ORAL PATHOLOGY EXAMS SCRIPT QUESTIONS AND
SOLUTIONS MARKED A+
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
,Pernicious anemia
Cushing's syndrome - ✔✔Plummer-Vinson syndrome
Plummer-Vinson syndrome characterized by an iron-deficiency anemia, atrophic
changes in the buccal, glossopharyngeal, and esophageal mucous metnbranes,
koilonycha (spoon-shaped./inger rail.s), and dysphagia. The dysphagia is due to an
esophageal stric- ture or web. SCC of the tongue and throat are complications. lt is
most common in mid- dle aged women, rarely in the male. The etiology unknown.
Because ofthe predisposition to the development ofcarcinoma ofthe oral mucous
membranes, it is essential that the di- agnosis be established early so that treatment
can be given ASAP This includes administration of iron, vitamin B complex and a high
protein diet. Aplastic anemia is a form of anemia in which the capacity of the bone
marrow to gen- erate red blood cells is defective. Two types: l. Primary: unknown cause,
affects young adults. The signs and symptoms include pallor, weakness, malaise,
dyspnea (dilfcul4, breathing), headache and vertigo. Oral symptoms include
spontaneous bleeding,bnstsing (petechlaeT and gingival infections. It is usually fatal. 2.
Secondary: caused by exposure to toxic agents, such as radiation, chemicals or drugs
(fbr exanple, chloramphenicol). It can occur at any age. Symptoms are the same as
primary. Prognosis is good once you remove the cause. *** Aplastic anemia is the most
serious and life-threatening blood dyscrasia associated s ith drus toxiciw.
What disorder is a result of a genetic mutation causing the substitution of glutamic acid
by a valine and results in dental radiographs with enlarged marrow spaces?
Cystic fibrosis
Muscular dystrophy
Polio
Sickle-cell anemia - ✔✔Sickle-cell anemia
Sickle-cell anemia is an inherited disease in which the red blood cells, normally disc-
shaped, become crescent shaped, As a result, they function abnomally and cause small
blood clots. These clots give rise to recurrent painful episodes called crises." Sickle-cell
anemia ofabnormal hemoglobin "sickle cell pain (also called sickle-cell disease) is the
result ofthe production S/ due to a genetic defect. It is carried as a trait by 10% of
African Americans and 0.2olo have sickle-cell anemia. lt is more common in fe-
(Hemoglobin males and usually clinically manifests itselfbefore the age of30. The typical
signs ofane- mia are present. The patient is weak, short ofbreath and easily fatigued.
Muscle and patns are common. Denlal radiographs ar€ oft€n of diagnostic value:
marrow spaces are markedly en- larged because ofthe loss ofmany trabeculae; the
trabeculae, which are present, are often abnormally prominent. Occasionally,
osteosclerotic areas are noted in the midst of large radiolucent marow spaces.
However, the lamina dura and the teeth are unaffected. See picture #18 in booklet \ote:
The gene defect is a known mutation ofa single nucleotlde (th),minelbr ofthe beta-globin
gene, which results in glutamic acid to be substituted by valine. Sicklecell anemia
occurs when a person inherits two abnormal ger'es (one front a person inherits one
, abnormal gene for the disease, they have what is called sickle cell trait. The life span
ofred blood cells is reduced from 120 to 20 days.
The category of pigmented (usually purple) lesions in the skin caused by extravasation
of blood from the capillaries is known as:
Petechiae
Ecchymosis
Varicose veins
Purpura - ✔✔Purpura
Purpura spots (pinpoint spots) are purplish discolorations in the skin produced by small
bleeding vessels near the surlace ofthe skin. Purpura may also occur in the mucous
mem- branes (such as the lining oJ the mouth) and in the intemal organs. Purpura by
itselfis only a sign of other underlying causes of bleeding. Purpura may occur with either
normal purpuras) or decreased platelet counts (thromboq)topenic purpltra.rr. Platelets
help maintain the integrity of the capillary lining and are platefet counts
hrcnlhrombocftopenic irnportant in the clotting process. Note: Large purpura spots (> 3
mn) are called ecchy- moses. Major kinds of purpura: . Thrombocytopenic purpura
(Werlhol's tlisease): a bleeding disorder characterized by a deficiency in the number
olplatelets. This resr.rlts in multiple bruises, petechiae, and hemonhage into the tissues
. Thrombotic thrombocytopenic purpura (TTP): a severe and frequently fatal form
characterized by a low platelet count in the blood due to consumption of platelets by
thrombosis in the terminal arterioles and capillaries ofmany organs Oral manifestations
of thrombocytopenic purpura: . Severe and profuse gingival hemorrhage . Petechiae
occur commonly on the palate Important: Tooth extractions are contraindicated due to
the tendency for excessive bleedin s.
All of the following statements are true EXCEPT one. which one is the EXCEPTION
Acute leukemias have a slow onset and progression
Acute leukemias are characterized by the appearance of immature, abnormal cells in
the bone marrow and peripheral blood and frequently in the liver, spleen, lymph nodes,
and other parenchymatous organs
The clinical picture of acute leukemias are marked by the effects ol anemia, which is
usually severe (/ittigue, molaise), an absence of functioning granulocles (proneness to
inlbction and inflammation), and thrombocytopenia (hemorrlrugic diathesis)
The spleen and liver usually are moderately enlarged, while enlarged lymph nodes are
seen mainly in acute lymphocytic leukemia.
Fever and a very high ESR are found Leukocyte counts vary greatly in the acute
leukemias - ✔✔Acute leukemias have a slow onset and progression
This is false; acute leukemias have a rapid ons€t and progression. -{cute leukemia is
characterized by malignant proliferation olwhite blood cell precursors I hle.\ts) in bone
marrow and lymph tissue and their accumulation in peripheral blood, bone rnanow, and
body tissues. Leukemic cells inhjbit normal bone marrow production rrf en throcytes.
SOLUTIONS MARKED A+
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
,Pernicious anemia
Cushing's syndrome - ✔✔Plummer-Vinson syndrome
Plummer-Vinson syndrome characterized by an iron-deficiency anemia, atrophic
changes in the buccal, glossopharyngeal, and esophageal mucous metnbranes,
koilonycha (spoon-shaped./inger rail.s), and dysphagia. The dysphagia is due to an
esophageal stric- ture or web. SCC of the tongue and throat are complications. lt is
most common in mid- dle aged women, rarely in the male. The etiology unknown.
Because ofthe predisposition to the development ofcarcinoma ofthe oral mucous
membranes, it is essential that the di- agnosis be established early so that treatment
can be given ASAP This includes administration of iron, vitamin B complex and a high
protein diet. Aplastic anemia is a form of anemia in which the capacity of the bone
marrow to gen- erate red blood cells is defective. Two types: l. Primary: unknown cause,
affects young adults. The signs and symptoms include pallor, weakness, malaise,
dyspnea (dilfcul4, breathing), headache and vertigo. Oral symptoms include
spontaneous bleeding,bnstsing (petechlaeT and gingival infections. It is usually fatal. 2.
Secondary: caused by exposure to toxic agents, such as radiation, chemicals or drugs
(fbr exanple, chloramphenicol). It can occur at any age. Symptoms are the same as
primary. Prognosis is good once you remove the cause. *** Aplastic anemia is the most
serious and life-threatening blood dyscrasia associated s ith drus toxiciw.
What disorder is a result of a genetic mutation causing the substitution of glutamic acid
by a valine and results in dental radiographs with enlarged marrow spaces?
Cystic fibrosis
Muscular dystrophy
Polio
Sickle-cell anemia - ✔✔Sickle-cell anemia
Sickle-cell anemia is an inherited disease in which the red blood cells, normally disc-
shaped, become crescent shaped, As a result, they function abnomally and cause small
blood clots. These clots give rise to recurrent painful episodes called crises." Sickle-cell
anemia ofabnormal hemoglobin "sickle cell pain (also called sickle-cell disease) is the
result ofthe production S/ due to a genetic defect. It is carried as a trait by 10% of
African Americans and 0.2olo have sickle-cell anemia. lt is more common in fe-
(Hemoglobin males and usually clinically manifests itselfbefore the age of30. The typical
signs ofane- mia are present. The patient is weak, short ofbreath and easily fatigued.
Muscle and patns are common. Denlal radiographs ar€ oft€n of diagnostic value:
marrow spaces are markedly en- larged because ofthe loss ofmany trabeculae; the
trabeculae, which are present, are often abnormally prominent. Occasionally,
osteosclerotic areas are noted in the midst of large radiolucent marow spaces.
However, the lamina dura and the teeth are unaffected. See picture #18 in booklet \ote:
The gene defect is a known mutation ofa single nucleotlde (th),minelbr ofthe beta-globin
gene, which results in glutamic acid to be substituted by valine. Sicklecell anemia
occurs when a person inherits two abnormal ger'es (one front a person inherits one
, abnormal gene for the disease, they have what is called sickle cell trait. The life span
ofred blood cells is reduced from 120 to 20 days.
The category of pigmented (usually purple) lesions in the skin caused by extravasation
of blood from the capillaries is known as:
Petechiae
Ecchymosis
Varicose veins
Purpura - ✔✔Purpura
Purpura spots (pinpoint spots) are purplish discolorations in the skin produced by small
bleeding vessels near the surlace ofthe skin. Purpura may also occur in the mucous
mem- branes (such as the lining oJ the mouth) and in the intemal organs. Purpura by
itselfis only a sign of other underlying causes of bleeding. Purpura may occur with either
normal purpuras) or decreased platelet counts (thromboq)topenic purpltra.rr. Platelets
help maintain the integrity of the capillary lining and are platefet counts
hrcnlhrombocftopenic irnportant in the clotting process. Note: Large purpura spots (> 3
mn) are called ecchy- moses. Major kinds of purpura: . Thrombocytopenic purpura
(Werlhol's tlisease): a bleeding disorder characterized by a deficiency in the number
olplatelets. This resr.rlts in multiple bruises, petechiae, and hemonhage into the tissues
. Thrombotic thrombocytopenic purpura (TTP): a severe and frequently fatal form
characterized by a low platelet count in the blood due to consumption of platelets by
thrombosis in the terminal arterioles and capillaries ofmany organs Oral manifestations
of thrombocytopenic purpura: . Severe and profuse gingival hemorrhage . Petechiae
occur commonly on the palate Important: Tooth extractions are contraindicated due to
the tendency for excessive bleedin s.
All of the following statements are true EXCEPT one. which one is the EXCEPTION
Acute leukemias have a slow onset and progression
Acute leukemias are characterized by the appearance of immature, abnormal cells in
the bone marrow and peripheral blood and frequently in the liver, spleen, lymph nodes,
and other parenchymatous organs
The clinical picture of acute leukemias are marked by the effects ol anemia, which is
usually severe (/ittigue, molaise), an absence of functioning granulocles (proneness to
inlbction and inflammation), and thrombocytopenia (hemorrlrugic diathesis)
The spleen and liver usually are moderately enlarged, while enlarged lymph nodes are
seen mainly in acute lymphocytic leukemia.
Fever and a very high ESR are found Leukocyte counts vary greatly in the acute
leukemias - ✔✔Acute leukemias have a slow onset and progression
This is false; acute leukemias have a rapid ons€t and progression. -{cute leukemia is
characterized by malignant proliferation olwhite blood cell precursors I hle.\ts) in bone
marrow and lymph tissue and their accumulation in peripheral blood, bone rnanow, and
body tissues. Leukemic cells inhjbit normal bone marrow production rrf en throcytes.
