CONTENTS:

Definition

Infectious diseases
◦ Bacterial diseases
◦ Viral disesases
◦ Fungal disease
Deficiency disease
Diseases of bones and joints

Diseases of the skin

Conclusion

References

1
DEFINITION:
 Disease: Any deviation from or interruption of
the normal structure or function of any part,
organ, or system (or combination) of the body
that is manifested by a characteristic set of
symptoms and signs and whose etiology,
pathology and prognosis maybe known or
unknown.

2
 Disorder: A derangement or abnormality of
function; a morbid physical or mental state.

3
 Syndrome: A set of symptoms that occur
together. In genetics, a pattern of multiple
malformations thought to be pathogenetically
related.

4
 Sign: Any objective evidence of a disease i.e.
such evidence as perceptible to the examining
physician.
 Symptom: any subjective evidence of a disease
or of a patient’s condition i.e. such evidence as
perceived by the patient.

5
 Infectious diseases
BACTERIAL INFECTIONS

6
SCARLET FEVER
 Scarlet fever occurs predominantly in children in
winter months.
 Caused by streptococcal organisms of beta
hemolytic type that elaborate an erythrogenic
toxin.
 SCARLET FEVER:
 Oral Manifestation: “stomatitis
scarlatina”. Mucosa of the palate appears
congested and the throat is often fiery red
 Tongue exhibits a white coating and
fungiform papillae are edematous and
hyperemic, projecting above the surface
as small red knobs--Strawberry tongue.
 The coating of the tongue is removed it
appears deep red and glistening and
smooth--Raspberry tongue.
 The clinical termination of the disease is
the desquamation of the skin

8
 Clinical features
1. Microorganism enters the body
through pharynx.
2. Incubation period of 3-5days.
3. Patient exhibits severe
pharyngitis, tonsillitis, headache,
chills, fever and vomiting.
4. Scarlet skin rash appears on the
2nd or 3rd day.
TREATMENT:
Antibiotics will ameliorate the disease
and will aid in controlling the
possible complications.
 DIPHTHERIA:
 Acute contagious disease.
 Cornybacterium diptheriae or Klebs-Loffler bacillus.
 Resides in URT.
 Droplet infection or direct contact.
 C/F: initially listelessness, malaise, headache, fever
and occasionally vomiting.
 Sore throat
 Mild redness and edema of pharynx.
 Cervical lymphadenopathy.

10
 Oral Manifestation: Characteristically, there
is formation of “diptheric membrane”.
 A false membrane, grayish, thick fibrinous,
gelatinous-appearing exudate which
contains dead cells, leukocytes and bacteria
overlying necrotic, ulcerated areas of the
mucosa and covering the tonsils , pharynx
and larynx .
 Soft palate may become paralysed .
 Patients have a peculiar nasal twang and
may exhibit nasal regurgitation.
 TUBERCULOSIS
 Mycobacterium tuberculosis
and rarely M. bovis.
 Clinical features:
 Episodic fever and chills.
 Easy fatigability and
malaise.
 Gradual loss of weight
accompanied by persistent
cough with or without
accompanied hemoptysis.

12
 Oral Manifestation
 Lesions may occur at any site on
the OMM, but the most common is
tongue followed by palate, lips,
buccal mucosa, gingiva and
frenula.
 They r irregular, deep or
superficial, painful which tends to
increase in size slowly.
 Tuberculuos gingivitis- unusual
form of TB which may appear as a
diffuse hyperemic, nodular or
papillary proliferation of the
gingival tissue.
LEPROSY
 caused by M. leprae.
 Ridley and Jopling have divided

leprosy into 2 polarized group:

 tuberculous leprosy (TT)

 lepromatous leprosy (LL).

 Oral Manifestation:

Generally consisted of small tumor

like mass “lepromas which
develop on tongue, lips and hard
palate.
Tendency to break down and
ulcerate.
Gingival hyperplasia with loosening
of teeth has also been described.

14
 ACTINOMYCOSIS
• Chronic granulomatous, suppurative and fibrosing disease
caused by anaerobic, gram – positive , nonacid-fast,
branched, filamentous bacteria.
• Common inhabitant of the oral cavity even in the complete
absence of any clinical manifestations of specific infection.
• Trauma plays a role in some cases by initiating a portal of
entry for the organisms, since they are highly invasive.
• Thus extraction of thr teeth or abrasion of the mucosa may
precede the infection.

 Actinomycosis israeli
◦ Cervicofacial actinimycosis
◦ Abdominal actinimycosis
◦ Pulmonary actinimycosis
 Cervicofacial actinimycosis: the most common form of the
disease.
 The soft tissue swellings eventually develop into 1 or more
abscess which tend to discharge upon a skin, liberating pus
containing sulfur granules.

15
 SYPHILIS:
 Treponema pallidum.
 acquired or congenital.
 Acquired Syphilis:
 Primary stage- This lesion is
called as the chancre.
 The chancre has been
demonstrated to develop on the
site of fresh extraction wound.
 Elevated, ulcerated nodule
showing local induration and
producing regional lymphadeniti.
 Such a lesion on the lip may have
a brownish, crusted appearance.

16
SYPHILIS:
 Secondary or Metastatic stage-
commence in about 6 weeks.
 The oral lesions are known as
“mucous patches” highly
infectious. Usually multiple,
painless, grayish –white plaques
overlying an ulcerated surface,
 Occur most commonly on
tongue, gingiva or buccal
mucosa.
 Often ovoid surrounded by an
erythematous halo.
 Serological reaction is positive.

17
 SYPHILIS:
 Tertiary lesions- also called as “late syphilis”.
 involves the cardiovascular system and
central nervous system
 non-infectious.
 Gumma is chief localized tertiary lesion and
occurs most frequently in the skin and
mucous membranes.
 Intraoral gumma most commonly involves the
tongue and palate.
 Appear as firm nodular mass in tissue which
may subsequently ulceralate and inacas eof
the lesion of the palate , cause perforation by
sloughing of the necrotic mass of tissue.

18
 SYPHILIS:
 Congenital

(Prenatal) Syphilis:
 frontal bossing,

 short maxilla,

 saddle nose,

 mulberry molars,

 relative protuberance

of mandible,
 rhagades and saber

shin.

19
SYPHILIS:
 Hutchison’s triad;
 hypoplasia of the
incisors and molar
teeth,
 eighth nerve deafness
and
 interstitial keratitis.

20
 GONORRHEA:
 It is primarily a venereal disease.
 Oral Manifestation:
 (Schmidt et al) pointed out the similarities of
gonococcal stomatis with erythema multiforme,
erosive and bullous lichen planus and herpetic
stomatitis.
 Lip may develop acute painful ulceration,
limiting motion, the gigniva may become
erythematous with or without necrosis.
 Tongue may present red, dry ulcerations or
become glazed and swollen with painful
erosions , with similar lesions on the buccal
mucosa and palate.
 Gonococcal pharyngitis and tonsillitis
 fever and regional lymphadenopathy.

21
 WEGENER'S GRANULOMATOSIS:
 necrotizing granulomas of
the upper and lower
respiratory tracts,
 Oral Manifestation: oral
cavity involvement occurs
in more than 50% of
patients.
 The gingivitis
 The "strawberry"
appearance of the
 large and necrotic tongue
ulcerations
22
LETHAL MIDLINE GRANULOMA
 caused by non-
Hodgkin's lymphoma
or polymorphic
 nasal stuffiness

 total destruction of

the entire palate and

severe facial
mutilation.
 mimics malignancy,

 The prognosis is poor,

23
 PYOGENIC GRANULOMA:
 response of the tissues to a non
specific infection.
 Etiology: originally believed to

be a botryomycotic infection;
 the result of some minor

trauma to the tissues

 most frequently on the gingiva,

also found on the lips tongue

and buccal mucosa and
occasionally on other areas.
 It is deep red or reddish purple,

Some lesions have a brown

cast if hemorrhage has
occurred into the tissues.
24
VIRAL INFECTIONS

25
HERPES SIMPLEX:
 Itis an acute infectious disease,
 Herpes virus hominis are

derived
 There are two immunologically

different types of HSV:

◦ Type I, usually affecting the face,
lips, oral cavity and upper body
skin;
◦ Type II usually affects the genitals
and skin of the lower body.
 the primary infection is
accompanied more frequently
by severe systemic
manifestation and occasionally
is fatal.

26
HERPES SIMPLEX:
Disseminated herpes
simplex of the newborn:
 uncommon disease

 These infants usually

manifest the disease by

the fourth to seventh day
of life,
 usually die on the 9th to

12th day of life.

 Surviving infants usually

show residual neurologic

involvement.

27
HERPES SIMPLEX:
 Primary herpetic
stomatitis:
 both children and
young adults.
 It rarely occurs
before the age of 6
mo,
 Shortly, yellowish,
fluid filled vesicles
develop.
28
HERPES SIMPLEX:
Recurrent or secondary, herpetic labialis and
stomatitis:
 The lesion may develop either on the lips or

intraorally. These vesicles are generally small.

29
 RECURRENT APHTHOUS STOMATITIS:
 Painful recurring solitary or
multiple ulcerations of the oral
mucosa.
Etiological factors:
 Bacterial infection-

Streptococcus sanguis,
Immunologic abnormality, Iron,
vitamin B12 or folic acid
deficiency.
Precipitating factors:
 Trauma, Endocrine conditions,

Psychic factors, Allergic factors.

30
 MEASLES (RUBEOLA, MORBILLI)
 fever malaise, cough,
conjunctivitis, photophobia,
lacrimation and eruptive
lesion of the skin and the
oral mucosa.
 Oral manifestation: koplik’s
spots

31
RUBELLA (GERMAN MEASLES)
 No koplik’s spots and
should not be
confused with
rubeola.
 Disease commonly
occurs in women in
first trimester
 blindness deafness
and enamel
hypoplasia

32
SMALL POX (VARIOLA)
 Ulceration of the oral
mucosa and pharynx,
trachea, esophagus
etc. tongue is swollen
and painful, making
swallowing difficult.

33
 CHICKENPOX (VARICELLA):
 Oral manifestations
include, small blister
like lesions on the oral
mucosa including the
buccal mucosa, tongue,
gingiva and palate.

34
 Herpes zoster (Shingles,
Zona):
 inflammation of dorsal

root ganglia.
 Oral manifestation:

trigeminal nerve,
 Painful vesicles may be

found in buccal mucosa,

tongue, larynx, pharynx
etc.
 Mumps:
 It is an acute contagious viral
infection
 The symptoms include
headache, dizziness, fever,
chills, vomiting.
 Salivary gland involvement
causes pain on mastication,
 in 70% cases bilateral parotid
involvement seen.
 Complication: other organs
may beaffected.
CANDIDIASIS:
 candida albicans, C. tropicalis, C.
crusei etc.
Classification:
Acute
 Acute Pseudomembranous oral

candidiasis
 Acute atrophic oral candidiasis

Chronic
 Chronic hyperplastic oral candidiasis

 Chronic mucocutaneous oral

candidiasis
 Chronic atrophic oral candidiasis
DISEASES OF BONES AND JOINTS
 Bone is a dense calcified tissue which is
specifically affected by a variety of diseases. some
characteristically are congenital while others
develop in early childhood, young adulthood or
even in later life.
OSTEOGENESIS IMPERFECTA:
 It is a serious disease of
unknown etiology
 (congenita or Vrolik’s
type)
 (tarda or Lobstein’s type
or gravis or levis or
osteopsathyrosis).
 Oral Manifestation:
CLEIDOCRANIAL DYSPLASIA:
 abnormality of the skull,
shoulder girdle, teeth and
jaws.
 High, narrow arched palate

 over-retention of

deciduous
 The root of the tooth is

usually short
 absence or paucity of

cellular cementum.
OSTEOPETROSIS:
 benign dominantly inherited
 malignant recessively

inherited form.
 Oral Manifestation: the

medullary spaces are reduced

 marked predilection for the

development of osteomyelitis
This is a complication of
dental extraction.
 Fractures of the jaw.
OSTEITIS DEFORMINS:
 Paget in 1877
 Clinical Features:
 Pathologic fractures are
common
 leontiasis ossea.
 Oral Manifestation:
maxillary enlargement,
 Teeth become loose and
migrate.
 inability to wear their
dentures
FIBROUS DYSPLASIA OF BONE:
 Polyostotic Fibrous
Dysplasia: it can be of 2
types-
 Jaffe’s type
 Albright’s
 Oral manifestation:
 expansion and
deformities of the jaws
FIBROUS DYSPLASIA OF BONE:
 Monostotic Fibrous
Dysplasia:
 children especially in the

maxilla and is impossible

to eradicate without
mutilating radical surgery.
 Oral manifestation: severe

 Mostly involves the

maxillary sinus, zygomatic

bone and floor of the
mouth.
INFLAMMATORY DISTURBANCES OF THE TM JOINT:

 Arthritis Due to Specific infection: It may follow a

dental infection or an adjacent cellulitis or
osteomyelitis.
 Clinical Features: severe pain of the joint. Healing
results in ankylosis of the joint.
INFLAMMATORY DISTURBANCES OF THE TM JOINT:

 Rheumatoid Arthritis:
hypersensitivity reaction
to bacterial toxins
 Clinical Features: slight
fever, fatigability,
swollen joints, with pain
and stiffness
INFLAMMATORY DISTURBANCES OF THE TM JOINT:

 Rheumatoid Arthritis
in Children (Still’s
Disease): may cause a
malocclusion of the class
II div I type with
protrusion of maxillary
incisors and an anterior
open bite.
DEFICIENCY DISEASES:
 The mouth is a sensitive indicator of nutritional status
because of the assorted hard and soft tissues of the oral
cavity and the specific nutritional needs of each.
Frequently, oral manifestations of nutri­tional disorders
reflect the initial sign of a deficiency. The severity of oral
involvement is generally not proportional to the nutritional
shortage, nor are there oral clinical characteristics specific
to any one nutritional disorder. Rather, the oral features are
variable in their appearance and a careful phys­ical
examination, history, laboratory studies, and a high degree
of suspicion are required to diagnose specific disorders.
ZINC DEFICIENCY
 Acrodermatitis enteropathica
 The disease manifests shortly

after birth
 symmetric skin eruption, and

resembling psoriasis.
 Angular cheilitis,

 Nonspecific superficial oral

ulcerations
 Secondary infection with

candidiasis Patients with poorly

controlled gastrointestinal
diseases may also develop zinc
deficiency
VITAMIN DEFICIENCIES:

 A vitamin is usually defined as an organic substance not

made by the body, which is soluble either in fat or water
and ordinarily is needed in only minute quantities to act
as a cofactor in a variety of metabolic reactions. As is
seen with vitamin A and vitamin D their role is more
hormonal than as a cofactor.
 The avitaminoses are due to the absence of the
minute amount of the biologically important materials
rather than the presence of certain biologically active
materials. They are called as diseases in a negative
sense rather than in a positive sense.
VITAMIN A:

 epithelial cells fail to

differentiate. enamel matrix is
arrested and/ or poorly defined.
 The dentin, too, is atypical in

structure,
 higher caries score.
 night blindness, xerophthalmia,

and keratomalacia, xerostomia

and burning of the mucous
membranes, are the result of
squamous metaplasia of the
minor and major salivary
glands.
VITAMIN D:

 
 one of a number of
compounds ofhydroxylated
cholecalciferols.
 best thought of as a

hormone.
 causes pronounced changes

in the permanent dentition

char­acterized by enamel
pitting and hypoplasia.
RICKETS
 premature infants being at the
highest risk.
 The changes in the bones are

found in epiphyseal plate, the

metaphysis and the shaft.
 Oral Manifestations:

 developmental abnormalities of

dentin and enamel,

 delayed eruption and

misalignment of teeth in the jaw,

 higher caries index

 abnormally wide predentin zone

and much interglobular dentin.

OSTEOMALACIA
 it is the adult equivalent
of juvenile (vitamin D
deficient) rickets.
VITAMIN D RESISTANT RICKETS

 also known as familial hypophophatemia

 Oral Manifestations:

 widespread formation of globular, hypocalcified dentin,

 common invasion of the pulp by microorganisms without demonstrable

destruction of the tubular matrix.

 periapical involvement of normal appearing teeth

 development of multiple gingival fistulas

HYPOPHOSPHATESIA
 It is a hereditary disease first
recognized by Rathbun in
1948.
 Oral Manifestation:

loosening and premature loss

of deciduous teeth,
 gingivitis;

 absence of cementum, so that

there is no sound functional

attachment of the tooth to the
bone by periodontal
ligament.
PANTOTHENIC ACID
 Glossitis and angular chelitis can be caused by a
deficiency in pantothenic acid.
VITAMIN K
 In 1929, Dam
 factors VII XI and X.

 hypoprothrombinemia due to

poor placental lipid transmission.

 Oral Manifestation- gingival

bleeding.
 Hypoprothrombinemia

 gingivae are the most frequent

oral site of involvement.

 Oral ecchymosis on the palate

and buccal mucosa may also be

commonly observed.
BIOTIN:
 frequently reported in
individuals consuming
large quantities of raw
eggs
 dry and crusted lips

 patchy atrophy of the

tongue papillae
resembling geographic
tongue, and diffusely
reddened oral mucous
membrane.
VITAMIN C
 More than 50% of patients
with scurvy develop a
hemorrhagic gingivitis.
 Aphthous-like ulcerations and
hemorrhages
 periodontal destruction and
alveolar bone degeneration
 premature loss of teeth.
 Oral Manifestation- In infants
the enlarged tissue may cover
the clinical crowns of the
teeth.
VITAMIN B COMPLEX
 The oral signs of deficiencies of the B
vitamins occur primarily in the oral soft
tissues: the tongue, mucous membrane,
gingiva and lips.
THIAMIN
 Beriberiis characterized
by multiple neuritis,
often associated with
congestive heart failure,
generalized edema and
sudden death
 oral manifestations:

vesicular eruption on the

buccal mucosa, floor of
the mouth and the palate.
RIBOFLAVIN

 Glossitis

 The filiform papilla become

atrophic
 tongue is magenta in appearance that

is easily distinguished from

cyanosis.
 Deep lesions usually leave scars on

healing.
 Burning and pain are generally mild

 Angular cheilitis

 Deep, moist, and crusted fissures at

the corners of the mouth

NIACIN
 pellagra.

 Niacin leads to the formation

of nicotinic acid amide that
leads to the formation of
coenzyme I and coenzyme II.
 beefy-red surface.

 severe gingivitis

 diarrhea, dementia, and a

marked photosensitivity,
most prominently involving
the neck and hands.
PYRIDOXINE
 itis actually a complex of three
related substances; pyridoxine,
pyridoxal, pyridoxamine.
 resemblance to pellagrous

stomatitis.
 angular cheilitis and a diffuse

glossitis.
 The lesions are painful and the

tongue often assumes a purplish

and atrophied ap­pearance.
 The fungiform papillae may

remain unchanged or enlarge

FOLIC ACID
 glossitis, diarrhea and
microcytic anemia.
 The papillas on the tongue

disappear one by one with the

filiform papilla being the first.
 folic acid inhibitors such as

methotrexate or those with

various gastrointestinal
diseases.
 results in prominent mucous

membrane changes.
 Pain and burning of the tongue
AMYLOIDOSIS

 represents a heterogeneous
group of disorders
 Primary systemic

amyloidosis affect the tongue

along the lateral borders of
the tongue.
 Secondary amyloidosis is

more common than the

primary, preceded by
rheumatoid arthritis, chronic
infectious diseases, and
Mediterranean fever.
ANEMIAS
 Glossitis may be the first
sign of folate or vitamin
B-12 deficiency. The
tongue appears reddened,
and the papillae are
atrophic, producing a
smooth ("bald")
appearance.
LANGERHANS HISTIOCYTOSIS: 
 Letterer-Siwe disease, is most common in infants and is
characterized by widespread involvement of the viscera,
potentially leading to death. Oral symptoms include
large ulcerations, ecchymoses, gingivitis, periodontitis,
and subsequent tooth loss.
 Hand-Schüller-Christian disease, is a childhood disease

that consists of the triad of diabetes insipidus, lytic bone

lesions, and proptosis. Oral manifestations include
irregular ulcerations of the hard palate, Gingival
inflammation and ulcerated nodules, difficulty in
chewing, and foul-smelling breath also occur.
SARCOIDOSIS:
 Sarcoidosis is an
idiopathic systemic
disease characterized by
bilateral hilar
lymphadenopathy and
noncaseating granulomas
in the lungs. Ocular and
cutaneous manifestations
are common.
SARCOIDOSIS:
 Oral manifestations multiple, nodular, painless ulcerations of
the gingiva, buccal mucosa, labial mucosa, and palate. biopsy
results reveal noncaseating granulomas surrounded by
multinucleate giant cells along with lymphocytic infiltrate.
Although less common, salivary gland involvement is a
possibility, leading to tumor-like swellings. Heerfordt
syndrome may arise if symptoms include parotid gland
swelling, xerostomia, uveitis, and facial nerve palsy. Rarely,
sarcoidosis may involve the tongue
MULTISYSTEM CONDITIONS
 Amyloidosis 
 Aphthous stomatitis 
 Lichen planus 
 Common drugs that cause lichenoid reactions
include ACE inhibitors, beta-blockers, NSAIDs,
diuretics, hydroxychloroquine, and others.
 Inhaled steroids
CROHN’S DISEASE
 idiopathic disorder that involves
the entire GI tract with
noncaseating granulomas, and
fissures. This disease is slightly
more prevalent among white
males. Symptoms of Crohn
disease include intermittent
attacks of diarrhea, constipation,
abdominal pain, and fever.
Patients may develop
malabsorption and subsequent
malnutrition. Fissures or fistulas
may occur in persons with
chronic disease.
CROHN’S DISEASE
 Orofacial symptoms
 (1) diffuse labial, gingival, or mucosal swelling;

 (2) cobblestoning of the buccal mucosa and

gingiva;
 (3) aphthous ulcers;

 (4) mucosal tags; and

 (5) angular cheilitis.

 Oral granulomas may occur without characteristic

alimentary involvement (orofacial granulomatoses).

ULCERATIVE COLITIS
 Ulcerative colitis is an
inflammatory condition with
some similarities to Crohn
disease. it is restricted to the
colon and is limited to the
mucosa and submucosa,
sparing the muscularis. Lesions
in the colon consist of areas of
hemorrhage and ulcerations
along with abscesses,in the oral
cavity as aphthous ulcerations
or superficial hemorrhagic
ulcers
GASTROESOPHAGEAL REFLUX DISEASE (GERD)

 Regurgitation of gastric
contents (pH 1-2) reduces
the pH of the oral cavity
below 5.5; Erosion of the
enamel exposes the
underlying dentin. Exposed
dentin is often sensitive to
temperature changes and,
secondary to its lower
mineral content, develops
caries much more quickly.
CHRONIC LIVER DISEASE
 Chronic liver disease impacts many systems of the
body. The coagulation pathway is one such system.
The liver synthesizes many of the clotting factors
necessary for hemostasis. can be manifested in the
mouth as petechiae or excessive gingival bleeding
with minor trauma. This is especially suggestive if it
occurs in the absence of inflammation.
CHRONIC LIVER DISEASE
 hepatitis C is the leading infectious cause of
chronic liver disease worldwide.
 The association between hepatitis C and oral lichen
planus is controversial.
APTHOUS STOMATITIS:
Canker sores are small ulcer craters in the lining of the mouth that are frequently painful
and sensitive. Canker sores are very common. About 20% of the population (one out of
five people) have canker sores at any one time. Canker sores are also medically known as
aphthous ulcers or aphthous stomatitis.
Women are slightly more likely than men to have recurrent canker sores. It can occur at

any age, but it is more commonly seen in teenagers. Genetic studies show that
susceptibility to recurrent outbreaks of the sores is inherited in some patients. This
partially explains why family members often share the condition.
Canker sores are generally classified into three groups based on size.

Minor sores have a diameter of 1millimeter (mm) to 10mm. They are the most common

(80% of all canker sores) and usually last about 7-10 days. 
Major sores (10% of all canker sores) have a diameter of greater than 10mm and they
may take anywhere between 10-30 days to heal. They may leave a scar after they heal.
Herpetiform ulcers (10% of all canker sores) are formed by a cluster of multiple small

individual sores (less than 3mm). They also usually heal within 7-10 days.
 Canker sores are usually found on the movable parts of the mouth, such as the tongue or the inside
lining of the lips and cheeks, and at the base of the gums. The ulcers begin as small oval or round
reddish swellings that usually burst within a day. The ruptured sores are covered by a thin white or
yellow membrane and edged by a red halo. Generally, the sores heal within two weeks without
scarring. Fever is rare, and the sores are rarely associated with other diseases. Usually, a person has
only one or a few canker sores at a time.
 Most people experience their first bout with canker sores between the ages of 10 and 20. Children
as young as 2 years old, however, can develop the condition. The frequency of canker sore
recurrences varies considerably. Some people have only one or two episodes a year, while others
may have a continuous series of canker sores.
 Pharmacologic agents are among the most common causes of recurrent aphthous lesions,
commonly known as canker sores. Some common culprits include nonsteroidal anti-inflammatory
drugs (NSAIDs), nicorandil, ACE inhibitors, but any drug can potentially produce an aphthous-like
reaction. These ulcerations are round, crateriform, yellowish depressions surrounded by an area of
erythema. The size varies from 1-3 mm (aphthous minor, approximately 80% of cases) to larger
than 1 cm (aphthous major, approximately 15% of cases). Patients may have outbreaks of multiple
ulcerations at one time. These are usually quite painful but typically are self-limiting and resolve in
7-10 days for aphthous minor and 14-21 days for aphthous major lesions.
 The most common adverse effect of many medications is dry mouth
(hyposalivation or xerostomia). The reasons for this vary from medication
to medication but can range from dehydration (eg, with diuretics) to
anticholinergic activity (eg, with some antidepressants). Dry mouth has a
number of consequences, including altered taste, increased risk of fungal
infection, increased caries risk, and increased prevalence of traumatic
ulceration due to lack of lubrication. Patients with severely impaired
salivary flow also have difficulty with eating, swallowing, and speech.
The former can result in decreased food intake and poor nutrition.
Numerous management options are available for decreased salivation,

which are beyond the scope of this chapter. These range from the simple,
such as increased hydration, to the complex, such as systemic
procholinergic agents to increase salivary production
REFERENCES:
Shafer, Hine, Levy; A Textbook of Oral Pathology; 4th edition
Cawson R.A., Odell E.W.; Essentials of oral Pathology and Oral Medicine

Sapp J.P., Eversole L.R., Wysocki G.P.; Contemporary oral and Maxillofacial Pathology

Saraf S., Textbook of Oral Pathology; 1st edition

Eversole L.R., Clinical Outline of Oral Pathology; 3 rd edition

Stewart R.E.; pediatric Dentistry, Scientific Foundation and Clinical Practice; 1 st edition

Jeffrey M Casiglia;Oral Manifestations of Systemic Diseases

Xiaojing Li; Systemic Diseases Caused by Oral Infection; Clinical Microbiology Reviews,

October 2000, p. 547-558, Vol. 13, No. 4.

Clong;Oral Manifestations of Systemic Diseases

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www.medicineworld.org

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