ORAL PATHOLOGY FINALS PAPER 2025/2026 QUESTIOS
AND SOLUTIONS GRADED A+
✔✔An enamel defect resulting from the incomplete formation of the enamel matrix is
called:
Enamel hypocalcification
Enamel hypoplasia
Regional odontodysplasia
Enamel Pearls - ✔✔Enamel hypoplasia is a developmcntal def'ect in which the enamel
ofthe tccth is hard in contcxt but thin and dcficient in amount. It results from incomplete
formation ofthe enamel matrix with a deficiency in the cementing substance. Enamel
hypoplasia a1l'ects both the deciduous and pcnna- nent teeth. It is usually due to illness
or injury during tooth formation or due to a Note: Thc gcnetic lbrms ofcnamel hypoplasia
arc generally considcred to be types ofamelogen- esis imperfecta. The clinical
appearance ofenamel hypoplasia includes: l) the lack ofcontact between teeth, 2) the
rapid breakdown ofocclusal surfaces, 3) a yellowish-brorvn stain that appears whcre the
dentin is exposed. Note: lfonly one permancnt tooth is affected, it is usually caused by
physical damagc or periapical infections to the primary tooth that this pernanent tooth
replaced. This is known as h-vpoplasia." Remember: Enarncl hypocalcification is a
hereditary dental dcfcct in which thc enamel is soft and "Turner's undercalcificd in
context yct normal in quantity. It is caused by the dcfective maturation of amcloblasts
ftrere r.r a defect in the mineraliz tion ofthe fonned genetic disorder matrir). The teeth
are chalky in consistency, the surfaces wear down rapidly and a yellow to brown stain
appears as the underlying dentin is exposcd. This condition affects both the deciduous
and permanent teeth as well. See picture #9 in bookl€t \ote: Regional odontodysplasia
involves the hard tissues that are derived from both epithelial (enarnel) an<l
mesenchymal (dentin and cemenhnt) components of thc tooth-fonning apparatus. Thc
tccth in a region or quadrant of the maxilla or mandible are affccted to thc extent that
they exhibit short roots, open apical foramina' and enlarged pulp chambers' The
thinness and poor mineralization quality ofthe enamel and dentin la
✔✔All of the following statements concerning amelogenesis inperfecta are true
EXCEPT one. Which one is the EXCEPTION
It is an inherited condition which is transmitted as a dominant trait Because ofthe
enamel malformation, the teeth of individuals with amelogenesis imperfecta are often
discolored, sensitive to temperature changes, and painful to brush
It only affects the permanent teeth
It causes the enamel of the teeth to be soft and thin
The teeth appear yellow. because the dentin is visible through the thin enamel
The teeth are easily damaged and susceptible to decay - ✔✔It only affects the
permanent teeth
-{melogenesis imp erlecta (AI) is a relatively rare group ofinherited disorders
characterized bl abnormal enamel formation. The term amelogenesis imperfecta is
,reserved for hereditary defects ofenamel that are not associated with defects in other
parts ofthe body or other health problems. lt is a hereditary ectod€rmal defect, unlike
dentinogenesis imperfecta which is a hereditary rnesodemral defect. The AI enamel
defects are highly variable and include abnomralities that are classified as hy- poplastic
defect in amount ofenamel),hypomaturatron ol'euottel crystallites), andhypocalcified
(defect in fnal grov'tlt and mqhration (defect in initial crystallite Jbnnation followed by
dete. ti\ e gt'ovlh). The enamel in both the hypomaturation and hypocalcified Al is not
mineralized to the level of normal enamel and can be described as hypomineralized Al
can be intrerited as an x-linked, autosomal recessive (,4RJ, or autosomal dominant The
color ofthe enamel ranges from white opaque to yellow to brown, it is reduced in volume
and pitled. Contact points between teeth are often open and occlusal surfaces and
incisal edges frequently are severely abraded. Although the enamel are soft and
irregular, there is no in- crease jn caries mte. Note: Open bite is a common clinical
finding. The radiographic findings are fiequently distinctive and pathognomonic. when
the enamel is totally absent, the radiographic appearance makes the diagnosis obvious.
When some enamel is present, thin radiopaque coverings on the proximal surfaces
ofthe teeth are noted. When the anatonic crown forms are normal or nearly normal, the
softness ofthe defective enamel may not be easily distinguished from the dentin. ln all
cases, howevel the dentin' mentum are unaffected by the disease process itself(arlr*e
dentinogenesis inp
✔✔The abnormal loss of tooth structure due to non masticatory physical friction is
referred to asa
Erosion
Abfraction
Attrition
Abrasion - ✔✔Abrasion
Types ofabrasion: . l. Toothbrush abrasion: most olten results in V-shaped wedges at
the cervical margin in the canine and premolar areas. lt is caused by the use ofa hard
toothbrush and/or a horizontal brushing stroke and/or a gritty dentifrice. 2. Occlusal
abrasion: results in flattened cusps on all posterior teeth and wom incisal edges. lt
results from the chewing or biting ofhard foods or objects and chewing tob- acco.
Attrition is the wearing away of enamel and dentin due to the normal function or most
commonly, due to the excessive grinding or gdtting together oftecth by the patient
lreJbrced to a.r bruxism). The most noticeable effects ofattrition are polished facets, flat
incisal edges. discolored surfaces ofthe teeth and exposed dentin. Facets usually
develop on the linguoin- cisal of the maxillary central incisors, the facioincisal of the
mandibular canines and the linguoincisal ofthe maxillary canines. See picture #14 in
booklet . Erosion is the loss of tooth structure from non-mechanical means. It can result
from drinking acidic liquids or eating acidic foods. It is common in bulimic individuals as
a re- sult of regurgitated stomach acids. It affects smooth and occlusal surlaces. See
picture #12 in booklet . Abfraction lesions are cervical erosive lesions that can not be
attributed to any partic- off starting at the base ofthe tooth and exposing the gum Iine
,ofthe tooth to excessive wear See picture #11 in booklet ular cause: causing the enamel
to "pop''
✔✔All of the following can cause intrinsic staining of the teeth except:
Dentinogenesis imperfecta
Erythroblastosis fetalis
Porphyria
Fluorosis
Diabetes mellitus
Pulpal injury
Intemal resorption
Tetracyclines - ✔✔Diabetes mellitus (see chart for more details)
Extrinsic stains can be caused by bacteria, iron, tobacco, foods, beverages, gingival
hem- orhage. restorative materials and medications. Treatment: . lIost extrinsic stains
can be removed with abrasives; reduce or eliminate cause of stain . Intrinsic stains may
need bleaching, esthetic restorations, or prosthetic rehabilitation
✔✔A patient with which typ€ of amelogenesis imperfecta will have teeth that
demonstrate enamel that varies from thin and smooth to normal thickness with grooves,
furrows and/or pits?
Type I (Hypoplastic)
Type II (Hypomaturation)
Type III (Hypocalcified) - ✔✔Type I (Hypoplastic) (see chart for more details)
Remember: L Amelogenesis imperfecta is a hereditary ectodermal defect, unlike
dentinogenesis imper_ fecta which is a hereditary mesodermal f. In all three types
ofame)ogenesis imperfecta, fected by the disease process itself defect. the dentin, pulp
and cementum are unaf- /anlte dentinogenesis imperfecta).
✔✔In type 1 dentin dysplasia roots appear extremely short and the pulp is
Normal
Somewhat smaller
Extremely large
Completely obliterated - ✔✔Completely obliterated
Dentin dysplasia is another autosomal dominant trait that affects dentin. AII teeth ofboth
dentitions are affected. This condition has not been associated with any systemic con-
nective tissue disorder. This is a rare condition that has been subdivided into type I or
radicular type and a more rare type II or coronal type: . . Type | (radicular . . cl.,-
.splasia): more common type Both dentitions are normal in color and shape The teeth
are generally mobile, frequently abscess and can be lost prematurely . Teeth show
greater resistance to caries than do normal teeth Radiographic features: . Extremely
, short roots . Obliterated pulp chambers and root canals before eruption . ( Residual
fragments of pulp tissue appear typically as horizontal lucencies cnevrons) . Periapical
radiolucencies Type Il (coronal . . . dy.splasia) (granulomo,s or c.vst-r') around the
defective roots Color of primary teeth is opalescent Color of permanent teeth is normal
Coronal pulps ofpermanent teeth are r"rsually enlarged ("thi,\tle lube") a J arc lilled rvith
globules of abnormal dentin Radiographic features: . Deciduous teeth are similar in
appearance to type I, but permanent teeth exhibit enlarged pulp chambers . ("thistle
.\bsence of neriaoical radiolucencie" nbe") in appearance
✔✔Leukemia is a group of bone mrrrow diseases involving an uncontrolled increase ln:
Red blood cells (Erythocytes)
Platelets
Plasma cells
White blood cells (Leukocytes) - ✔✔White blood cells (Leukocytes)
Leukemia is a lomr ofcancer that begins nbe") in appearance jn the blood-forming cells
ofthe bone marrow soft, innet part o.l'1he botret. Undcr nomal circumstances, the blood-
fonning, or hematopoictic, cclls of thc bone marrow make leukocytes to defend thc body
against infectioLls organlsms such as r inrses and bacteria. But il'sot'ne leukocytes are
damaged and remain in an inmlature fbrm' they becornc poor int'ection fighters that
multiply excessivcly and do not dic olfas thcy should. The leukcmic cells accumulate
and lesscn the production of oxygcn-carrying red blood cclls /ery- rlr r or r les/. blood-clo
tting cells (plaletets), and normal lcukocytes. If untrcated, the surplus leukemic cells or
er$helm the bone marrow, enter the bloodstream. and eventually invadc other parts
ofthe btrdr. such as the lymph nodes, spleen, livcr, and central nervous syslern (brcin,
"^Pfualcoldr' * ar. the bchar ior of leukcmia is different than that of other canccrs, which
usually bcgin in major organs and ultimatcl), spread to thc bone marrow. Thcrc are more
than a dozen varictics ofleukenia, but thc follorving four types arc thc most com- nlon: L
-\cute lymphocytic lcnkcrlta (ALL). most common type in children 1. .\cute myelogenous
le]rlemia j. -1. Chronic lymphocytic lcukernia (AML.): most malignant type fczlr: least
malignant type Chronic myclogenous leukcmia (CML)t 2 distinct phases, invariably latal
lmportant: . . . Leukemia is classified by thc dominant cell type and by the duration from
onset to death Leukemia can modify thc inflammalory reaction Leukemia's affect on
teeth/gingiva: Duc to a decrease in immune responsc, periodontal problenrs can be
aggravated. Gingival enlargement can be a finding rvith leukemia Additionally, deficits
with platelets can bc scen intraorally with increased hemorrhag
✔✔A 48 year old female patient walks into your office. She states that she is diagnosed
with some disease which she can't remember the name of. Her physician wants her to
follow up with you, her dentist, regularly to watch out for cancer of the tongue and
throat. She also has a bald tongue, and states that her fingernails "look funny." What
disease does she have?
Aplastic anemia
Plummer-Vinson syndrome
AND SOLUTIONS GRADED A+
✔✔An enamel defect resulting from the incomplete formation of the enamel matrix is
called:
Enamel hypocalcification
Enamel hypoplasia
Regional odontodysplasia
Enamel Pearls - ✔✔Enamel hypoplasia is a developmcntal def'ect in which the enamel
ofthe tccth is hard in contcxt but thin and dcficient in amount. It results from incomplete
formation ofthe enamel matrix with a deficiency in the cementing substance. Enamel
hypoplasia a1l'ects both the deciduous and pcnna- nent teeth. It is usually due to illness
or injury during tooth formation or due to a Note: Thc gcnetic lbrms ofcnamel hypoplasia
arc generally considcred to be types ofamelogen- esis imperfecta. The clinical
appearance ofenamel hypoplasia includes: l) the lack ofcontact between teeth, 2) the
rapid breakdown ofocclusal surfaces, 3) a yellowish-brorvn stain that appears whcre the
dentin is exposed. Note: lfonly one permancnt tooth is affected, it is usually caused by
physical damagc or periapical infections to the primary tooth that this pernanent tooth
replaced. This is known as h-vpoplasia." Remember: Enarncl hypocalcification is a
hereditary dental dcfcct in which thc enamel is soft and "Turner's undercalcificd in
context yct normal in quantity. It is caused by the dcfective maturation of amcloblasts
ftrere r.r a defect in the mineraliz tion ofthe fonned genetic disorder matrir). The teeth
are chalky in consistency, the surfaces wear down rapidly and a yellow to brown stain
appears as the underlying dentin is exposcd. This condition affects both the deciduous
and permanent teeth as well. See picture #9 in bookl€t \ote: Regional odontodysplasia
involves the hard tissues that are derived from both epithelial (enarnel) an<l
mesenchymal (dentin and cemenhnt) components of thc tooth-fonning apparatus. Thc
tccth in a region or quadrant of the maxilla or mandible are affccted to thc extent that
they exhibit short roots, open apical foramina' and enlarged pulp chambers' The
thinness and poor mineralization quality ofthe enamel and dentin la
✔✔All of the following statements concerning amelogenesis inperfecta are true
EXCEPT one. Which one is the EXCEPTION
It is an inherited condition which is transmitted as a dominant trait Because ofthe
enamel malformation, the teeth of individuals with amelogenesis imperfecta are often
discolored, sensitive to temperature changes, and painful to brush
It only affects the permanent teeth
It causes the enamel of the teeth to be soft and thin
The teeth appear yellow. because the dentin is visible through the thin enamel
The teeth are easily damaged and susceptible to decay - ✔✔It only affects the
permanent teeth
-{melogenesis imp erlecta (AI) is a relatively rare group ofinherited disorders
characterized bl abnormal enamel formation. The term amelogenesis imperfecta is
,reserved for hereditary defects ofenamel that are not associated with defects in other
parts ofthe body or other health problems. lt is a hereditary ectod€rmal defect, unlike
dentinogenesis imperfecta which is a hereditary rnesodemral defect. The AI enamel
defects are highly variable and include abnomralities that are classified as hy- poplastic
defect in amount ofenamel),hypomaturatron ol'euottel crystallites), andhypocalcified
(defect in fnal grov'tlt and mqhration (defect in initial crystallite Jbnnation followed by
dete. ti\ e gt'ovlh). The enamel in both the hypomaturation and hypocalcified Al is not
mineralized to the level of normal enamel and can be described as hypomineralized Al
can be intrerited as an x-linked, autosomal recessive (,4RJ, or autosomal dominant The
color ofthe enamel ranges from white opaque to yellow to brown, it is reduced in volume
and pitled. Contact points between teeth are often open and occlusal surfaces and
incisal edges frequently are severely abraded. Although the enamel are soft and
irregular, there is no in- crease jn caries mte. Note: Open bite is a common clinical
finding. The radiographic findings are fiequently distinctive and pathognomonic. when
the enamel is totally absent, the radiographic appearance makes the diagnosis obvious.
When some enamel is present, thin radiopaque coverings on the proximal surfaces
ofthe teeth are noted. When the anatonic crown forms are normal or nearly normal, the
softness ofthe defective enamel may not be easily distinguished from the dentin. ln all
cases, howevel the dentin' mentum are unaffected by the disease process itself(arlr*e
dentinogenesis inp
✔✔The abnormal loss of tooth structure due to non masticatory physical friction is
referred to asa
Erosion
Abfraction
Attrition
Abrasion - ✔✔Abrasion
Types ofabrasion: . l. Toothbrush abrasion: most olten results in V-shaped wedges at
the cervical margin in the canine and premolar areas. lt is caused by the use ofa hard
toothbrush and/or a horizontal brushing stroke and/or a gritty dentifrice. 2. Occlusal
abrasion: results in flattened cusps on all posterior teeth and wom incisal edges. lt
results from the chewing or biting ofhard foods or objects and chewing tob- acco.
Attrition is the wearing away of enamel and dentin due to the normal function or most
commonly, due to the excessive grinding or gdtting together oftecth by the patient
lreJbrced to a.r bruxism). The most noticeable effects ofattrition are polished facets, flat
incisal edges. discolored surfaces ofthe teeth and exposed dentin. Facets usually
develop on the linguoin- cisal of the maxillary central incisors, the facioincisal of the
mandibular canines and the linguoincisal ofthe maxillary canines. See picture #14 in
booklet . Erosion is the loss of tooth structure from non-mechanical means. It can result
from drinking acidic liquids or eating acidic foods. It is common in bulimic individuals as
a re- sult of regurgitated stomach acids. It affects smooth and occlusal surlaces. See
picture #12 in booklet . Abfraction lesions are cervical erosive lesions that can not be
attributed to any partic- off starting at the base ofthe tooth and exposing the gum Iine
,ofthe tooth to excessive wear See picture #11 in booklet ular cause: causing the enamel
to "pop''
✔✔All of the following can cause intrinsic staining of the teeth except:
Dentinogenesis imperfecta
Erythroblastosis fetalis
Porphyria
Fluorosis
Diabetes mellitus
Pulpal injury
Intemal resorption
Tetracyclines - ✔✔Diabetes mellitus (see chart for more details)
Extrinsic stains can be caused by bacteria, iron, tobacco, foods, beverages, gingival
hem- orhage. restorative materials and medications. Treatment: . lIost extrinsic stains
can be removed with abrasives; reduce or eliminate cause of stain . Intrinsic stains may
need bleaching, esthetic restorations, or prosthetic rehabilitation
✔✔A patient with which typ€ of amelogenesis imperfecta will have teeth that
demonstrate enamel that varies from thin and smooth to normal thickness with grooves,
furrows and/or pits?
Type I (Hypoplastic)
Type II (Hypomaturation)
Type III (Hypocalcified) - ✔✔Type I (Hypoplastic) (see chart for more details)
Remember: L Amelogenesis imperfecta is a hereditary ectodermal defect, unlike
dentinogenesis imper_ fecta which is a hereditary mesodermal f. In all three types
ofame)ogenesis imperfecta, fected by the disease process itself defect. the dentin, pulp
and cementum are unaf- /anlte dentinogenesis imperfecta).
✔✔In type 1 dentin dysplasia roots appear extremely short and the pulp is
Normal
Somewhat smaller
Extremely large
Completely obliterated - ✔✔Completely obliterated
Dentin dysplasia is another autosomal dominant trait that affects dentin. AII teeth ofboth
dentitions are affected. This condition has not been associated with any systemic con-
nective tissue disorder. This is a rare condition that has been subdivided into type I or
radicular type and a more rare type II or coronal type: . . Type | (radicular . . cl.,-
.splasia): more common type Both dentitions are normal in color and shape The teeth
are generally mobile, frequently abscess and can be lost prematurely . Teeth show
greater resistance to caries than do normal teeth Radiographic features: . Extremely
, short roots . Obliterated pulp chambers and root canals before eruption . ( Residual
fragments of pulp tissue appear typically as horizontal lucencies cnevrons) . Periapical
radiolucencies Type Il (coronal . . . dy.splasia) (granulomo,s or c.vst-r') around the
defective roots Color of primary teeth is opalescent Color of permanent teeth is normal
Coronal pulps ofpermanent teeth are r"rsually enlarged ("thi,\tle lube") a J arc lilled rvith
globules of abnormal dentin Radiographic features: . Deciduous teeth are similar in
appearance to type I, but permanent teeth exhibit enlarged pulp chambers . ("thistle
.\bsence of neriaoical radiolucencie" nbe") in appearance
✔✔Leukemia is a group of bone mrrrow diseases involving an uncontrolled increase ln:
Red blood cells (Erythocytes)
Platelets
Plasma cells
White blood cells (Leukocytes) - ✔✔White blood cells (Leukocytes)
Leukemia is a lomr ofcancer that begins nbe") in appearance jn the blood-forming cells
ofthe bone marrow soft, innet part o.l'1he botret. Undcr nomal circumstances, the blood-
fonning, or hematopoictic, cclls of thc bone marrow make leukocytes to defend thc body
against infectioLls organlsms such as r inrses and bacteria. But il'sot'ne leukocytes are
damaged and remain in an inmlature fbrm' they becornc poor int'ection fighters that
multiply excessivcly and do not dic olfas thcy should. The leukcmic cells accumulate
and lesscn the production of oxygcn-carrying red blood cclls /ery- rlr r or r les/. blood-clo
tting cells (plaletets), and normal lcukocytes. If untrcated, the surplus leukemic cells or
er$helm the bone marrow, enter the bloodstream. and eventually invadc other parts
ofthe btrdr. such as the lymph nodes, spleen, livcr, and central nervous syslern (brcin,
"^Pfualcoldr' * ar. the bchar ior of leukcmia is different than that of other canccrs, which
usually bcgin in major organs and ultimatcl), spread to thc bone marrow. Thcrc are more
than a dozen varictics ofleukenia, but thc follorving four types arc thc most com- nlon: L
-\cute lymphocytic lcnkcrlta (ALL). most common type in children 1. .\cute myelogenous
le]rlemia j. -1. Chronic lymphocytic lcukernia (AML.): most malignant type fczlr: least
malignant type Chronic myclogenous leukcmia (CML)t 2 distinct phases, invariably latal
lmportant: . . . Leukemia is classified by thc dominant cell type and by the duration from
onset to death Leukemia can modify thc inflammalory reaction Leukemia's affect on
teeth/gingiva: Duc to a decrease in immune responsc, periodontal problenrs can be
aggravated. Gingival enlargement can be a finding rvith leukemia Additionally, deficits
with platelets can bc scen intraorally with increased hemorrhag
✔✔A 48 year old female patient walks into your office. She states that she is diagnosed
with some disease which she can't remember the name of. Her physician wants her to
follow up with you, her dentist, regularly to watch out for cancer of the tongue and
throat. She also has a bald tongue, and states that her fingernails "look funny." What
disease does she have?
Aplastic anemia
Plummer-Vinson syndrome
