

Question.22. Describe environmental enamel hypoplasia.

Answer. Environmental enamel hypoplasia may be defied as an incomplete or defective formation of the organic enamel matrix of teeth.

• Enamel hypoplasia (EH) is a quantitative defect associated with a reduced localized thickness of enamel, following disruption of the secretory phase of amelogenesis.
• The enamel may be translucent or opaque, with single or multiple pits or grooves and partial or complete absence of enamel over signifiant areas of dentin. The enamel hypoplasia defects tend to occur in the incisal or cuspal one­third of the crown.
• Defect which is caused by environmental factors, either dentition may be involved and sometimes only a single tooth; both enamel and dentin are usually affcted, at least to some degree.
• It is known that a number of diffrent factors, each capable of producing injury to the ameloblasts, may give rise to the condition, including:
  • Nutritional defiiency (vitamins A and D)
  • Exanthematous diseases (e.g. measles, chickenpox, scarlet fever)
  • Congenital syphilis
  • Hypocalcemia
  • Birth injury, Prematurity and Rh hemolytic disease
  • Local infection or trauma
  • Ingestion of chemicals (chiefl floride)
  • Idiopathic
• In mild environmental hypoplasia, there may be only a few small grooves, pits, or fisures on the enamel surface.
  If the condition is more severe, enamel may exhibit rows of deep pits arranged horizontally across the surface of the tooth.
  There may be only a single row of such pits or several rows indicating a series of injuries.
• In most severe cases, a considerable portion of enamel may be absent, suggesting a prolonged disturbance in the function of the ameloblasts.
• Hypoplasia results only if the injury occurs at the time teeth are developing, or more specifially during the formative stage of enamel development.
  Once the enamel has calcifid, no such defect can be produced.
  Thus, knowing the chronologic development of the deciduous and permanent teeth,it is possible to determine from the location of the defect on the teeth the approximate time at which the injury occurred.

Enamel Hypoplasia Due to Vitamin A Defiiency

Although tissues of ectodermal origin i.e., the epidermis is primarily affcted in vitamin A defiiency, teeth also record this defiiency.

Avitaminosis A is evidenced by marked metaplasia of the enamel organ, which results in defective enamel formation.

This view originates from histological changes seen initially in the oral mucosa and extending to the degeneration of the epithelial­derived ameloblasts, which results in a hypoplastic enamel matrix.

If vitamin A defiiency is severe,ameloblast cells will become completely atrophied, which results in an absence of enamel formation.

In less severe cases, the columnar ameloblasts apparently shorten, and adjacent enamel exhibits hypoplasia.

If vitamin A defiiency is relieved during subsequent tooth development, normal enamel is produced,although defective tissue is not repaired.

Enamel Hypoplasia Due to Vitamin D Defiiency

Vitamin D is essential for deposition of calcium and phosphorus in hard tissues.

Its presence increases the absorption of dietary calcium and maintains proper levels of calcium and phosphorus in the blood.

Primary defiiency of vitamin D results from insuffient exposure to the sun and insuffient dietary intake.

Secondary defiiencies result from abnormal intestinal resorption.

Secondary defiiencies may be overcome by alteration of dietary intake of calcium and phosphorus.

A severe vitamin D defiiency in children results in rickets, a condition characterized by insuffient deposition of calcium salts in bony tissue.

Dental features of rickets include enamel hypoplasia due to failure of tooth mineralization. Enamel hypoplasia is of pittd type.

Enamel hypoplasia Due to exanthematous Diseases

Some studies have indicated that exanthematous diseases,including measles, chickenpox and scarlet fever, are etiologic factors.

In general, it might be stated that any serious nutritional deficiency or systemic disease is potentially capable of producing enamel hypoplasia, since ameloblasts are one of the most sensitive groups of cells in body in terms of metabolic function.

The type of hypoplasia occurring from these defiiency or disease states is usually of the pittng variety.

Since the pits tend to stain, the clinical appearance of the teeth may be very unsightly.

Clinical studies indicate that most cases of enamel hypoplasia involve those teeth that form within the fist year after birth, although teeth that form somewhat later may be affcted.

Thus the teeth most frequently involved are the central and lateral incisors, cuspids and fist molars.

Enamel Hypoplasia Due To Congenital Syphilis

Congenital syphilis arises from transplacental fetal infection with Treponema pallidium acquired during pregnancy from an untreated mother.

The disease is divided into an early stage that usually occur before 3 months, but may be seen up to 2 years, and late stage disease that occurs after 2 years.

Late congenital syphilis affct the amelogenesis of the molars and incisors.

Both Hutchinson teeth and mulberry molars are seen in about 65% of patients.

These characteristic teeth present at around 6 years; they are centrally notched, widely spaced, peg­shaped upper permanent central incisors.

Patients with congenital syphilis may also have mulberry molars, which are fist molars dwarfed by a small occlusal surface, and are characterized by roughened lobulated hypoplastic enamel leading to caries.

The surface has numerous poorly formed cusps which overcome to form a dome­shaped tooth, which is considerably narrower at the grinding surface than at its base.

Enamel Hypoplasia Due To Hypocalcemia

Tetany induced by a decreased level of calcium in the blood, may result from several conditions, the most common being vitamin D deficiency and parathyroid deficiency (parathyroprivic tetany).

In tetany the serum calcium level may fall as low as 6–8 mg per l00 mL, and at this level enamel hypoplasia is frequently produced in teeth developing concomitantly This type of enamelhypoplasia is usually of the pittng variety and thus does not diffr from that resulting from a nutritional disturbance or exanthematous disease.

Enamel Hypoplasia Due To Birth Injuries

The neonatal line or ring, described by Schour in 1936 and present in deciduous teeth and fist permanent molars, may be thought of as a type of hypoplasia because there is a disturbance produced in the enamel and dentin, which is indicative of trauma or change of environment at the time of birth.

Enamel Hypoplasia Due To Local Infection Or Trauma

A type of hypoplasia occasionally seen is unusual in that only a single tooth is involved, most commonly one of the permanent maxillary incisors or a maxillary or mandibular premolar.

There may be any degree of hypoplasia, ranging from a mild, brownish discoloration of the enamel to a severe pittng and irregularity of the tooth crown.

Another frequent pattrn of enamel defects seen in permanent teeth is caused by periapical inflmmatory disease of the overlying deciduous tooth. The altered tooth is called Turner’s tooth.

 

Question.23. Write short note on cleft lip.

Answer. Cleft lip is a developmental anomaly characterized by wedge shaped defect in the lip which results from failure of two parts of the lip to fuse together at the time of development.

Etiology

• Nutritional factors such as defiiency of or excess of vitamin A and defiiency of riboflvin.
• Maternal smoking (during pregnancy) is a very high­risk factor.
• Psychogenic, emotional or traumatic stress in pregnant mothers.
• Relative ischemia to the area due to defective vascular supply.
• Mechanical obstruction by enlarged tongue.
• High dose of steroid therapy during pregnancy.
• Localized mucopolysaccharide metabolism defect in the area.
• Infections.
• Substances such as alcohol, drugs or toxins in the circulation.

Pathogenesis

• Cleft in lower lip usually occurs either due to failure of the copula to form the mandibular arch or due to persistence of the central groove of the mandibular process.
• Cleft of the upper lip and premaxilla occur due to failure of mesodermal penetration and subsequent obliteration of the ectodermal grooves between the median nasal process, lateral nasal process and the maxillary process, which occurs during the seventh week of intrauterine life.

Clinical Features

• Occur most commonly in males.
• Most common type of isolated cleft lip only is unilateral complete type.
• Breastfeeding is impossible to babies having cleft lip, as they cannot generate suffient suction.
• There is diffilty in correct phonation and articulation of speech.
• Mental trauma to the child due to the unusual appearance.

Treatment

• Cosmetic repair of face and lips
• Proper development of speech
• Prevention of maxillary arch collapse

 

Question.24.Write short note on florosis.

Answer. Fluorosis is a toxic manifestation of chronic floride intake.

• It can be described as a diffse symmetric hypomineralization disorder of ameloblasts.
• Fluorosis is irreversible and only occurs with exposure to floride when enamel is developing.
• Instead of being a normal creamy-white translucent color, florosed enamel is porous and opaque.
• Teeth can resemble a ghostly white chalk colored (light refractivity is greatly reduced because the enamel’s prism structure is defective).
• Cloudy striated (lines of demarcation) enamel, white specks or blotches, ‘snow-capping’, yellowish-brown spots, or brown pits on teeth are all characteristic of florosis.
• In its more severe form, florosed enamel is structurally weak (britte) and prone to erosion and breakage, especially when drilled and filed.
• Even in the milder forms, there is increased enamel attition.
• To prevent florosis from occurring in the most prominent and/or most susceptible teeth, the most critical time to avoid floride exposure is the fist three to six years of a child’s life.

Fejerskov et al. (1977) stated that the effct of floride on enamel formation can follow several possible pathogenic pathways:

• Effct on ameloblasts:
  • Secretory phase:
    • Diminished matrix production
    • Change of matrix composition
    • Change in ion transport mechanism
  • Maturation phase: Diminished withdrawal of protein and water
• Effct on nucleation and crystal growth in all stages of enamel formation
• Effct on calcium homeostasis generally with dental florosis as an indirect result
  • • After the tooth erupts and calcifiation has been completed, ingested floride does not have adverse dental consequences.
    • Fluorosis is seen to affct mainly permanent dentition and very high floride levels (>10 ppm) are required in drinking water for it to cross placental barrier and affct primary dentition.

 

Question.25.Enumerate the developmental disturbances affcting the structures of teeth and discuss in detail amelogenesis imperfecta.
Or
Enumerate developmental disturbances affecting structures of teeth. Write in detail about amelogenesis imperfecta.

Answer.

Enumeration Of Developmental Disturbances Affecting Structure Of Teeth

• Amelogenesis imperfecta
• Dentinogenesis imperfecta
• Enamel hypoplasia
• Dentin dysplasia
• Regional odontodysplasia
• Dentin hypocalcifiation

Amelogenesis Imperfecta

Amelogenesis imperfecta is a group of hereditary disorders characterized by alteration of the quantity and quality of enamel in humAns and is frequently associated with a signifiant dental disease. Witkop and Sauk (1976)

Classifiation of Amelogenesis Imperfecta

Witkop, 1988 Four major categories based primarily on phenotype (hypoplastic, hypomaturation, hypocalcified,hypomaturation­hypoplastic with taurodontism) subdivided into 15 subtypes by phenotype and secondarily by mode of inheritance.

• Type I–Hypoplastic
• Type IA–Hypoplastic, pittd autosomal dominant
• Type IB–Hypoplastic, local autosomal dominant
• Type IC–Hypoplastic, local autosomal recessive
• Type ID–Hypoplastic, smooth autosomal dominant
• Type IE–Hypoplastic, smooth X­linked dominant
• Type IF–Hypoplastic, rough autosomal dominant
• Type IG–Enamel agenesis, autosomal recessive
• Type II–Hypomaturation
• Type IIA–Hypomaturation, pigmented autosomal recessive
• Type IIB–Hypomaturation, X­linked recessive
• Type IIC–Hypomaturation, snow­capped teeth, X­linked
• Type IID–Hypomaturation, snow­capped teeth, autosomal dominant?
• Type IIIA–Autosomal dominant
• Type IIIB–Autosomal recessive
• Type IV–Hypomaturation­hypoplastic with taurodontism
• Type IVA–Hypomaturation­hypoplastic with taurodontism, autosomal dominant
• Type IVB–Hypoplastic­hypomaturation with taurodontism, autosomal dominant

Histopathology

• There is a disturbance in the diffrentiation or viability of ameloblasts in the hypoplastic type, and this is reflcted in defect in matrix formation up to and including total absence of matrix.
• In the hypocalcifiation type there are defects of matrix structure and of mineral deposition.
• In the hypomaturation type there are alterations in enamel rod and rod sheath structures.
• Ground section of the teeth involved showed very thin enamel, composed of laminations of irregularly arranged enamel prisms.

Radiographic Features

• The enamel may appear totally absent on the radiograph,or when present may appear as a very thin layer chiefl over the tips of cusps and on the inter­proximal surfaces.
• In other cases the calcifiation of the enamel may be so affcted that it appears to have the same approximate radiodensity as the dentin, making diffrentiation, between the two diffilt.

Treatment

• There is no defiite treatment of amelogenesis imperfecta.
• Composite veneering can be done to improve esthetics of teeth.

Question.26. Describe histologic features with diagram of ghost teeth.

Answer. It is also known as regional odontodysplasia.

Following are the histologic features of ghost teeth:

• In ground section enamel thickness varies.
• Prism structure of enamel is irregular and it lacks laminated appearance.
• Dentin show clefts which are scattred through mixture of interglobular dentin and amorphous material.
• Reduction in amount of dentin is seen.
• Widening of predentin layer is present.
• Large areas of interglobular dentin are seen.
• Pulp contains free or attched pulp stones which exhibit tubules or have laminated calcifiation.
• Follicular tissue surrounding the crown is enlarged and exhibit collections of basophilic enamel like calcifiations called as enameloid conglomerates.

 

Question.27.Classify enamel hypoplasia. Describe in detail about environmental factors causing enamel hypoplasia.

Answer.

Classifiation of Enamel Hypoplasia

• Mild: Presence of few small grooves, pits and fisures on enamel
• Moderate: Presence of rows of deep pits arranged horizontally over surface.
• Severe: Portion of enamel may be absent

 

Question.28. Write short note on hypodontia.

Answer. It is the developmental alteration in number of teeth.

• Hypodontia denotes the lack of development of one or more teeth.
• Oligodontia is a type of hypodontia which indicates lack of development of six or more teeth.

Etiology

• Genetic: Various syndromes are associated such as hereditary ectodermal dysplasia, craniofacial dysostosis etc.
• At present scenario evolution is there towards some teeth.
• X­ray radiation causing damage to developing tooth bud results in absence of teeth.

Clinical Features

• Hypodontia is very uncommon in deciduous dentition.
• When hypodontia is present it frequently involves lateral incisors.
• In permanent dentition third molars are more commonly affcted and after these second premolars and lateral incisors are absent.
• Hypodontia is also associated with microdontia.

Treatment

• Fixed prosthesis should be given to patient in form of bridges.
• Removable partial dentures can also be given.

 

Question.29. Discuss in detail about etiology, clinical features and treatment of cleft lip and palate. Add a note on syndromes associated.

Answer.

Clinical Features

• It is seen more common in females as compared to males.
• Cleft is seen over the hard and soft palate and it can also be seen in the cleft of soft palate alone.
• Extension of cleft palate varies, i.e. it involves uvula or soft palate, at times it extend over the complete palate,it also sometimes involve alveolar ridge unilaterally or bilaterally.
• Patient feels diffilty in drinking and eating since liquid and food regurgitates through the nose.
• Patient have problem in speaking.
• Upper lateral incisors of patient are short or may be absent.
• Crossbite is present.

Treatment Of Cleft Lip And Cleft Palate

• Cleft palate is usually repaired in l2–l8 months. Early repair causes retarded maxillary growth. Late repair causes
  speech defect.
• Both soft and hard palates are repaired.
• Abnormal insertion of tensor palati is released. Mucoperiosteal flps are raised in the palate which is sewed together.
• If maxillary hypoplasia is present, then osteotomy of the maxilla is done. With orthodontic teeth extraction and alignment of dentition is done.
• Regular examination of ear, nose and throat during followup period, i.e. postoperative speech therapy.
• Whenever complicated problems are present, staged surgical procedure is done.
• Wardil-Kilner push back operation-by raising mucoperiosteum flps based on greater palatine vessels.
• Hearing support is given using hearing aids if defect is present; control of otitis media.
• Speech problems occur due to velopharyngeal incompetence; articulation problems also can occur speech therapy is given. It is corrected by pharyngoplasty, veloplasty,speech devices.
• Dental problems like uneruption, unalignment are common. They should be corrected by proper dentist opinion,and reconstructive surgery.

Orthodontic management with alveolar bone graft, maxillary osteotomy is done in 8–11 years.

Syndromes Associated With Cleft Lip And Cleft Palate

There are multiple syndromes associated but most common syndrome associated is Pierre­Robin syndrome. This syndrome is characterized by cleft palate, micrognathia and glossoptosis.
Other syndromes associated are as follows:

1. Goldenhar syndrome: Cleft palate, microstomia, hypoplastic zygomatic arch.

• Marfan’s syndrome: Cleft palate, skeletal defects, ocular lens defect.
• Down’s syndrome: Cleft palate, teeth anomalies, fisured tongue, malocclusion.
• Patau syndrome: Cleft lip and cleft palate, polydactyly and heart anomalies.
• Orofacial digital syndrome: Cleft lip, digital malformation,deformed facial features.
• Treacher Collin syndrome: Cleft lip and cleft palate, facial deformities.
• Median cleft face syndrome: Cleft palate, nasal cleft and frontonasal dysplasia.
• Otopalatodigital syndrome: Cleft palate, mandibular micrognathia, facial deformity.
• Blepharocheilodontic syndrome: Eye anomalies, cleft lip and palate, microdontia.

 

Question.30. Write short note on developmental disturbances in number of teeth.
Or
Describe in detail developmental disturbances affecting number of teeth.

Answer. Developmental disturbances in number of teeth

• Anodontia
• Hypodontia
• Hyperdontia

Hyperdontia

• Hyperdontia is the development of an increased number of teeth.
• The additional teeth are known as supernumerary teeth.
• Accessory teeth may be present at or shortly after birth.
• Teeth present in newborn baby are known as natal teeth while teeth arising in fist 30 days of life are known as neonatal teeth.
• These teeth may represent pre­deciduous supernumerary teeth.

 

Question.31.Enumerate the diffrent developmental disturbances of teeth on basis of size, number and shape. Describe in detail the developmental disturbances in structure of tooth.

Answer.

Developmental Disturbances in structure of tooth

Following are the developmental disturbances in structure of tooth:

• Amelogenesis imperfecta or hereditary enamel dysplasia or hereditary brown enamel or hereditary opalescent teeth.
• Environmental enamel hypoplasia.
• Dentinogenesis imperfecta.
• Dentin dysplasia.
• Regional odontodysplasia or odontodysplasia or odontogenic dysplasia, odontogenesis imperfecta or ghost teeth
• Dentin hypocalcifiation.

Regional odontodysplasia

• It is also known as odontodysplasia or ghost teeth.
• In this both ectodermal and mesodermal tooth components are affcted.
• In this tooth is hypocalcifid and hypoplastic.

Etiology

• Due to abnormal migration of neural crest cells
• Due to medication taken during pregnancy
• In local trauma or infection
• In cases of radiation therapy
• Due to somatic mutations
• Local circulatory defiiency

Clinical Features

• Both the dentitions, i.e. deciduous and permanent dentitions are affcted.
• Slight female predilection is present.
• Maxillary teeth are more commonly involved as compared to mandibular teeth. More often involved are maxillary anterior teeth.
• Many of the affcted teeth are failed to erupt.
• Erupted teeth have small irregular crowns that are yellow to brown with rough surface.
• Presence of caries and periapical inflmmatory lesions are common.
• Gingival swelling is present adjacent to the affcted tooth.

Treatment

• Prosthetic replacement of teeth should be done.
• In some of teeth root canal should be done followed by capping of teeth.

 

Question.32.Write short note on Turner’s tooth.

Answer. Turner’s tooth is also known as Turner’s hypoplasia.
It is a localized enamel hypoplasia caused due to local infection or trauma and tooth affcted is known as
Turner’s tooth.

Pathogenesis

• If a deciduous tooth is affcted by dental caries when crown of succeeding permanent tooth is formed, bacterial infection involving periapical tissues may occur and this disturbs the ameloblastic layer of permanent tooth bud which leads to hypoplastic crown.
• During trauma when deciduous tooth get lodged in alveolus and disturb the budding permanent tooth bud,this results in yellowish or brownish stain or pigmentation of enamel on labial surface, at times pittng of enamel and irregularity of tooth crown is also present.

Clinical Features

• The enamel defects vary from focal areas of white, yellow, or brown discoloration to extensive hypoplasia, which can involve the entire crown.
• Anterior teeth are involved less frequently because crown formation is usually complete before the development of any apical inflmmatory disease in the relatively cariesresistant anterior deciduous dentition.
• Maxillary central incisors are affcted in the majority of the cases; the maxillary lateral incisors are altered less frequently.

 

Question.33.Describe developmental disturbances affcting shape of tooth.

Answer. Following are the developmental disturbances affcting shape of tooth:

• Enamel pearl
• Mulberry molar
• Globodontia
• Hutchinson’s incisor.

Twinning

Cleavage of tooth germ leads to formation of supernumerary tooth which is duplicate image of tooth from which it is developed.

Talon Cusp

• It resembles as an eagle’s talon which projects lingually from cingulum areas of a maxillary or mandibular permanent incisor.
• Talon’s cusp is more prevalent in person’s with RubinsteinTaybi syndrome.
• It blends smoothly with the tooth except that there is deep developmental groove where cusp blends with sloping lingual tooth surface.
• Talons’s cusp consists of normal enamel and dentin and consists of horn of pulp tissue.
• Major signifiance of talon’s cusp is that there is occlusal interference and there is also high incidence of caries.

Dens evaginates

• It is also known as Leong’s premolar, occlusal tuberculated premolar and occlusal enamel pearl.
• It is a developmental condition which appears clinically as an accessory cusp or a globule of enamel on occlusal surface between buccal and lingual cusps of premolar.
• Dens evaginatus occur due to proliferation and evagination of an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early development of tooth.
• Clinical signifiance is that the extra cusp may contribute to incomplete eruption, displacement of teeth and pulp exposure with subsequent infection following occlusal wear or fracture.

Enamel Pearl

• It is also known as enameloma or ectopic enamel.
• Enamel pearl is a nodule of enamel which is 1 to 2 mm in diameter which form on the root, at root bifurcation, at root trifurcation.
• Enamel pearl originates due to activity of remnants of Hertwig’s epithelal before it get reduced to cell rest of Malasez.
• Clinical signifiance is that these pearls give rise to periodontal problems.

Mulberry Molar

• It occurs in syphilis.
• Posterior tooth is involved.
• In this hyperplastic enamel occur with the spherical aggregates or the globules over surface of dentin.

Globodontia

• Globodontia is the enlarged bulbous malformed posterior tooth with no discernable cusps or grooves. In this teeth have a clover leaf appearance.
• In globodontia relation between cusps and groove get eliminated.
• This condition occur both in deciduous or permanent dentition.

Hutchinson’S Incisor

• It occurs in syphilis.
• In this incisal edge show notching.
• Tooth has shape of screw driver.

 

Question.34. Enumerate causes of enamel hypoplasia and describe amelogenesis imperfecta in detail.

Answer.

Enumeration Of Causes Of Enamel Hypoplasia

Following are the causes of enamel hypoplasia:

• Nutritional defiiency (Vitamins A, C and D)
• Exanthematous diseases, i.e. measles, chicken pox and scarlet fever
• Congenital syphilis
• Hypocalcemia
• Birth injury, prematurity, Rh hemolytic disease
• Local infection or trauma
• Ingestion of chemicals such as floride
  Idiopathic causes

 

Question.35. Write short note on Melkersson–Rosenthal syndrome.

Answer. This syndrome is the triad of chelitis granulomatosa,fisured tongue, facial palsy.

• Melkersson–Rosenthal syndrome is occasionally a manifestation of Crohn disease or orofacial granulomatosis.
• A genetic predisposition may exist in Melkersson–
  Rosenthal syndrome.
• Histologically the swellings of syndrome consist of chronic inflmmatory cell infitration which shows peri and para vascular aggregation of lymphocytes,plasma cells and histiocytes.
  At places non­caseating granuloma formation is seen along with epithelioid cells and LanghAns type giant cells.
• Six pattrns of fisured tongue are associated with the Melkersson, Rosenthal syndrome, i.e. central longitudinal fisuring, transverse fisuring originating from central fisure, plication, lateral longitudinal fisuring, transverse fisuring with central fisure and lateral longitudinal fisuring.

 

Question.36. Write short note on talon’s cusp.

Answer. Talon’s cusp is a well delineated accessory cusp which resembles as eagle’s talon which project lingually from cingulum areas of maxillary or mandibular permanent incisor.

• Talon’s cusp consists of normal enamel and dentin and has a horn of pulp tissue.
• Talon’s cusp blends smoothly with the tooth except that there is deep developmental groove where the cusp blends with sloping lingual tooth surface.
• Due to presence of Talon’s cusp patient’s face the problem with esthetics. There is also presence of occlusal interference and high incidence of caries is also noticed.
• Talon’s cusp is associated with Rubinstein Taybi’s syndrome as well as Sturge-Weber syndrome.

 

Question.37. Write short note on facial hemiatrophy.

Answer. It is also known as Parry Romberg syndrome.
It is the slowly progressive atrophy of soft tissue mainly half of the face and is also characterized by wasting of subcutaneous fat which sometimes accompanied by atrophy of skin, cartilage,bone and muscle.

Clinical Features

• It occurs during fist and second decades of life.
• Females are more commonly affcted as compared to males.
• It occurs more commonly over the left side of face.
• Onset of facial hemiatrophy is marked by white line furrow.
• Earliest sign is the presence of painless cleft.
• Patients can show sharp line of demarcation which resemble as large scar in between normal and abnormal skin.
• This is known as Coup de sabre.
• Overlying the atrophic fat a bluish hue may appear on the skin.

Oral Manifestations

• Presence of severe facial hemiatrophy which leads to facial deformation and mastication.
• Presence of hemiatrophy of lips and tongue.
• Delayed eruption is present which leads to malocclusion.
• Presence of incomplete root formation.
• During opening the mouth jaw is deviated towards affected side.

Differential Diagnosis

• Post traumatic atrophy: Brief history from patient is important.
• Goldenhar syndrome: It is non­progressive and is congenital.
  Mandibulofacial dysostosis: It is hereditary and cleft palate is present.

Treatment

• Surgical reconstruction is done.
• Malocclusion should be corrected by orthodontic treatment.

 

Question.38. Write short note on mesiodens.

Answer. Mesiodens is a supernumerary tooth in maxillary anterior incisor region.

• Mesiodens represents one of the more common supernumerary teeth and can erupt spontaneously.
• Mesiodens supernumerary tooth was classifid according to its location, i.e. it is located at or near to midline in incisal
  region of maxilla between the central incisors.
• According to the shape and size, two subclasses are considered in the classifiation of mesiodens; namely, eumorphic and dysmorphic.
  The eumorphic subclass is usually similar to a normal­sized central incisor, whereas the dysmorphic teeth have diffrent shapes and sizes and are categorized into conical, tuberculate, supplemental and odontomes.
  Out of these conical form is most common type.
• Mesiodens may be seen as an isolated fiding or as part of a syndrome, specially cleft lip and palate, cleidocranial dysostosis and Gardner’s syndrome.
• Mesiodens can occur either as single tooth or it is paired.
  It can be impacted or inverted.
• Mesiodens is a small tooth consisting of cone shaped crown and short root.
• Mesiodens can lead to retarded eruption, displacement or resorption of adjacent root.
• Mesiodens can frequently cause improper alignment.
• It usually results in oral problems such as malocclusion,food impaction, poor esthetics, and cyst formation.
• Immediate removal of mesiodens is usually indicated in the following situations; inhibition or delay of eruption,displacement of the adjacent tooth, interference with orthodontic appliances, presence of pathologic condition, or spontaneous eruption of the supernumerary tooth.

 

Question.39.List developmental disturbances affcting the tooth.
Discuss taurodontism and dilacerations.

Answer. Developmental disturbances affecting the tooth

Developmental Disturbances affecting structure of tooth

• Amelogenesis imperfecta
• Dentinogenesis imperfecta
• Enamel hypoplasia
• Dentin dysplasia
• Regional odontodysplasia
• Dentin hypocalcifiation

Developmental disturbances affecting number of tooth

• Anodontia
• Hypodontia
• Hyperdontia

Developmental disturbances affecting shape of tooth

• Gemination
• Twinning
• Fusion
• Concrescence
• Dilaceration
• Talon cusp
• Dens invaginatus
• Dens evaginatus
• Taurodontism
• Hypercementosis
• Enamel pearl
• Mulberry molar
• Globodontia
• Hutchinson’s incisor

Enumeration Of Anomalies Affecting Size Of Tooth

• Microdontia
• Macrodontia