quiz 3 - abnormalities of the teeth

Question 1

what is the etiology of developmental Alterations in tooth size?

Answer 1

genetic and environmental influences
deciduous teeth - intrauterine influences
permanent teeth - environment
tooth size is variable among races and sexes.

Question 2

What is microdontia?

Answer 2

One or more teeth that is or are physically smaller than normal.

Occurrence:
more common in females
Associated with hypodontia

Question 3

What are the clinical features of microdontia?

Answer 3

True generalized microdontia: all teeth are smaller than normal.
Uncommon, seen e.g. pituitary dwarfism.
Relative microdontia: normal sized teeth in larger than normal jaws, (macrognathia)(not microdontia)

Question 4

What is the treatment for microdontia?

Answer 4

Treatment is not necessary unless for aesthetic purposes..

maxillary pig collaterals are often restored to full size by porcelain crowns

Question 5

What is isolated of microdontia?

Answer 5

It is not uncommon
most frequently seen in maxillary lateral incisors, “peg laterals”. Peg lateral tends to occurred bilaterally, has short roots and appears to be familial as autosomal dominant with incomplete penetrance.
This condition also affects maxillary third molars and supernumerary teeth.
Associated with hypodontia.

Question 6

What is macrodontia? Occurrence? Clinical features?

Answer 6

It is one or more teeth, which is/are physically larger than normal

occurrence: more common in males

Clinical features: associate with hyperdontia

True generalized macrodontia is rare, associated with pituitary gigantism.
Relative macrodontia: Normal sized teeth within small jaws.

Regional or localized macrodontia: it’s only occasionally found and often associated with hemifacial hyperplasia, which also shows unilateral premature eruption.

Question 7

What is the treatment for macrodontia/

Answer 7

Treatment is not necessary unless for aesthetic purposes.

the term macrodontia should not be used to describe teeth that have been altered by fusion or gemination.

Question 8

What is gemination? etiolog? What is the occurrence?

Answer 8

A single enlarged tooth or joined (eg. double) two in which the tooth count is normal when the anomalous tooth is counted as one
Etiology: developmental
Occurrence:
Occur in both dentitions
Higher frequency in the anterior teeth
Maxillary permanent incisors most often affected

Question 9

What is fusion? etiology? Occurrence?

Answer 9

A single and large tooth or jointed tooth in which the tooth counts reveals a missing tooth when the anomalous tooth is counted as one.
etiology: developmental
Occurrence: occur in both dentitions.
Higher frequency in the anterior teeth and tends to occur in the mandible.

Question 10

Random notes

Answer 10

gemination demonstrated a single root canal.

Fusion demonstrates separated canals but this does not hold true in all cases.

A variety of appearances are noted with both gemination and fusion resulting in a anatomically correct but larger tooth. e.g. bifid crown w/2 separated roots

Question 11

What are complications with fusion and gemination?

Answer 11

With fusion or gemination in deciduous dentition can result in:

crowding
abnormal spacing
delayed or ectopic eruption of the underlying permanent teeth

Question 12

What is the treatment for gemination and fusion?

Answer 12

When germination or fusion is detected in deciduous teeth, the progression of eruption of the permanent teeth should be monitored clinically and radiographically.
Extraction may be necessary to prevent an abnormality any eruption.
In permanent to dentition the treatment ranges from selected shaping shaping with or without placement of full crowns to surgical removal with prosthetic replacement.

Question 13

What is concrescence? etiology? Occurrence? Complications? Treatment?

Answer 13

It is the union of two fully formed teeth, joined along the route surfaces by cementum.

etiology: maybe caused by proximity of roots of developing teeth or do to excessive production of cementum secondary to periApical inflammation

Occurrence: maxillary molars most often affected

Complications: concrescence become significant if one of the teeth and involved requires extraction.

Treatment: often no treatment is required unless the union interferes with eruption; then surgical removal may be warranted.

Question 14

what is cusp of carabelli? Description? Occurrence? Clinical features? Treatment?

Answer 14

Description: an additional cost typically seen on the palatal surface of the mesio-lingual cusp of a maxillary molar.
Occurrence: most common example of supernumerary cusps, maybe seen in both dentitions. Prevalence high in whites (90%), rare in Asians.
Clinical features: ranges from definite cusp to a small indented pit or fissure. One present is usually most prominent on the first maxillary molar, and less obvious on the second and third molar.
Treatment: no treatment is required unless a deep groove is present; then, it should be sealed to prevent dental caries.

Question 15

What is a prostostylid?

Answer 15

And analogous accessory cusp is seen occasionally on the mesiobuccal cusp of a mandibular permanent or deciduous Molar.

Question 16

What is an accessory cusp - talon cuspid (dens evaginatus of anterior teeth)? Occurrence?

Answer 16

An additional cusp located on the lingual surface of an anterior tooth.

occurrence: predominantly on the permanent maxillary lateral, lingual aspect (55%) or central incisors (33%). Less frequently on the mandibular anterior teeth.

Uncommon. More frequently and Asians, native Americans, the Inuit, those of Arab descent and patients with Rubinstein-Taybi syndrome.
Rare in the deciduous dentition
In isolated cases, genetic influences appear to have an effect.

Question 17

What are the clinical features of talon cuspid (dens evaginatus of anterior teeth)?

Answer 17

The abnormal cusp arises from the cingulum portion of the tooth (typically maxillary incisor) and usually it extends to the incisal edge imparting a T-shape that resembles an “eagles talon”.

Maybe a unilateral or bilateral
Most talon cusps contain a pulpal extension.
Lingual pits may be present.

Question 18

What is dens evaginatus (central tubercle)? Occurrence?

Answer 18

A focal area of crown that projects outward and produces what appears as an extra-cusp centrally located on occlusal surface of premolars.

Occurrence: rare in whites, most common in Asians, the Inuit and Native Americans.
Typically on the premolar teeth, It Is usually bilateral, And demonstrate a marked mandibular predominance.
Occasionally in molars.

Question 19

What is dens evaginatus (central tubercle) treatment?

Answer 19

Maybe associated with shovel shaped teeth.
the cusp contain enamel, dentin and pulp

treatment:
often produce occlusal problems, then gradual grinding or removal of the cusp is indicated
Attempts to maintain vitality is only a partial success
If shovel shaped incisors are present, check for pit and fissures that should be sealed to prevent caries.

Question 20

What is dens invaginatus (dens in dente)? Occurrence?

Answer 20

A deep enamel-lined pit that extends for varying depths into the underlying dentin, often displacing pulp chamber and sometimes altering the shape of the root.

Occurrence:
Prevalence varies from 0.4% to 10% of all patients
Most common in permanent maxillary lateral incisors, followed by central incisors, premolars, canines and molars
Uni or bilateral and the involvement may be singular, multiple or bilateral

Question 21

what does dens invaginatus (dens in dente) do? treatment?

Answer 21

Dens invaginatus predispose the tooth to early decary and pulpitis.
Classified into three types, Type I “coronal” is seen more frequently.
Occasionally the invagination Is large resembling a tooth within a tooth “DENS IN DENTE”
The invagination may be dilated deforming creating the tooth “DILATED ODONTOME”
I radiograph is useful for diagnosis.

Treatment: prophylactic filling is recommended. Treatment ranges from endodontic therapy to extraction.

Question 22

What are enamel pearls? etiology?

Answer 22

Presence of a small, spherical enamel projection located on the roof surface. Maybe 1 to 4 pearls on a single tooth. The enamel pearl may consist of enamel only or enamel, dentin and pulp.

etiology: thoughts to arise from a localized bulging contact of the odontoblastic layer which may provide a prolonged contact between Hertwig’s root sheath developing detin which triggers induction of enamel formation.

Question 23

What are the clinical features and treatment of enamel pearls?

Answer 23

Clinical features:
Radio graphically, how well defined radiopaque nodule(s) along the root’s surface.
Weak point of periodontal attachment and point of plaque retention.

Treatment:
meticulous oral hygiene is recommended.
If removal is contemplated, remember that some enamel pearls contained vital pulp tissue.

Question 24

What are cervical enamel extensions? Occurrence? Clinical features?

Answer 24

Focal apical extension of the coronal enamel Beyond the normal CEJ onto the root of the tooth.

occurrence:
Prevalence varies from 8.6% two thirty-two point six % of all patients and is higher in Asians.
Most frequently in mandibular molars (1st, 2nd, and 3rd molars respectively)

Clinical features:
Associated with localized loss of periodontal attachment with bifurcation involvement.
Associated with development of an inflammatory cyst (buccal bifurcation cyst).

Question 25

What is the treatment for cervical enamel extensions?

Answer 25

Therapy is directed at achieving a more durable attachment and providing access to the area for appropriate cleaning.
Flattening or removing the enamel in the combination with a new attachment procedure and furcation plasty may provide a more durable attachment and access for cleaning.
buccal bifurcation cyst when present needs to be removed.

Question 26

what is taurodontism? Prevalence? Etiology?

Answer 26

And enlargement of the body and pulp chamber of a multi-rooted tooth, with apical displacement of the pulpal floor and furcation of the roots. (tauro: bull, dont: tooth)

Prevalence it Is highly variable 0.5% to 46%. Varying degrees of severity.

etiology: probably results from late invagination of Hertwig’s root sheath, the mechanism that determines the shape of the tooth roots.

Question 27

What are the clinical features of taurodontism? diagnosis and treatment?

Answer 27

The body of the tooth is enlarged at the expense of the roots. Constriction at the tooth cervix (CEJ) is absent or reduced. Teeth have a rectangular appearance.
Permanent teeth are more frequently affected and maybe unilateral or bilateral.
May be an isolated incident, or maybe a component of a specific syndrome e.g. Down’s syndrome.

Diagnosis is based on the radiographic appearance.

Treatment is not required but can be a complicating factor during root canal procedures

Question 28

what are supernumerary roots? what is the localization, complications, and treatment?

Answer 28

And increased number of roots on the tooth.

localization:
most commonly seen in permanent molars (especially third molars) from either arch followed by mandibular cuspids and premolars.
Reported in both dentitions.

Complications: detection is important when extractions or root canal treatment are undertaken.

Treatment: no treatment is required but the detection of the accessory root is of critical importance when endodontic therapy of exodontia is undertaken.

Question 29

what is dilaceration? etiology? localization? treatment? complications?

Answer 29

an abnormal curvature to the root or less frequently the crown of a tooth.

Etiology: most cases are idiopathic, other cases appear to be related to trauma to the tooth bud during root development. Pathologic process adjacent to the developing tooth may also be a cause.

Localization: any tooth but most common and permanent maxillary incisors followed by mandibular anterior dentition.

Treatment: no treatment for minor dilacerations. Teeth with delayed of abnormal eruption may be exposed and orthodontically moved into position. Extraction in some cases.

Complications: caution must be exercised if the involved tooth requires endodontic therapy or extraction. Failure of eruption.

Question 30

what appearance will translucent or opaque enamel be?

Answer 30

the color of normal teeth varies depending on the shade, translucency, and thickenss of the ename.

Translucent enamel: teeth appear yellow at cervical one third and bluish-white at the incisal edge.

Opaque enamel: teeth are more uniform gray-white.

Question 31

What are extrinsic stains and intrisnic stains?

Answer 31

occur from surface accumulations of an exogenous pigment an typically can be removed with a surface treatment.
Intrinsic stains: arise from endogenous material that incorporate into the enamel or Dentin and cannot be removed by prophylaxis with toothpaste or pumice.

Question 32

What is the etiology of Extrinsic stains?

Answer 32

Tobacco, food for example with chlorophyll, and beverage for example coffee and tea.
chromogenic bacteria Can’t produce colorations from green, black, brown to orange. In black-brown stains are probably secondary to the formation of ferric sulfide from an interaction between bacterial hydrogen sulfide and iron and the saliva or gingival curricular fluid.
Gingival hemorrhage: the color results from the breakdown of hemoglobin into green biliverdin.

Medications for example with the use of 8% Stannous fluoride probably secondary to combination of the stannous ion with bacterial sulfides.

Antiseptics: chlorhexidine may produce a yellowish brown stain that predominately involves the interproximal surfaces air gingival margins. The degree of sustaining depends on concentration and patient susceptibility.

Question 33

What is the treatment of extrinsic stains?

Answer 33

Prophylactic procedures including polishing with fine pumice and improve oral hygiene.

stains on the surface of teeth that can be removed with abrasives.

Question 34

What is the etiology of intrinsic stains?

Answer 34

Trauma: the Frequent finding after trauma, especially in deciduous dentition. Post traumatic injuries may create pink, yellow or dark gray discoloration.

Medications for example the ingestion of tetracycline during the mineralization of the organic matrix of developing teeth and bone results in permanent incorporation of the drug into the mineral component of these tissues. this drug can cross the placental barrier (avoid during pregnancy and in children up to age 8 years).

Restorative materials: especially amalgams on large class II proximal restorations on molars and deep lingual metallic restorations on anterior incisors.

Amelogenesis imperfecta, dnetinogenesis imperfecta and dental fluorosis.

congenital erythropoietic porphyria: an autosomal recessive disorder of porphyrin metabolism that is responsible for the development of a defective pathway for the metabolism of hematoporphyrins, resulting in the accumulation of excessive porphyrins in the blood and urine.

Doscoloration occurs because excess porphyrins are present in the blood during the mineralization of the teeth. Affected teeth are pinkish brown.

erythoblastosis fetalis: a hemolytic anemia that begins in uterus. IT results from incompatible factors in the blood of the mother and fetus. The result of the extensive hemolysis is the elevated bilirubin blood pigments. The pigment becomes deposited in the developing teeth of the fetus and teeth show from yellow to deep shades of green colors.

Treatment: focuses on aesthetic solution.

Question 35

what is the developmental alterations in number of teeth pathogenesis?

Answer 35

probably related to the development of excess or loss of dental lamina and influenced by genetic and environmental factors.

Question 36

what is anodontia? occurrence? treatment?

Answer 36

a total lack of tooth development.

occurrence: total anodontia (lack of all teeth) is a rare condition and is often associated with the hereditary condition ectodermal dysplasia.
treatment: prosthetic replacement.

Question 37

what is hypodontia? etiology?

Answer 37

Lack of development of one or more teeth.

Oligodontia: a subdivision of hypodontia, indicates the lack of development of six or more teeth.

The loss of developing tooth buds in most instances appears to be genetically controlled; however, the environment most likely influences the final results or, in some cases, may be responsible completely for the lack of tooth formation.
The dental lamina is extremely sensitive to external stimuli (trauma, infection, radiation, chemotherapy, endocrine disturbances and the severe intrauterine disturbances) and damage before tooth formation can result in hypodontia.

Research has identified a gene mutation in only a small percentage of non-syndromic hypodontia.

The currently implicated genes include PAX9 gene, the AXIN2 gene, and the He-Zhao deficiency.
The most critical discovery related to hypodontia is the AXIN2 gene mutation. This pattern of oligodontia it Is inherited as an autosomal dominant disorder with most commonly missing teeth being the permanent second and third molars, Second premolars, lower incisors and maxillary lateral incisors. The AXIN2 Gene mutation also has been associated with development of adenomatous polyps of the colon and colorectal carcinomas.
Patients with similar examples of oligodontia should be questioned for family history of colon cancer, with a further medical evaluation

Question 38

What are the clinical features of Hypodontia? treatment?

Answer 38

The most commonly affected teeth are third molars followed by second premolars and lateral incisors.
hypodontia is associated with microdontia, reduced alveolar development, increased freeway space and retained primary teeth.
More frequently and the females (1.5:1)
hypodontia maybe associated with syndromes; oligodontia often noted rather than hypodontia. e.g. hypohidrotic ectodermal dysplasia.

treatment: depends on severity from none to prosthetic replacement.

Question 39

What is the occurrence of hypodontia?

Answer 39

Failure if teeth to form is one of the most common dental developmental abnormalities, with reported prevalence of 1.6% to 9.6% in the permanent teeth when the absence of third molars is excluded.
The prevalence increases to 20% if 3rd molars are considered.
hypodontia in deciduous dentition is uncommon and prevalence ranges from 0.5% to 0.9% and when present often affects lateral incisors.

Question 40

What is the definition of hyperdontia? occurrence?

Answer 40

The development of an increased number of teeth
additional teeth are turned supernumerary.

occurrence: prevalence of permanent teeth and awaits 0.1% to 3.8% and is lower in primary teeth 0.3% to 0.8%

Most cases are single tooth hyperdontia (76% to 86%) in a permanent teeth; 95% in maxilla with predilection for an interior region, followed by maxillary fourth molars and mandibular fourth molars, premolars, canines and lateral incisors. Most are unilateral.

Question 41

What are the clinical features of hyperdontia?

Answer 41

Male predominance
non-syndromic multiple supernumerary teeth occur most frequently in the mandible.
Maybe associated with Gardner’s syndrome and Cleidocranial dysplasia.
Supernumerary teeth are divided into supplemental (normal size and shape) or rudimentary (abnormal shape and smaller size) types.
hyperdontia associated with macrodontia.

Question 42

What are some terms to describe supernumerary teeth? treatment?

Answer 42

mesiodens - between the maxillary anterior incisors
distomolar (distodens) - fourth molar
paramolar - situated lingually or buccally to a molar tooth
natal teeth - teeth present in newborns, most are mandibular incisors.
neonatal teeth - teeth arising within the first 30 days of life, most are prematurely erupted portions of the deciduous dentition

Treatment of hyperdontia is early removal of the accessory tooth.

Question 43

What is primary impaction? etiology and occurrence?

Answer 43

Teeth that ceased to irrupt before emergence are impacted.
etiology: due to obstruction from crowding or from some other physical barrier (e.g. Insufficient maxillofacial development, overlying cyst or tumor, trauma, thickened overlying bone or soft tissue).

Occurrence: impaction of deciduous teeth is very rare, if present involves second molars.

A common event in permanent teeth, most often mandibular third molar, followed by maxillary third molars, maxillary cuspids.
Less commonly, premolars, mandibular canines, maxillary premolars, and the second molars.

Question 44

What are the clinical features of primary impaction? Treatment? Other choices?

Answer 44

Impaction may be partially erupted or completely covered by bone and is classified according to the angulation of the tooth.

Treatment: treatment varies but surgical removal is more frequent.

Other choices: Long term observation, orthodontically assisted eruption, and transplantation.

Question 45

what are the risks of non-intervention? intervention?

Answer 45

non-intervention:

1. development of pathologic conditions. e.g, cyst and tumors
2. crowding of dentition
3. resorption and worsening of the periodontal status of adjacent teeth

intervention: sensory loss, alveolitis, trismus, infection, fracture and TMJ injury to adjacent teeth.

Question 46

What is ankylosis? etiology? occurrence?

Answer 46

Cessation of eruption after emergence is termed ankylosis and hookers from the fusion of tooth within the surrounding bone.

Etiology: pathogenesis is unknown. It may be secondary to one of many factors such as inflammation and the subsequent bone repair and with focal loss of periodontal ligament, bone and cementum become mixed, causing fusion of the tooth to bone.

Occurrence: any age but usually in association with erupted primary molars. Prevalence of clinically detectable ankylosis in children is 1.3 to 8.9%
ankylosis in the permanent teeth is uncommon and usually end teeth that have been avulsed and re-implanted.

Question 47

What are the clinical features of ankylosis?

Answer 47

D affected tooth is below The adjacent dentition in a patient with a history of previous full occlusion.
Radio graphically, absence of periodontal ligament space maybe noted, but is often in the bifurcation, making detection difficult.
A sharp, solid sound may be noted on percussion of the affected tooth but detected only when 20% of the root is fused to the bone

Question 48

What are the complications of ankylosis?

Answer 48

ankylosed teeth that are allowed to remain in position can lead to

1. occlusal and periodontal problems
2. over irruption of the opposing teeth
3. the adjacent teeth often inclined toward be affected tooth
4. occasionally, impaction of the underlying permanent tooth.

Question 49

What is the treatment for ankylosis?

Answer 49

Extraction of the ankylosed primary tooth is necessary to allow in eruption of the underlying permanent tooth and space maintenance.
In a permanent teeth or primary teeth without underlying successors, prosthetic buildup can be placed to augment the occlusal height.

Question 50

What are post developmental loss of tooth structure?

Answer 50

Attrition
 abrasion
erosion
 abfraction
 internal/external resorption

Lost a tooth structure can begin on the enamel surface of the crown through attrition, abrasion, erosion or abfraction.
Acquired environmental loss of tooth structure is often multifactorial.

Question 51

What is attrition?

Answer 51

Loss of tooth structure caused by tooth to tooth contact during a occlusion and mastication.
part is physiologic but when it is extensive and affects appearance, function or dental sensitivity, The process must be considered pathologic.
Attrition can occur in both dentition’s.

Question 52

What are the clinical features of attrition?

Answer 52

Most often involve the occlusal and incisal surfaces and a link you’ll of anterior maxillary teeth and labial of the anterior mandibular teeth.
Large flat, smooth and shiny wear faces are found in a relationship that correspond to the pattern of occlusion.
Interproximal contact points also are affected from vertical movement of the teeth during function..
The destruction it can be accelerated by poor quality or absence of an animal, premature contacts, edge to edge occlusion, intra-oral abrasives, diet, erosion and grinding habits.

Question 53

What is abrasion?

Answer 53

The pathologic loss of tooth structure as a result of an abnormal habit or an abnormal use of abrasive substances orally.
The most common source is aggressive toothbrushing that combines an abrasive toothpaste with heavy pressure and a horizontal brushing stroke and present as horizontal cervical notches on buccal surface of exposed radicular cementum and dentin.

Question 54

What are other causes of abrasion?

Answer 54

Thread biting
pipe stems
Bobby pin produces a notch in incisal surfaces
inappropriate dental floss produces loss of inter-proximal radicular cementum and Dentin
Toothpicks use
Tobacco chewing can also be the cause of abrasion.

Question 55

What is erosion?

Answer 55

The loss of tooth structure from a nonbacterial chemical process.
presence of acids, either from foods (lemon, soft drinks, vinegar), medications, or internal sources (e.g. gastric secretions “perimolysis”) from voluntary and involuntary regurgitation
Also, external sources e.g. Acidic industrial atmosphere or poorly monitored pH swimming pools.
Sometimes no obvious cause can be found.

Question 56

What are the clinical features of erosion?

Answer 56

The classic pattern of dental erosion is the cupped lesion (Central depression of dentin Surrounded by elevated enamel).
erosion commonly affects the facial surfaces of the maxillary anteriors and appears as shallow spoon-shaped depressions in the cervical portion of the crowns (often associated with dietary sources).
Posterior teeth often exhibit loss of occlusal surface, and the edges of metallic restorations may be above the level of the tooth structure.
Occasionally, the entire buccal cusps are lost and replaced by ski slope-like depressions that extend from the lingual cusp to the buccal CEJ.

Question 57

other random erosion notes

Answer 57

Internal source is most often gastric secretions from regurgitation, hiatal hernia, chronic vomiting.
This pattern shows generalized tooth loss on lingual surfaces. The exposed dentin has a concave surface and the shows of peripheral white line of enamel.
The posterior teeth frequently exhibit extensive loss of the occlusal surface and amalgam margins are above the surface of the dentin.

Question 58

What is the best treatment for attrition, abrasion and erosion?

Answer 58

Best treated with early diagnosis and intervention to restrict the severity of tooth loss.

Question 59

What is the abstraction?

Answer 59

loss of tooth structure that results from repeated tooth flexure caused by occlusal stress.
clinically, it appears as wedge shaped defects Limited to the cervical area of the teeth. some lesions are subgingival.
More common in the mandible and with bruxism.

Diagnosis: defects are deep, narrow and V-shaped.

Question 60

What is internal resorption?

Answer 60

Loss of tooth structure can also begin on dentin or cementum by internal or external resorption.

Internal resorptionis a relatively rare form of tooth loss that begins within the pulpal Chambers of intact teeth destroying Dentin as it extends outward in uniform pattern toward the tooth surfaces.

The cells in the dental pulp accomplish the resorption.
Usually occurs in late adult life.

Question 61

What is the etiology of internal resorption? Clinical features?

Answer 61

Most cases follow injury to pulp tissue e.g., physical trauma or caries related pulpitis.

clinical features:
Usually asymptomatic and discovered through routine radiographs.
Usually a single tooth affected, Although cases of more than one tooth affected has been seen.

Question 62

What are the two main patterns of internal resorption?

Answer 62

1. inflammatory resorption: the resorbed dentin is replaced by inflamed granulation tissue.
   - when it affects the coronal pulp, the crown shows a pink discoloration described as “ pink tooth of Mummery”
   - when it occurs in the root, a balloon like radiograph dilation of the canal is seen.
   - internal resorption Secondary to infectious pulpitis may stop upon necrosis of the responsible cells within the pulp
   - although many cases are progressive, some cases are self limiting and usually arise in traumatized teeth or those that have recently undergone orthodontic or periodontal therapy
2. replacement or metaplastic resorption: portions of the pulp dentinal wall are resorbed and replaced with bone or cementum-like bone.
   - Radio graphically, it appears as an enlargement of the canal, which is filled with material that is less radiodense than the surrounding dentin.
   - the outline of distraction is less defined than seen in inflammatory resorption

Question 63

What is the treatment for internal resorption?

Answer 63

Root canal therapy before perforation
once there is communication between pulp and periodontal ligament, the prognosis for saving the tooth is very poor.
Extraction often is necessary for radicular perforation that do not respond to therapy

Question 64

what is external resorption? etiology?

Answer 64

loss of tooth structure that begins on the outer surface and extends inwards toward the pulp.

• the resorption is accomplished by cells located on the periodontal ligament
• a common process

etiology: specific etiology uncertain and probably may have one of several causes: trauma is often associated, pressure from tumor, cyst, adjacent tooth growth, mechanical forces (orthodontic therapy), inflammatory effects, or idiopathic.

Question 65

what are clinical features of external resorption?

Answer 65

usually presents with a “moth-eaten” radiographic pattern
this may occur in one or more teeth
several teeth may be involved and may not be obvious cause (musltiple idiopathic root resorption).
one of two patterns may be seen.

1. resorption occurs immediately apical to CEJ on root surface
2. resorption starts at tooth apex and progress occlusally.
   - external resorption can create defects in crowns of teeth before eruption - it is not pre-eruptive caries.

Question 66

what is treatment for external resorption?

Answer 66

identification and elimination of any accelerating factor.
removal of all soft tissue from the sites of dental destruction
therapy directed against local periodontal pathogens may be helpful in some cases.
over an extend clinical course, resorption eventually causes loss of the affected tooth.

Question 67

how do you know if it is internal or external resorption?

Answer 67

when it is difficult to distinguish external from internal resorption, the mesial-buccal-distal rule can be used through 2 radiographic exposures: one perpendicular and one mesial.
the external resorption appears to shift away from the pulp canal when the radiographs are compared.
cone CT should be considered if the standard views provide insufficient information.

Question 68

what is hypoplasia, diffuse opacities, and demarcated opacities?

Answer 68

environmental: during enamel formation, ameloblasts are susceptible to various external factors that may be reflected in erupted teeth.
Enamel defects are classified into one of the three patterns:
- hypoplasia occurs in the form of pits, grooves or large areas of missing enamel.
- diffuse opacities appear as variations in the translucency of the enamel. Enamel has an increased white opacity with no clear boundary with the adjacent normal enamel.
- demarcated opacities show areas of decreased translucence, increased opacity and a sharp boundary with the adjacent enamel.

Question 69

what is turner’s hypoplasia? occurrence?

Answer 69

enamel defect seen in permanent teeth secondary to periapical inflammatory disease of the overlying deciduous tooth or trauma.

ocurrence: most frequently in premolars and maxillary incisors.
about 45% of all children sustain injuries to their primary teeth.

Question 70

what are clinical features of turner’s hypoplasia? treatment?

Answer 70

clinical features: the defect varies white, yellow or brown color to extensive hypoplasia.

treatment: depending on the severity (restoration of the tooth for aesthetic purposes).

Question 71

what is dental fluorosis?

Answer 71

ingestion of excess amounts of fluoride during tooth formation, usually in drinking water can result in enamel defects.
the optimum fluoride dose is 1 part per million gallons of water.
fluoride appears to create its significant enamel defects through retention of amelogenin proteins in the enamel structure, forming hypomineralized enamel.
As fluoride levels increase, hypoplasia of enamel in addition to brown discoloration may be seen.
Can produce pitting in the enamel or “chalky” surface to the enamel. Teeth are resistant to caries.

Question 72

what is the diagnosis for dental fluorosis?

Answer 72

the defect presents in bilaterally and symmetric distribution
evidence of prior excessive fluoride intake or elevated levels of fluoride in the enamel or other tissues
primarily an aesthetic problem

Question 73

what is syphilitic hypoplasia?

Answer 73

congenital syphilis is due to a transplacental infection with Treponema pallidum. In utero infection by T. pallidum may result in enamel hypoplasia of the permanent incisors and first molars.
- the affected incisors (Hutchinson’s incisors) are shaped like screwdrivers: broad cervically and narrow incisally, with a notched incisal edge

Question 74

what does the first molars look like in syphilitic hypoplasia?

Answer 74

first molars appear as irregularly shaped crowns made-up of multiple tiny globules of ename instead of cusps (Mulberry molars).
Most defects in the enamel are cosmetic rather than functional.
Aesthetically or functionally defective teeth can be restored through a variety of cosmetically pleasing techniques.

Question 75

What is amelogenesis imperfecta?

Answer 75

A group of inherited conditions affecting the enamel of teeth in the abence of a systemic disorder.
Genes taht encode for enamel proteins (amelogin, enamelin, others) are mutated in patients with this condition.

Question 76

What is the etiology of amelogenesis imperfecta?

Answer 76

at least 14 different hereditary subtypes of AI exist, with numerous patterns of inheritance and a wide variety of clinical manifestations.
It may be inherited as an autosomal dominant, autosomal recessive, or X-liked disorder
to date, mutations of seven genes have been associated with this (AMELIX gene, ENAM gene, MMP-20 gene, KLK4 gene, DLX3 gene, FAM83H, and WDR72 gene).
Each gene can be mutated in a variety of ways, often creating diverse and distinct phenotypic patterns.

Question 77

What is enamel formation like and what are the hereditary defects of the formation of enamel divided into?

Answer 77

enamel formation is a multi-step process and its development of enamel can be divided into three major stages

1. elaboration of the organic matrix
2. mineralization of the matrix
3. maturation of the enamel.

hereditary defect of the formation of enamel are divided as: hypoplastic, hypocalcified, and hypomaturation

occurrence: estimated frequency varies between 1:718 and 1:14,000 of the population
In general, both the deciduous and the permanent dentitions are diffusely involved.

Question 78

what is hypoplastic meaning with amelogenesis imperfecta?

Answer 78

tooth enamel does not develop to a normal thickness because of failure of ameloblasts to lay down enamel matrix properly.

• On radiographs the abnormal enamel contrasts normally with dentin, thin peripheral outline of radiopaque enamel.
• Clinically, it ranges from pits and grooves in one patient to complete absence in another.
• Because of reduced enamel thickness in some cases, abnormal contour and absent interproximal contact points may be evident
• The color of teeth varies from tooth to tooth and patient to patient from white opaque to yellow to brown

Question 79

what does hypocalcified mean with amelogenesis imperfecta?

Answer 79

enamel quantity is normal bu no significant mineralization occurs; therefore, enamel is very soft and easily lost.

• the color of the teeth color range from yellow-brown or orange but often becomes stained brown to black.
• cervical enamel is better calcified and generally remains on the crown.
• on radiographs the enamel has a moth-eated appearance and is less radiopaque than dentin
• unerupted teeth and anterior open bite are not rare.

Question 80

what does hypomaturation mean with amelogenesis imperfecta?

Answer 80

defect in the maturation of the ename’s crystal structure. The enamel is of normal thickness but not of normal hardness and translucency.

• affected teeth are normal in shape but exhibit a mottle, appearance with opaque white-yellow discoloration.
• the enamel is softer than normal and tends to chip from the underlying dentin.
• the radiodensity of enamel is almost equal to that of normal dentin.
• although the enamel is soft and irregular, teeth are not caries prone.
• the mildes form of hypomaturation is the snow-capped teeth where enamel is of normal hardness and exhibits a white opaque zone on the incisal or occlusal one quarter to one third of the crown. Both dentitions are affected.

Question 81

what is amelogenesis imperfecta with taurodontism (hypomaturation-hypoplastic AI)?

Answer 81

The thin enamel is yellow to brown and pitted.
On radiographs the enamel has a radiodensity similar to dentin, large pulp chambers may be seen in single-rooted teeth in addition to varying degrees of taurodontism.
In some types there is an increased prevalence of anterior open bite, delayed eruption or tooth impaction.

Question 82

What is the treatment like for amelogenesis imperfecta?

Answer 82

• It is generally not easy to diagnose the exact type of amelogenesis imperfecta clinically because of the frequent similarity among different varieties.
• The mode of inheritance must be kept in mind, and an accurate family history should always be taken.

Treatment

• depend on severity and subtype.
• the main problems are aesthetics, dental sensitivity and loss of vertical dimension. Restorative measurements.

Question 83

What is dentinogenesis imperfecta, hereditary opalescent dentin? etiology?

Answer 83

A hereditary developmental disturbance of the dentin in the absence of any systemic disorder.
DI arise as an isolated disorder of teeth with no systemic manifestations
DI can occur in association with a number of syndromes, e.g. Osteogenesis Imperfecta that has dental manifestations that mimic DI, but are related to different gene mutation.

Etiology:

• autosomal dominant disorder and occurs in about 1:8000 whites in USA.
• DI is associated with mutation of the DSPP (dentin sialophosphoprotein) gene.

Question 84

what are the clinical features of Dentinogenesis Imperfecta?

Answer 84

• All teeth in both dentitions are affected
• Deciduous teeth are affected more severely followed by permanent incisors and first molars with second and third molars being least altered.
• Teeth have a blue-to-brown discoloration, often with a distinctive translucence.
• Enamel often separates easily from the underlying defective dentin. Once exposed, the dentin often shows accelerated attrition.
• Dentin is abnormally soft, providing inadequate functional support to the overlying enamel, therefore, enamel chips away easily. Despite the exposure of dentin, teeth are not particularly prone to dental caries.

Question 85

What are the teeth like in dentinogenesis imperfecta?

Answer 85

radiographically teeth have bulbous crowns, cervical constrictions, thin roots an early obliteration of the root canals and pulp chambers.
Some teeth may show normal thickness of enam, extremely thin dentin, and dramatically enlarged pulps called shell teeth.
This abnormality is most frequent in deciduous teeth in presence of DI or may be unassociated with DI as an isolated finding in both dentitions.

Question 86

Dentinogenesis imperfecta treatment?

Answer 86

• Protecting teeth from wear; improving esthetics; eventual construction of dentures.
• The entire dentition is a risk because of numerous problems.
• The teeth are not good candidates for full crown because of cervical fracture or for abutments for partial denture because of root fracture.
• Similar dental changes of DI may be seen in conjuction with systemic hereditary disorder of bone, osteogenesis imperfect.
  Dentin defects associated with this bone disease are termed osteogenesis imperfecta with opalescent teeth.

Question 87

What is dentin dysplasia? what types are there?

Answer 87

An autosomal dominant inherited disorder that affects dentin.
- classified into two major patterns.
Type I: Radicular dental dysplasia.
Type II: Coronal dental dysplasia. It is currently thought to be a variation of dentinogenesis.
Two types are rare but Type I is more common.

Question 88

What is dentin dysplasia type I (DD Type I - radiuclar type) rootless teeth like?

Answer 88

• deciduous and permanent dentitions affected.
• deciduous often more severly involved; variability most prominent in permanent teeth.
• the enamel and coronal dentin are normal clinically and well formed, but radiuclar dentin loses all organization and subsequently is shortened dramatically.
• roots are missing or rudimentary in form showing markedly tapered forms (rootless teeth)
• early exfoliation is commonly seen
• pulp often completely obliterated but may show crescent or chevron-shaped pulp chamber (horizontal lucencies). Pulp obliteration often causes pulpal necrosis and periapical pathosis without obvious cause.
• Mandibular molars commonly have W-shaped roots.

Question 89

What is dentin dysplasia type II (DD Type II) coronal type like?

Answer 89

• Type II associated mutation of the DSPP (dentinsialophosphoprotein) gene.
• The root length is normal in both dentitions
• Deciduous teeth closely resemble those of dentinogenesis imperfect. The teeth show a blue-to-amber-to-brown translucence.
• Radiographically, the dental changes include bulbous crown, cervical constriction, thin roots, and early obliteration of the pulp.
• Permanent teeth demonstrate normal clinical coloration, but radiographically, coronal pulps are enlarged with apical extension of the pulp chamber “thistle tube-shaped or flame-shaped” and pulp stones. Root length in both dentitions is normal. The pulp canals are narrow.

Question 90

What is the treatment for dentin dysplasia type I and II?

Answer 90

Type 1: Directed toward retention of teeth as long as possible, no good prognosis.
Type II: Directed toward retention of teeth as long as possible and meticulous oral hygiene.

Question 91

What is regional odontodysplasia (ghost teeth)?

Answer 91

• An uncommon, localized developmental abnormality of extensive adverse effects on formation of ename, dentin and pulp.
• Most cases are Idiopathic.
• The most popular theory is an alteration in vascular supply.

Question 92

What is the localization like for regional odontodysplasia (ghost teeth)?

Answer 92

• Occur in both dentitions
• Most frequently seen in anterior maxilla
• Ipsilateral involvement of both arches
• Bilateral changes in the same jaw have been reported

Question 93

What are the clinical features of regional odontodysplasia?

Answer 93

• Many of affected teeth fail to erupt.
• Erupted teeth show small yellow to brown crowns with rough surfaces.
• Caries and periapical lesions are common.
• The most common presenting signs and symptoms include:
  - delayed or failure of eruption
  - early exfoliation, abscess formation
  - malformed teeth
  - non-inflammatory gingival enlargement
• Radiographically, faint outlines of teeth (enamel and dentin) with large pulpal chambers and short roots “ghost teeth”.

Question 94

What is the treament for regional odontodysplasia?

Answer 94

• Therapy is directed toward retention of the affected teeth, whenever possible, to allow for appropriate development and preservation of the surrounding alveolar ridge.
• Because of the poor quality of the affected teeth, their removal is usually indicated.
• the resulting edentulous area can be restored with prosthetic appliances or implants.