A guide to common oral lesions
Foliate papillae
Description: Foliate papillae appear as an area of vertical folds and grooves located on the extreme
posterior-lateral surface of the tongue. They are occasionally mistaken for tumors or inflammatory
disease. The grooves are best seen when air from an air syringe is directed at them. Their long axis is “up
and down”, that is they are at right angles to the long axis of the tongue. Our experience has been that
they are usually bilaterally symmetrical. In most people, the papillae are small and inconspicuous,
whereas in others they are prominent. Lingual tonsils are found immediately beneath the foliate papillae
and, when hyperplastic, cause a prominence of the papillae. Those familiar with the basic fold and groove
structure of the foliate papillae are not apt to confuse these normal structures with an abnormality.
ETIOLOGY: They are normal anatomical structures.
TREATMENT: None required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Hyperplastic lingual tonsils, squamous carcinoma, soft tissue tumors
Lymphoid aggregates
DESCRIPTION: Lymphoid aggregates appear as small, slightly elevated nodules that may be normal
colored or have a slight yellow-orange hue. Those illustrated here are in the soft palate. They may be
found anywhere in the mucosa but are especially common where the mouth meets the throat, including
the base of the tongue. This lymphoid rich area has been called Waldeyer’s ring. When they occupy the
same area as the foliate papillae, the papillae may take on a more nodular appearance. In the tongue they
have been referred to as “lingual tonsils.”
ETIOLOGY: They are normal structures, components of Waldeyer’s ring.
TREATMENT: None required.
PROGNOSIS: Good. They may enlarge or regress in relationship to oral or upper respiratory infections.
DIFFERENTIAL DIAGNOSIS: Although foliate papillae and lymphoid aggregates of lingual tonsils may
occupy the same area, they are different entities.
Mucocele
DESCRIPTION: A mucocele is a collection of saliva in the oral mucosa. They are soft elevations whose
color ranges from that of normal mucosa to light blue or even white. Patients with mucoceles regularly
state that the lesion “gets larger, then smaller, then larger again.” This has become an important
diagnostic sign. The mucosa of the lower lip and buccal mucosa are the most common sites, but any
area that contains intraoral salivary glands is a potential site.
ETIOLOGY: Traumatic severance of salivary ducts permitting salivary escape into mucosa is the accepted
etiology.
TREATMENT: Surgical excision deep enough to include the underlying gland that feeds it.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Salivary gland neoplasms (especially mucoepidermoid carcinoma), varix,
and hemangioma.
Irritation fibroma (traumatic fibroma)
DESCRIPTION: Traumatic fibroma is a dome-shaped soft tissue mass usually found on buccal mucosa
along the line of occlusion. Less frequently they may be found on lips and tongue. They are among the
most common oral soft tissue lesions. The color is usually the same as the surrounding mucosa and the
consistency is surprisingly soft. Patients are generally aware of the lesion being present months to years
with little change. Histologically, they exhibit fibrous hyperplasia that is collagenous and acellular.
ETIOLOGY: The presumed etiology is trauma to the affected mucosa. Accidental biting probably accounts
for most of these lesions.
TREATMENT: Excision
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Salivary gland tumors and other soft tissue tumors may have a similar
appearance but are usually more firm. Other lesions such as mucocele may also resemble traumatic
fibroma.
Leukoedema
DESCRIPTION: Leukoedema appears as a filmy, opaque, white to slate gray discoloration of mucosa,
chiefly buccal mucosa. Redundancy of the mucosa may impart a folded or wrinkled appearance to the
relaxed mucous membrane. It partially disappears when the mucosa is stretched. It is stated to be seen
in 90% of Blacks and 10–90% in Whites. This variation may be due to the difficulty in observation of
leukoedema in non-pigmented mucosa. Leukoedema is accentuated in smokers.
ETIOLOGY: Leukoedema is a variation of normal that should not be confused with something ominous.
Intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin is
thought to account for the white appearance. Microscopic examination reveals superficial squamous cells
have a clear, seemingly empty cytoplasm but it has not been shown that there is an increase in
intracellular water. Thus, the term edema is questionable.
TREATMENT: None required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: White sponge nevus, hereditary benign intraepithelial dyskeratosis, and
dyskeratosis congenital. All are extremely rare
.
Pyogenic granuloma
DESCRIPTION: Pyogenic granuloma is a red, nodular overgrowth of granulation tissue that arises from
the mucosal or skin surface. Approximately two-thirds of oral lesions are found on the gingival followed
in descending order by the lips, tongue, buccal mucosa, palate, vestibule and edentulous areas. The
interdental papilla of the maxillary facial gingival is the single most common site. A review of more than
800 cases disclosed the mean size to be approximately 1.0 cm with a range of 3 mm to 4 cm. Females
were more often affected (72%). Duration varied widely with a mean of 5.5 months. Because of the
vascular nature of pyogenic granuloma, they bleed easily and some cause mild pain. They commonly
develop during pregnancy. The association with pregnancy is so common that the lesion has also been
called granuloma gravidarum or pregnancy tumor. Because pus is infrequently found in this lesion, the
term pyogenic granuloma is a misnomer but remains the preferred term.
ETIOLOGY: The stimulus that provokes this overgrowth of granulation tissue is unknown although mild
trauma and infection are prominently mentioned.
TREATMENT: Conservative excision. They may recur.
PROGNOSIS: Good.
DIFFERENTIAL DIAGNOSIS: Peripheral giant cell granuloma and peripheral ossifying fibroma.
DESCRIPTION: Varices appear as red, blue, or deep purple broad-based elevations in oral mucosa. The
size is usually less than 5 mm. The buccal mucosa is a common place to find them, however, they are
also found in lip mucosa and ventral and lateral mucosa of the tongue and floor of the mouth. On ventral
tongue they are apt to be multiple and the term “caviar tongue” has been commonly used to describe
them. They are seen more commonly in the elderly.
ETIOLOGY: A varix is a distended vein that elevates the overlying mucosa. The reason for venous
distention is unclear but may be related to weakening of the vessel wall secondary to aging.
TREATMENT: None usually required. They often thrombose but this is of little clinical consequence.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Mucocele, hemangioma and angina bullosa hemorragica.
Description: Foliate papillae appear as an area of vertical folds and grooves located on the extreme
posterior-lateral surface of the tongue. They are occasionally mistaken for tumors or inflammatory
disease. The grooves are best seen when air from an air syringe is directed at them. Their long axis is “up
and down”, that is they are at right angles to the long axis of the tongue. Our experience has been that
they are usually bilaterally symmetrical. In most people, the papillae are small and inconspicuous,
whereas in others they are prominent. Lingual tonsils are found immediately beneath the foliate papillae
and, when hyperplastic, cause a prominence of the papillae. Those familiar with the basic fold and groove
structure of the foliate papillae are not apt to confuse these normal structures with an abnormality.
ETIOLOGY: They are normal anatomical structures.
TREATMENT: None required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Hyperplastic lingual tonsils, squamous carcinoma, soft tissue tumors
Lymphoid aggregates
DESCRIPTION: Lymphoid aggregates appear as small, slightly elevated nodules that may be normal
colored or have a slight yellow-orange hue. Those illustrated here are in the soft palate. They may be
found anywhere in the mucosa but are especially common where the mouth meets the throat, including
the base of the tongue. This lymphoid rich area has been called Waldeyer’s ring. When they occupy the
same area as the foliate papillae, the papillae may take on a more nodular appearance. In the tongue they
have been referred to as “lingual tonsils.”
ETIOLOGY: They are normal structures, components of Waldeyer’s ring.
TREATMENT: None required.
PROGNOSIS: Good. They may enlarge or regress in relationship to oral or upper respiratory infections.
DIFFERENTIAL DIAGNOSIS: Although foliate papillae and lymphoid aggregates of lingual tonsils may
occupy the same area, they are different entities.
Mucocele
DESCRIPTION: A mucocele is a collection of saliva in the oral mucosa. They are soft elevations whose
color ranges from that of normal mucosa to light blue or even white. Patients with mucoceles regularly
state that the lesion “gets larger, then smaller, then larger again.” This has become an important
diagnostic sign. The mucosa of the lower lip and buccal mucosa are the most common sites, but any
area that contains intraoral salivary glands is a potential site.
ETIOLOGY: Traumatic severance of salivary ducts permitting salivary escape into mucosa is the accepted
etiology.
TREATMENT: Surgical excision deep enough to include the underlying gland that feeds it.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Salivary gland neoplasms (especially mucoepidermoid carcinoma), varix,
and hemangioma.
Irritation fibroma (traumatic fibroma)
DESCRIPTION: Traumatic fibroma is a dome-shaped soft tissue mass usually found on buccal mucosa
along the line of occlusion. Less frequently they may be found on lips and tongue. They are among the
most common oral soft tissue lesions. The color is usually the same as the surrounding mucosa and the
consistency is surprisingly soft. Patients are generally aware of the lesion being present months to years
with little change. Histologically, they exhibit fibrous hyperplasia that is collagenous and acellular.
ETIOLOGY: The presumed etiology is trauma to the affected mucosa. Accidental biting probably accounts
for most of these lesions.
TREATMENT: Excision
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Salivary gland tumors and other soft tissue tumors may have a similar
appearance but are usually more firm. Other lesions such as mucocele may also resemble traumatic
fibroma.
Leukoedema
DESCRIPTION: Leukoedema appears as a filmy, opaque, white to slate gray discoloration of mucosa,
chiefly buccal mucosa. Redundancy of the mucosa may impart a folded or wrinkled appearance to the
relaxed mucous membrane. It partially disappears when the mucosa is stretched. It is stated to be seen
in 90% of Blacks and 10–90% in Whites. This variation may be due to the difficulty in observation of
leukoedema in non-pigmented mucosa. Leukoedema is accentuated in smokers.
ETIOLOGY: Leukoedema is a variation of normal that should not be confused with something ominous.
Intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin is
thought to account for the white appearance. Microscopic examination reveals superficial squamous cells
have a clear, seemingly empty cytoplasm but it has not been shown that there is an increase in
intracellular water. Thus, the term edema is questionable.
TREATMENT: None required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: White sponge nevus, hereditary benign intraepithelial dyskeratosis, and
dyskeratosis congenital. All are extremely rare
.
Pyogenic granuloma
DESCRIPTION: Pyogenic granuloma is a red, nodular overgrowth of granulation tissue that arises from
the mucosal or skin surface. Approximately two-thirds of oral lesions are found on the gingival followed
in descending order by the lips, tongue, buccal mucosa, palate, vestibule and edentulous areas. The
interdental papilla of the maxillary facial gingival is the single most common site. A review of more than
800 cases disclosed the mean size to be approximately 1.0 cm with a range of 3 mm to 4 cm. Females
were more often affected (72%). Duration varied widely with a mean of 5.5 months. Because of the
vascular nature of pyogenic granuloma, they bleed easily and some cause mild pain. They commonly
develop during pregnancy. The association with pregnancy is so common that the lesion has also been
called granuloma gravidarum or pregnancy tumor. Because pus is infrequently found in this lesion, the
term pyogenic granuloma is a misnomer but remains the preferred term.
ETIOLOGY: The stimulus that provokes this overgrowth of granulation tissue is unknown although mild
trauma and infection are prominently mentioned.
TREATMENT: Conservative excision. They may recur.
PROGNOSIS: Good.
DIFFERENTIAL DIAGNOSIS: Peripheral giant cell granuloma and peripheral ossifying fibroma.
Torus palatinus and torus mandibularis
DESCRIPTION: Bony exostoses in the midline of the hard palate and on the lingual aspect of the mandible
are referred to as torus palatinus and torus mandibularis respectively. Some studies suggest they are
inherited whereas others suggest environmental factors. They start in childhood and reach peak incidence
in young adults. Once they have reached “programmed size”, their growth stops. Some are so subtle they
hardly constitute an abnormality, whereas others are so large they frighten the uninitiated observer. In
the mandible, they may form a row of nodules as illustrated. In most individuals they occur bilaterally.
Those in the palate may be divided by deep grooves to form a cluster of nodules. Exostoses entirely
similar to tori occur elsewhere on the alveolar bone, but there is no specific name for them. It has been
estimated that palatal tori occur in 20-35% of the population. Mandibular tori are less common, about
10% of the population are affected.
ETIOLOGY: Tori are developmental over-growths of normal bone and as previously stated they may be
inherited.
TREATMENT: Tori and other exostoses seldom cause symptoms. Because they extend above the level of
surrounding normal mucosa, they invite trauma. Small traumatic ulcers are therefore commonly seen on
the mucosa that covers tori, more commonly palatal tori. Tori may interfere with prosthetic appliances
and, for that reason, may require removal.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Tori have such a characteristic clinical appearance and history that
differential diagnosis is seldom a problem.
Varix (plural: varices)DESCRIPTION: Bony exostoses in the midline of the hard palate and on the lingual aspect of the mandible
are referred to as torus palatinus and torus mandibularis respectively. Some studies suggest they are
inherited whereas others suggest environmental factors. They start in childhood and reach peak incidence
in young adults. Once they have reached “programmed size”, their growth stops. Some are so subtle they
hardly constitute an abnormality, whereas others are so large they frighten the uninitiated observer. In
the mandible, they may form a row of nodules as illustrated. In most individuals they occur bilaterally.
Those in the palate may be divided by deep grooves to form a cluster of nodules. Exostoses entirely
similar to tori occur elsewhere on the alveolar bone, but there is no specific name for them. It has been
estimated that palatal tori occur in 20-35% of the population. Mandibular tori are less common, about
10% of the population are affected.
ETIOLOGY: Tori are developmental over-growths of normal bone and as previously stated they may be
inherited.
TREATMENT: Tori and other exostoses seldom cause symptoms. Because they extend above the level of
surrounding normal mucosa, they invite trauma. Small traumatic ulcers are therefore commonly seen on
the mucosa that covers tori, more commonly palatal tori. Tori may interfere with prosthetic appliances
and, for that reason, may require removal.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Tori have such a characteristic clinical appearance and history that
differential diagnosis is seldom a problem.
DESCRIPTION: Varices appear as red, blue, or deep purple broad-based elevations in oral mucosa. The
size is usually less than 5 mm. The buccal mucosa is a common place to find them, however, they are
also found in lip mucosa and ventral and lateral mucosa of the tongue and floor of the mouth. On ventral
tongue they are apt to be multiple and the term “caviar tongue” has been commonly used to describe
them. They are seen more commonly in the elderly.
ETIOLOGY: A varix is a distended vein that elevates the overlying mucosa. The reason for venous
distention is unclear but may be related to weakening of the vessel wall secondary to aging.
TREATMENT: None usually required. They often thrombose but this is of little clinical consequence.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Mucocele, hemangioma and angina bullosa hemorragica.
Osteoporotic bone marrow defect
DESCRIPTION: As the name implies, this is a localized increase of hematopoietic bone marrow that
creates a radiolucent radiographic defect. They occur more commonly in women in the midyears and
show a predilection for the molar region of the mandible. They are especially common in extraction sites.
Scattered trabeculae may extend short distances into the defect or, in some instances, through it giving
the defect a fairly characteristic appearance. Naturally there are no clinical symptoms.
ETIOLOGY: The etiology remains unknown. No connection has been found linking the osteoporotic bone
marrow defect with anemia or systemic need for increased erythrocytes.
TREATMENT: Once the diagnosis is established, no treatment is required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: This defect may easily be mistaken for a cyst or tumor. In those cases where
there is doubt about the diagnosis, biopsy should be done.
DESCRIPTION: As the name implies, this is a localized increase of hematopoietic bone marrow that
creates a radiolucent radiographic defect. They occur more commonly in women in the midyears and
show a predilection for the molar region of the mandible. They are especially common in extraction sites.
Scattered trabeculae may extend short distances into the defect or, in some instances, through it giving
the defect a fairly characteristic appearance. Naturally there are no clinical symptoms.
ETIOLOGY: The etiology remains unknown. No connection has been found linking the osteoporotic bone
marrow defect with anemia or systemic need for increased erythrocytes.
TREATMENT: Once the diagnosis is established, no treatment is required.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: This defect may easily be mistaken for a cyst or tumor. In those cases where
there is doubt about the diagnosis, biopsy should be done.
Aphthous stomatitis
(Canker sores, recurrent aphthous stomatitis, RAS)
DESCRIPTION: This is one of the most common oral diseases. The exact incidence is unknown, but
estimates range from 20% to 60% of the population. Lesions appear as painful ulcers ranging in size from
less than 1 mm to 2 centimeters. They may be single or multiple. Small lesions (less than 0.5 cm) have
been referred to as minor aphthae and large lesions (more than 0.5 cm) have been called major aphthae.
An uncommon presentation of this disease appears as multiple, pinpoint areas of ulceration that seldom
exceed 1 mm. This has been referred to as the herpetiform pattern, an unfortunate terms since herpes
virus is not the cause.
Each lesion begins as a red macule, less often a papule but not as a blister. It soon ulcerates and the
ulcer becomes covered by a pyogenic membrane producing the characteristic yellow-white center with
surrounding erythematous flare. The shape is usually round to oval but may be elongated in natural folds
such as the vestibule. Aphthous stomatitis occurs on freely movable mucosa that does not overlie bone.
The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached
gingival, hard palate and dorsal tongue are seldom affected.
Aphthous lesions affect all age groups from young to old but young adults and females are more
affected. Elapsed time between recurrences is extremely variable; some unfortunate patients have almost
continuous disease whereas others go from months to years between episodes.
ETIOLOGY: The cause is unknown. The concept that canker sores are caused by a microbiologic agent
has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies
and complement within epithelium and basement membrane during the early stages of the disease
suggests a humoral immune response, and the influx of lymphocytes rather than neutrophils in early
lesions points to a cellular immune reaction as well. It is yet to be learned if the immune response is
directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To
further cloud the issue, a variety of other factors have been implicated. Withdrawal of certain foods such
as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing toothpastes, has
been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have
brought about a cure.
Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery
suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation
also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been
reported to worsen when cigarette smoking is discontinued. There are too many theories for them all to
be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of
diseases all manifested by painful mouth sores.
TREATMENT: To reduce pain, patients with few lesions may be treated with topical medications such as
Orabase® with Benzocaine, Zilactin®, or Soothe-N-Seal®. Anti-inflammatory agents such as topical
steroids or Aphthasol® have also been shown to be effective. For severe or widespread disease, systemic
prednisone such as a Medrol 4 mg Dosepak® is helpful. Long-term systemic steroid therapy may be
associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts,
depression, fluid retention and exacerbation of diabetes.
PROGNOSIS: Cure is seldom achieved but palliation and long-term remission may be achieved by above
mentioned treatment. Without treatment, healing time varies from 4 days for a small lesion to a month or
more for major aphthae. Major aphthae may also cause scarring.
DIFFERENTIAL DIAGNOSIS: Aphthous stomatitis must be differentiated from herpetic stomatitis, the
disease with which it is most often confused. Recurrent intraoral herpes occurs almost exclusively on
mucosa overlying bone. The hard palate is the most common site. Lesions indistinguishable from
aphthous stomatitis have been reported in Behcet’s syndrome, Reiter’s syndrome, Crohn’s disease and
celiac disease.
DESCRIPTION: This is one of the most common oral diseases. The exact incidence is unknown, but
estimates range from 20% to 60% of the population. Lesions appear as painful ulcers ranging in size from
less than 1 mm to 2 centimeters. They may be single or multiple. Small lesions (less than 0.5 cm) have
been referred to as minor aphthae and large lesions (more than 0.5 cm) have been called major aphthae.
An uncommon presentation of this disease appears as multiple, pinpoint areas of ulceration that seldom
exceed 1 mm. This has been referred to as the herpetiform pattern, an unfortunate terms since herpes
virus is not the cause.
Each lesion begins as a red macule, less often a papule but not as a blister. It soon ulcerates and the
ulcer becomes covered by a pyogenic membrane producing the characteristic yellow-white center with
surrounding erythematous flare. The shape is usually round to oval but may be elongated in natural folds
such as the vestibule. Aphthous stomatitis occurs on freely movable mucosa that does not overlie bone.
The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached
gingival, hard palate and dorsal tongue are seldom affected.
Aphthous lesions affect all age groups from young to old but young adults and females are more
affected. Elapsed time between recurrences is extremely variable; some unfortunate patients have almost
continuous disease whereas others go from months to years between episodes.
ETIOLOGY: The cause is unknown. The concept that canker sores are caused by a microbiologic agent
has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies
and complement within epithelium and basement membrane during the early stages of the disease
suggests a humoral immune response, and the influx of lymphocytes rather than neutrophils in early
lesions points to a cellular immune reaction as well. It is yet to be learned if the immune response is
directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To
further cloud the issue, a variety of other factors have been implicated. Withdrawal of certain foods such
as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing toothpastes, has
been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have
brought about a cure.
Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery
suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation
also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been
reported to worsen when cigarette smoking is discontinued. There are too many theories for them all to
be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of
diseases all manifested by painful mouth sores.
TREATMENT: To reduce pain, patients with few lesions may be treated with topical medications such as
Orabase® with Benzocaine, Zilactin®, or Soothe-N-Seal®. Anti-inflammatory agents such as topical
steroids or Aphthasol® have also been shown to be effective. For severe or widespread disease, systemic
prednisone such as a Medrol 4 mg Dosepak® is helpful. Long-term systemic steroid therapy may be
associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts,
depression, fluid retention and exacerbation of diabetes.
PROGNOSIS: Cure is seldom achieved but palliation and long-term remission may be achieved by above
mentioned treatment. Without treatment, healing time varies from 4 days for a small lesion to a month or
more for major aphthae. Major aphthae may also cause scarring.
DIFFERENTIAL DIAGNOSIS: Aphthous stomatitis must be differentiated from herpetic stomatitis, the
disease with which it is most often confused. Recurrent intraoral herpes occurs almost exclusively on
mucosa overlying bone. The hard palate is the most common site. Lesions indistinguishable from
aphthous stomatitis have been reported in Behcet’s syndrome, Reiter’s syndrome, Crohn’s disease and
celiac disease.
Oral cryptococcosis:
-Cryptococcosis is a rare fungal disease, caused by cryptococcus nepformans. Two varieties of the
organism have been identified, C.Neoformans Var. Neoformans and C.Neoformans Var. Gatti.
The fungus is found all over the world in soil. It may also be associated with bird droppings, and it is
acquired through inhalation of the spores.
Sometimes the infection is asymptomatic. In immunocompromised patients, it can spread to anywhere in
the body, including the central nervous system, and it can be lethal.
-Recently, there's been large increase in the incidence of Cryptococcal infections. The main predisposing
factors are HIV Infections, Diabetis, Immunosuppresive therapy.
-Two forms of the disease have been recognized- PULMONARY which is the commonest and
Disseminated which may involve CNS, Lymph nodes, Skin, GIT and Oral mucosa.
-In Oral cavity, It presents as abnormai chronic ulcerations with vegetating surface, tender on palpation.
-Tongue, Palate, Gingiva, Tooth socket are the most common sites.
-DIAGNOSIS: Culture test, Detection of cryptococcus in the serum.
-TREATMENT: Systemic amphotericin B, Fluconazole, & Itraconazole
-Cryptococcosis is a rare fungal disease, caused by cryptococcus nepformans. Two varieties of the
organism have been identified, C.Neoformans Var. Neoformans and C.Neoformans Var. Gatti.
The fungus is found all over the world in soil. It may also be associated with bird droppings, and it is
acquired through inhalation of the spores.
Sometimes the infection is asymptomatic. In immunocompromised patients, it can spread to anywhere in
the body, including the central nervous system, and it can be lethal.
-Recently, there's been large increase in the incidence of Cryptococcal infections. The main predisposing
factors are HIV Infections, Diabetis, Immunosuppresive therapy.
-Two forms of the disease have been recognized- PULMONARY which is the commonest and
Disseminated which may involve CNS, Lymph nodes, Skin, GIT and Oral mucosa.
-In Oral cavity, It presents as abnormai chronic ulcerations with vegetating surface, tender on palpation.
-Tongue, Palate, Gingiva, Tooth socket are the most common sites.
-DIAGNOSIS: Culture test, Detection of cryptococcus in the serum.
-TREATMENT: Systemic amphotericin B, Fluconazole, & Itraconazole
Denture sore mouth (DSM) and Papillary hyperplasia (PH)
DESCRIPTION: Long treated as separate entities, there is evidence that PH and DSM may be different
expressions of the same disease. Both are related to the wearing of dentures. The mildest form of denture
sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As
the condition worsens, large confluent areas turn crimson red. This is the classic form of DSM. In later
stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary
hyperplasia. In some cases of PH, the mucosa has a more mossy than mulberry appearance and the
hyperplasia is not apparent until a gentle blast of air opens the crevices revealing the papillary nature of
the lesion. Whether or not DSM.
ETIOLOGY: The cause is unknown but there is evidence that Candida albicans is at least contributory.
DSM has been called chronic atrophic candidiasis. Organisms are found more often in PH and DSM than
in normal controls. Treatment with the antifungal drugs such as nystatin, clotrimazole and fluconazole
have been reported to bring about remission in most cases, especially in DSM. Since organisms have
been shown to colonize the tissue surface of the denture, sterilization of the denture with fungicide is
indicated. Factors other than Candida albicans seem to be involved, but it is difficult to assess the role of
denture trauma and bacterial pathogens. Because the disease is limited to the area covered by the
denture, it is often assumed that the patient is allergic to denture base material.. There is little evidence to
support his view. Patients with palatal lesions ordinarily do not have lesions under the lower denture as
would be expected if the patient were truly allergic.
TREATMENT: We know of no effective therapy other than fungicides such as nystatin, clotrimazole,
ketoconazole or fluconazole in the usual doses for oral candidiasis. Good oral and denture hygiene may
help. The denture should fit well and not be worn at night. In cases of excessively redundant papillary
hyperplasia, surgical reduction may provide a better denture base.
PROGNOSIS: The condition is benign. For many years, papillary hyperplasia had the undeserved
reputation of being premalignant. It is not.
DIFFERENTIAL DIAGNOSIS: The disease has such a characteristic appearance that diagnosis is seldom a
problem.
DESCRIPTION: Long treated as separate entities, there is evidence that PH and DSM may be different
expressions of the same disease. Both are related to the wearing of dentures. The mildest form of denture
sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As
the condition worsens, large confluent areas turn crimson red. This is the classic form of DSM. In later
stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary
hyperplasia. In some cases of PH, the mucosa has a more mossy than mulberry appearance and the
hyperplasia is not apparent until a gentle blast of air opens the crevices revealing the papillary nature of
the lesion. Whether or not DSM.
ETIOLOGY: The cause is unknown but there is evidence that Candida albicans is at least contributory.
DSM has been called chronic atrophic candidiasis. Organisms are found more often in PH and DSM than
in normal controls. Treatment with the antifungal drugs such as nystatin, clotrimazole and fluconazole
have been reported to bring about remission in most cases, especially in DSM. Since organisms have
been shown to colonize the tissue surface of the denture, sterilization of the denture with fungicide is
indicated. Factors other than Candida albicans seem to be involved, but it is difficult to assess the role of
denture trauma and bacterial pathogens. Because the disease is limited to the area covered by the
denture, it is often assumed that the patient is allergic to denture base material.. There is little evidence to
support his view. Patients with palatal lesions ordinarily do not have lesions under the lower denture as
would be expected if the patient were truly allergic.
TREATMENT: We know of no effective therapy other than fungicides such as nystatin, clotrimazole,
ketoconazole or fluconazole in the usual doses for oral candidiasis. Good oral and denture hygiene may
help. The denture should fit well and not be worn at night. In cases of excessively redundant papillary
hyperplasia, surgical reduction may provide a better denture base.
PROGNOSIS: The condition is benign. For many years, papillary hyperplasia had the undeserved
reputation of being premalignant. It is not.
DIFFERENTIAL DIAGNOSIS: The disease has such a characteristic appearance that diagnosis is seldom a
problem.
Epulis fissuratum (Inflammatory fibrous hyperplasia)
DESCRIPTION: This lesion occurs in those who wear prosthetic appliances. The lesion consists of two or
more folds of soft tissue separated by a central groove into which fits the appliance border. It most often
is found in the buccal vestibule of the anterior maxilla, but any mucosal area touched by a denture border
is vulnerable including the lingual aspect of the mandible. In a study of 583 cases, 64% were found in
females.
Those in the fifth and sixth decade are most often affected. Duration ranged from one week to 10 years,
40% of the patients reported a duration of 6 months to two years. Symptoms are absent except in
ulcerated lesions which may be painful. Histologically, the excessive tissue is composed of cellular,
inflamed fibrous connective tissue.
ETIOLOGY: This is an inflammatory fibrous hyperplasia or oral mucosa caused by ill-fitting or over-
extended denture borders.
TREATMENT: Surgical excision of the lesion and reduction of the denture border.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The lesion has such a characteristic clinical appearance that differential
diagnosis is not a problem. Persistent ulcerated areas in epulis fissuratum should be biopsied to rule out
squamous carcinoma. Folds similar to epulis fissuratum may be seen in Crohn’s disease
DESCRIPTION: This lesion occurs in those who wear prosthetic appliances. The lesion consists of two or
more folds of soft tissue separated by a central groove into which fits the appliance border. It most often
is found in the buccal vestibule of the anterior maxilla, but any mucosal area touched by a denture border
is vulnerable including the lingual aspect of the mandible. In a study of 583 cases, 64% were found in
females.
Those in the fifth and sixth decade are most often affected. Duration ranged from one week to 10 years,
40% of the patients reported a duration of 6 months to two years. Symptoms are absent except in
ulcerated lesions which may be painful. Histologically, the excessive tissue is composed of cellular,
inflamed fibrous connective tissue.
ETIOLOGY: This is an inflammatory fibrous hyperplasia or oral mucosa caused by ill-fitting or over-
extended denture borders.
TREATMENT: Surgical excision of the lesion and reduction of the denture border.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The lesion has such a characteristic clinical appearance that differential
diagnosis is not a problem. Persistent ulcerated areas in epulis fissuratum should be biopsied to rule out
squamous carcinoma. Folds similar to epulis fissuratum may be seen in Crohn’s disease
Plaque induced gingivitis
DESCRIPTION: Inflammation of the gingiva is among the mildest but most common human ailments. The
gingival that envelops the neck of the teeth is swollen, red and bleeds easily. It is not painful. It may show
patchy involvement with skip areas or it may involve virtually the entire marginal gingiva. If untreated,
some patients show progression to bulky enlargement of the gingiva called hyperplastic gingivitis.
Gingivitis is stated to be enhanced by pregnancy and puberty.
ETIOLOGY: The gingival inflammation is the response to bacterial plaque on the adjacent tooth surface.
TREATMENT: Treatment consists of regular dental prophylaxis and the good oral hygiene.
PROGNOSIS: The disease is easily treated and the prognosis is good. If ignored, inflammation may
spread to deeper periodontal tissues in which case the patient is said to have periodontitis.
DIFFERENTIAL DIAGNOSIS: Mucosal pemphigoid, lichen planus, dilantin hyperplasia, and leukemic
infiltrate.
DESCRIPTION: Inflammation of the gingiva is among the mildest but most common human ailments. The
gingival that envelops the neck of the teeth is swollen, red and bleeds easily. It is not painful. It may show
patchy involvement with skip areas or it may involve virtually the entire marginal gingiva. If untreated,
some patients show progression to bulky enlargement of the gingiva called hyperplastic gingivitis.
Gingivitis is stated to be enhanced by pregnancy and puberty.
ETIOLOGY: The gingival inflammation is the response to bacterial plaque on the adjacent tooth surface.
TREATMENT: Treatment consists of regular dental prophylaxis and the good oral hygiene.
PROGNOSIS: The disease is easily treated and the prognosis is good. If ignored, inflammation may
spread to deeper periodontal tissues in which case the patient is said to have periodontitis.
DIFFERENTIAL DIAGNOSIS: Mucosal pemphigoid, lichen planus, dilantin hyperplasia, and leukemic
infiltrate.
Angular cheilosis
DESCRIPTION: This lesion appears as fissuring and maceration at the labial commissures. The term
cheilitis and cheilosis have both been used to describe the same disease.
ETIOLOGY: It is doubtful that this condition is caused by vitamin deficiency in the United States. Studies
have shown that the two most common organisms responsible for this condition are Candida albicans
and Staphylococcus aureus. This condition is commonly seen in older patients having loss of vertical
dimension, in younger patients with orthodontic appliances, and those with a lip licking habit.
TREATMENT: In those patients who have obvious overclosure, restoration of vertical dimension is of
benefit. Application of antifungal ointment to eliminate Candida organisms is indicated.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The disease is so characteristic that it cannot be confused with any other
lesion.
DESCRIPTION: This lesion appears as fissuring and maceration at the labial commissures. The term
cheilitis and cheilosis have both been used to describe the same disease.
ETIOLOGY: It is doubtful that this condition is caused by vitamin deficiency in the United States. Studies
have shown that the two most common organisms responsible for this condition are Candida albicans
and Staphylococcus aureus. This condition is commonly seen in older patients having loss of vertical
dimension, in younger patients with orthodontic appliances, and those with a lip licking habit.
TREATMENT: In those patients who have obvious overclosure, restoration of vertical dimension is of
benefit. Application of antifungal ointment to eliminate Candida organisms is indicated.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The disease is so characteristic that it cannot be confused with any other
lesion.
Peripheral giant cell granuloma
DESCRIPTION: The peripheral giant cell granuloma appears as a nodular soft tissue mass arising from
gingival or alveolar mucosa. The color may be red but is often a blue-grey. Most are approximately a
centimeter in size, although they may be larger. The peak age is around 40 years but they occur in all
ages with a female prevalence. There is almost equal distribution between maxillary and mandibular
gingival. The term “peripheral” is included in the name to separate this lesion from a histologically similar
lesion which occurs inside the jaws. Jaw lesions are referred to as the “central” giant cell granuloma. The
peripheral granuloma may cause pressure resorption of underlying alveolar bone and less commonly
resorption of the adjacent tooth. They are not painful. Histologically this lesion consists of fibroblasts and
multinucleated giant cells.
ETIOLOGY: Unknown
TREATMENT: Conservative excision. The recurrence rate is approximately 10%.
PROGNOSIS: Good.
DIFFERENTIAL DIAGNOSIS: Pyogenic granuloma and peripheral ossifying fibroma.
DESCRIPTION: The peripheral giant cell granuloma appears as a nodular soft tissue mass arising from
gingival or alveolar mucosa. The color may be red but is often a blue-grey. Most are approximately a
centimeter in size, although they may be larger. The peak age is around 40 years but they occur in all
ages with a female prevalence. There is almost equal distribution between maxillary and mandibular
gingival. The term “peripheral” is included in the name to separate this lesion from a histologically similar
lesion which occurs inside the jaws. Jaw lesions are referred to as the “central” giant cell granuloma. The
peripheral granuloma may cause pressure resorption of underlying alveolar bone and less commonly
resorption of the adjacent tooth. They are not painful. Histologically this lesion consists of fibroblasts and
multinucleated giant cells.
ETIOLOGY: Unknown
TREATMENT: Conservative excision. The recurrence rate is approximately 10%.
PROGNOSIS: Good.
DIFFERENTIAL DIAGNOSIS: Pyogenic granuloma and peripheral ossifying fibroma.
Drug-induced gingival hyperplasia (Dilantin hyperplasia)
DESCRIPTION: Drug-induced gingival enlargement was first described almost 50 years ago with the use
of the anticonvulsant Dilantin (phenytoin). Other drugs especially calcium channel blockers such as
Procardia (nifedipine) and cyclosporine have also been implicated. Dilantin causes gingival enlargement
in almost 50% of those that regularly take it, while only about 25% of patient talking cyclosporine and
calcium channel blockers have enlargement. Poor oral hygiene and especially dental plaque accentuate
the enlargement. Superimposed gingivitis also causes boggy and red tissues that mask the true nature of
the enlargement.
ETIOLOGY: Drug induced. As stated above, the condition may become aggravated by superimposed
gingivitis and periodontitis. There is evidence that associated drugs may impair the secretion of
collagenase by gingival fibroblasts permitting the accumulation of excessive gingival collagen.
TREATMENT: The inflammatory component may be reduced by good dental hygiene. The fibrous
overgrowth requires surgical removal. Discontinuance of associated drugs may result in gradual
regression of the overgrowth within one year.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Hereditary gingival fibromatosis, hyperplastic gingivitis from dental neglect,
and leukemic infiltrates of the gingiva.
of the anticonvulsant Dilantin (phenytoin). Other drugs especially calcium channel blockers such as
Procardia (nifedipine) and cyclosporine have also been implicated. Dilantin causes gingival enlargement
in almost 50% of those that regularly take it, while only about 25% of patient talking cyclosporine and
calcium channel blockers have enlargement. Poor oral hygiene and especially dental plaque accentuate
the enlargement. Superimposed gingivitis also causes boggy and red tissues that mask the true nature of
the enlargement.
ETIOLOGY: Drug induced. As stated above, the condition may become aggravated by superimposed
gingivitis and periodontitis. There is evidence that associated drugs may impair the secretion of
collagenase by gingival fibroblasts permitting the accumulation of excessive gingival collagen.
TREATMENT: The inflammatory component may be reduced by good dental hygiene. The fibrous
overgrowth requires surgical removal. Discontinuance of associated drugs may result in gradual
regression of the overgrowth within one year.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: Hereditary gingival fibromatosis, hyperplastic gingivitis from dental neglect,
and leukemic infiltrates of the gingiva.
Traumatic ulcer
DESCRIPTION: An ulcer by definition is a localized area on the skin or mucosa in which the surface
epithelium has been destroyed. The shape and size of traumatic ulcers are so variable as to defy a simple
description. They are usually painful and of short duration.
ETIOLOGY: Common causes of traumatic ulcers include: denture irritation, biting injuries, burns and
friction irritation from sharp or fractured teeth.
TREATMENT: The treatment is to remove the cause if it is known. Relief of pain can be achieved with
topical agents such as Orabase-B® with Benzocaine, Zilactin® or Soothe-N-Seal.
PROGNOSIS: The ulcer should heal if the cause is removed. An ulcer which does not heal within two to
three weeks should be biopsied to rule out malignancy.
DIFFERENTIAL DIAGNOSIS: Traumatic ulcers must be differentiated from squamous carcinoma,
bacterial, fungal and viral diseases, and other oral mucosal diseases.
DESCRIPTION: An ulcer by definition is a localized area on the skin or mucosa in which the surface
epithelium has been destroyed. The shape and size of traumatic ulcers are so variable as to defy a simple
description. They are usually painful and of short duration.
ETIOLOGY: Common causes of traumatic ulcers include: denture irritation, biting injuries, burns and
friction irritation from sharp or fractured teeth.
TREATMENT: The treatment is to remove the cause if it is known. Relief of pain can be achieved with
topical agents such as Orabase-B® with Benzocaine, Zilactin® or Soothe-N-Seal.
PROGNOSIS: The ulcer should heal if the cause is removed. An ulcer which does not heal within two to
three weeks should be biopsied to rule out malignancy.
DIFFERENTIAL DIAGNOSIS: Traumatic ulcers must be differentiated from squamous carcinoma,
bacterial, fungal and viral diseases, and other oral mucosal diseases.
Geographic tongue
(benign migratory glossitis, erythema migrans)
DESCRIPTION: The lesions of this disease on the tongue are so characteristic that recognition should be
instantaneous. The dorsal tongue displays map-like areas that are smooth and red with a whitish-yellow
perimeter. The disease may involve any oral mucosal surface in which case the name erythema migrans
is more appropriate. Atrophy of the filliform papillae is usually a finding on the dorsal tongue.
All ages are affected. We have seen it in a child six months old. The number of lesions varies from one to
many. Old lesions heal and new ones form, waxing and waning in rhythm with most due to unknown
forces. Some complain of a burning sensation.
ETIOLOGY: Unknown although a hypersensitivity reaction to unknown antigens has been suspected.
TREATMENT: None is usually required. In those with symptoms, topical steroid ointment or gel may be
beneficial. Secondary fungal colonization should also be suspected in symptomatic lesions.
PROGNOSIS: This is a chronic disease lasting months to years with periods of remission and
exacerbation.
DIFFERENTIAL DIAGNOSIS: Typical lesions are diagnostic. Variable clinical presentation may suggest
lichen planus or candidiasis.
(benign migratory glossitis, erythema migrans)
DESCRIPTION: The lesions of this disease on the tongue are so characteristic that recognition should be
instantaneous. The dorsal tongue displays map-like areas that are smooth and red with a whitish-yellow
perimeter. The disease may involve any oral mucosal surface in which case the name erythema migrans
is more appropriate. Atrophy of the filliform papillae is usually a finding on the dorsal tongue.
All ages are affected. We have seen it in a child six months old. The number of lesions varies from one to
many. Old lesions heal and new ones form, waxing and waning in rhythm with most due to unknown
forces. Some complain of a burning sensation.
ETIOLOGY: Unknown although a hypersensitivity reaction to unknown antigens has been suspected.
TREATMENT: None is usually required. In those with symptoms, topical steroid ointment or gel may be
beneficial. Secondary fungal colonization should also be suspected in symptomatic lesions.
PROGNOSIS: This is a chronic disease lasting months to years with periods of remission and
exacerbation.
DIFFERENTIAL DIAGNOSIS: Typical lesions are diagnostic. Variable clinical presentation may suggest
lichen planus or candidiasis.
Condensing osteitis
DESCRIPTION: Condensing osteitis is a reaction to infection. It differs from other periapical inflammatory
diseases in that there is a bone production rather than bone destruction. The result is a radiopaque lesion.
This sclerotic reaction is apparently brought about by good patient resistance coupled with a low degree
of virulence of the offending bacteria. It is more commonly seen in the young and seems to show special
predilection for the periapical region of lower molars. The associated tooth is carious or contains a large
restoration. We are reluctant to state the reaction of the tooth to pulp testing because of lack of sufficient
personal experience and paucity of published information. Theoretically, the results should be abnormal.
Current level of knowledge suggests that the pulp is irreversibly inflamed. Uncommonly, condensing
osteitis occurs as a reaction to periodontal infection rather than dental infection.
ETIOLOGY: Infection of periapical tissues by organisms of low virulence.
TREATMENT: Vitality of the overlying tooth should be investigated. If the pulp is inflamed or necrotic,
endodontics or extraction are the options.
PROGNOSIS: In those cases in which the offending tooth is extracted, the area of condensing osteitis may
remain in the jaws indefinitely, and is termed osteosclerosis or bone scar.
DIFFERENTIAL DIAGNOSIS: Idiopathic osteosclerosis and cementoblastoma. An abnormal result with
pulp testing strongly suggests condensing osteitis and tends to rule out osteosclerosis and
cementoblastoma.
DESCRIPTION: Condensing osteitis is a reaction to infection. It differs from other periapical inflammatory
diseases in that there is a bone production rather than bone destruction. The result is a radiopaque lesion.
This sclerotic reaction is apparently brought about by good patient resistance coupled with a low degree
of virulence of the offending bacteria. It is more commonly seen in the young and seems to show special
predilection for the periapical region of lower molars. The associated tooth is carious or contains a large
restoration. We are reluctant to state the reaction of the tooth to pulp testing because of lack of sufficient
personal experience and paucity of published information. Theoretically, the results should be abnormal.
Current level of knowledge suggests that the pulp is irreversibly inflamed. Uncommonly, condensing
osteitis occurs as a reaction to periodontal infection rather than dental infection.
ETIOLOGY: Infection of periapical tissues by organisms of low virulence.
TREATMENT: Vitality of the overlying tooth should be investigated. If the pulp is inflamed or necrotic,
endodontics or extraction are the options.
PROGNOSIS: In those cases in which the offending tooth is extracted, the area of condensing osteitis may
remain in the jaws indefinitely, and is termed osteosclerosis or bone scar.
DIFFERENTIAL DIAGNOSIS: Idiopathic osteosclerosis and cementoblastoma. An abnormal result with
pulp testing strongly suggests condensing osteitis and tends to rule out osteosclerosis and
cementoblastoma.
Peripheral ossifying fibroma
DESCRIPTION: This lesion appears as a mass arising from the gingiva adjacent to teeth or between
teeth. It favors teenagers and young adults. Those arising between teeth may separate the teeth and
produce pressure resorption of the interdental bone. It’s not unusual to see a “saddle” lesion straddling
the ridge with a labial and lingual lobe. Color is normal or slightly red. Histologically the bulk of this
lesion is moderately cellular fibrous connective tissue frequently containing foci of bone, cementum, or
dystrophic calcification. When inflammation is present, plasma cells frequently predominate.
ETIOLOGY: Unknown
Treatment: Excision. The recurrence rate is about 15%. Extraction of the adjacent teeth is seldom
necessary.
Prognosis: Good
Differential Diagnosis: Peripheral fibroma bears a great resemblance to pyogenic granuloma and
peripheral giant cell granuloma. Histologic examination is necessary to distinguish between them.
DESCRIPTION: This lesion appears as a mass arising from the gingiva adjacent to teeth or between
teeth. It favors teenagers and young adults. Those arising between teeth may separate the teeth and
produce pressure resorption of the interdental bone. It’s not unusual to see a “saddle” lesion straddling
the ridge with a labial and lingual lobe. Color is normal or slightly red. Histologically the bulk of this
lesion is moderately cellular fibrous connective tissue frequently containing foci of bone, cementum, or
dystrophic calcification. When inflammation is present, plasma cells frequently predominate.
ETIOLOGY: Unknown
Treatment: Excision. The recurrence rate is about 15%. Extraction of the adjacent teeth is seldom
necessary.
Prognosis: Good
Differential Diagnosis: Peripheral fibroma bears a great resemblance to pyogenic granuloma and
peripheral giant cell granuloma. Histologic examination is necessary to distinguish between them.
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