VI.

Ulcerative conditions
Ulcers represent one of the most frequent lesions in dentistry.
Etiologically speaking, they are extremely varied and can be classified as
follows:
Reactive lesions:
Ulcerations: mechanical
chemical
thermal
Bacterial conditions:
Syphilis
Gonorrhoea
Tuberculosis
Actinomycosis
Noma
Conditions associated with immunological deficiencies:
Recurrent aphtous ulcerations
Behet syndrome
Reiter syndrome
Erythematosus lupus
Allergic reactions
Cyclic neutropenia
Reactive lesions
MECHANICAL ULCERATIONS: most ulcers occurring on the soft
parts of the oral cavity are of mechanical nature and are located on the
lower lip, tongue, jugal mucosa and oral floor. These ulcers are not related
to gender or age. In newborns with natal or neonatal teeth the traumatic
ulceration that usually occurs on the ventral surface of the tongue 1/3
anterior is called Riga-Fede disease.

Root residues, sharp edges of the teeth, periodontal carious lesions,

crochets from partial dental prosthesis, malpositioned teeth, unstable full
dental

prosthesis,

etc

could

determine

acute

or

chronic

traumatic

ulcerations.
In less common circumstances in people suffering from psychic
conditions, lesions can be self-induced by abnormal behaviours such as lip,
tongue or cheek biting.
Traumatic ulcerations can also be iatrogenic. Thus, ulcerations of
mucosa could be caused while removing cotton rolls or compresses from the
mucosa, while pressing too hard the saliva vacuum or by accidental injury of
soft mucosa with mills or disks.
CHEMICAL

ULCERATIONS:

chemical

substances

can

cause

ulcerations because of their components (acids or bases) that have an

irritating or allergenic effect. Consequently, there will appear lesions of the
mucosa caused by the patient or iatrogenic.
Furthermore, there are cases of lesions of the mucosa caused by
aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue
necrosis with painful erosions occurs on that specific spot and it will heal in
a week time.
Also, chemical substances used in dental practice could cause
iatrogenic ulcerative lesions of the oral mucosa when applied incorrectly.
Thus,

phenol,

trichloroacetic

acid

eugenol,

silver

nitrate,

formaldehyde, sodium hypochlorite, etc could cause burns of the oral

mucosa and superficial ulcerations that will heal spontaneously within 4-7
days.
THERMAL ULCERATIONS: intra-oral thermal burns are quite rare.
They can be caused by hot liquids or food and they are mostly located on
the lips, tongue and mouth floor .
Also, acrylic resins resulting from polymerization or monomer excess
as well as some blueprints materials (wax, hydrocolloids) could cause burns
on the oral mucosa.

All lesions caused by erythema, erosions or vesicles will heal within a

week.
Bacterial infections
SYPHILIS: it is a sexually transmitted infection caused by the
spirochete anaerobic bacterium, Treponema pallidum. Depending on the
transmission route, syphilis can be either transmitted or congenital. The
primary route of transmission is sexual and only in extremely exceptional
cases contamination could come through an infected blood transfusion.
Treponema can be passed from mother to fetus or during birth causing
congenital syphilis.
Sexually transmitted syphilis has three longitudinal phases:
-

primary

secondary

latent (tertiary)

Primary syphilis: the specific lesion of syphilis is chancre, most

frequently located on the genital area, although in 2-5% of the cases it can
be located in the oral cavity.
Averagely, the incubation period is about 3 weeks long.
The incubation period can be shorter, depending on the large number
of spirochetes inoculated during the infective sexual contact and the
correlation to an ongoing solution facilitating the premature occurrence of
syphiloma.
The occurrence of primary sores can be delayed (60 90 days from
the infective sexual contact) by the use of sub-curative doses of
treponemicidal antibiotics for common, inter-current, medical conditions
and thus making it impossible to conduct a prophylaxis for syphilis.
The most frequently affected areas in the oral cavity, after lips and
commissures, are:
-

tongue

palate

gingiva (the incisive canine area)

tonsils

From a clinical point of view, chancre first resembles a macula that

progressively turns into an inflammatory papule that quickly erodes and
becomes a painless, neat lesion, with slightly bold margins, hard base and
surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
Chancre usually occurs as a singular sore, although multiple sores are
possible to occur and succeed in evolution.
The size of the sore varies from a few mm to 3 cm (the maximum
diameter).
Primary

lesion

is

accompanied

by

one-sided,

regional

lymphadenopathy (rarely bilateral) with enlarged, mobile lymph glands that

are sensitive to touch. Lymphadenopathy occurs a week after the chancre
and persists for weeks and sometimes months after chancre disappeared.
The sore usually reabsorb and spontaneously heal in 3-6 days without
any treatment; a barely visible scar will remain.
Diagnosis of primary syphilis is based on:
-

anamnesis

clinical aspect

bacterial tests

serologic tests

Bacterial diagnosis consists of a microscopic dark field examination

of the serosity obtained from compressing the base of the chancre, since it
is not possible to cultivate Treponema palladium.
The bacterial microscopic examination is performed only during the
first 2 3 weeks of chancre evolution until serosity turns positive. In the
case of oral chancre Treponema palladium must be differentiated from
other commensal spirochetes and the only certain method to do so is by
microscopic examination, direct immunofluorescence staining.
During primary stage of syphilis, serologic tests can turn out
negative.
At the end of the primary stage of syphilis (about a month after
inoculation)

VDRL

(Venereal

Disease

Research

Laboratory),

immunofluorescence reaction FTA Abs (Fluorescent Treponemal

Antibody Absorption) or the TPHA (Treponema palladium haemaglutination

assay) turn out positive.
Differential diagnosis includes:
-

traumatic ulcers

aphthae

T.B.C. lesions (tuberculous ulcers)

Epidermoid carcinoma

SECONDARY SYPHILIS: sores usually occur 4-10 weeks after the

initial infection. From a clinical point of view, there can be observed general
manifestations of the disease and skin mucous manifestations. General
manifestations precede or accompany the lesions on the skin and mucosa
and are represented by:
-

painful lymphadenopathy

malaise

headache

weight loss

fever

musculoskeletal pain

biologic

changes

(hyperleukocytosis,

hypochromic

anemia,

increase of VSH values)

Skin

lesions

are

polymorphous,

generalized,

superficial

and

resolutive; initially they are represented by a macular rash that later turns
papillary squamous. This exanthema occurs on the face, palms and plantar
area.
Oral manifestations are mostly associated with skin lesions and
continue to evolve for 3 12 weeks, whereupon they will disappear leaving
no scars. These oral manifestations are common in 1/3 cases of syphilis.
The initial manifestation is similar to the coetaneous one and it is
characterized by a dark-red macular eruption (syphilitic rosella) located
mainly on the posterior side of the oral cavity. Further on, there will appear
mucous plaques representing the most frequent manifestation of this

stage. From a clinical point of view, they are oval, slightly bolded and
turning into opalescent, white-grey plaques and surrounded by an
erythematous margin. The superficial layer is removed and slightly painful,
possibly bleeding ulcers are revealed.
These ulcers are mostly located on the lips, tongue, jugal mucosa and
palate. Sometimes, they can be found on the tonsils. These lesions are
highly contagious.
In this stage of the disease, there can be seen syphilitic condyloma
(vegetative syphilides) that are exophytic, papillomatous lesions located
on the commissures or the palate. They will be highly infectious if they turn
into ulcerations.
Laboratory examinations
-

serologic tests are positive

dark

field

microscopic

examination

and

immunofluorescence

examination can show Treponema palladium and are useful in establishing

diagnosis.
Differential diagnosis in the initial stage includes:
-

infectious mononucleosis

erosive drug eruptions

LATENT SYPHILIS (TERTIARY)

It is rarely common today and it usually manifests after a period of 3
10 years and sometimes even 30 years may pass until this stage of syphilis
is diagnosed. Some 1/3 cases of syphilis will develop the third stage and
only when improper treatment was prescribed.
It is mainly characterized by:
-

neurological manifestations (meningitis, progressive generalized

paralysis, locomotive ataxia)

cardiovascular lesions (ascending aorta aneurysms and cardiac

failure)

lesions of the skin and mucosa (gumma and syphilitic tubercle)

bone lesions that mainly affect the leg bone, skull bones, and nose
and maxillary bones.

Oral manifestations include:

-

gumma

atrophic glossitis

sclerotic glossitis

Gumma is an inflammatory, granular and circumscribed lesion first

occurring under skin or under mucosa and later on spreading towards
superficial or more profound layers.
From an evolution point of view, gumma knows 4 stages:
-

rawness

softening

ulceration

healing

The size of the lesion varies from 1 to 10 cm.

It is most frequently located on the hard palate (extending to oralnasal fistula) and the palatine velum.
Atrophic glossitis (or interstitial) is the consequence of a vasculitis
that evolves into an obliterating endarteritis, causing the atrophy of both
the mucosa and the muscle of the tongue. Consequently, the dorsal part of
the tongue becomes neat and atrophic.
Sclerotic glossitis is the result of tongue becoming deformed once a
gumma has healed. Consequently, the tongue has a lobulated appearance
with deep and irregular ditches.
CONGENITAL SYPHILIS: it is commonly met in children born from
infected mothers; during the 5th month of pregnancy treponemes can pass
through the placenta and infect the fetus.
Spirochetemia can cause miscarriages or it can produce numerous
inflammatory and destructive lesions to many organs of the fetus.
Early congenital syphilis occurs in children aged between 0 and 2,
while late congenital syphilis occurs in children grater than 2.
Early congenital syphilis (neonatal) is a severe form affecting
many

internal

organs

(constant

splenomegaly,

congestive

hepatitis,

edematous nephritis, pneumonia). Skin and mucous lesions are also quite

severe (palmar-plantar pemphigus, papillary, erythematous-papular analgenital and facial syphilides).

When affecting the facial area, it is most commonly met in the
perioral, pathognomonic part and it is characterized by rhagades (Parrots
radial scars). The line between skin and vermillion is not clear.
Syphilitic coryza manifests with swelling, congestion and erosion of
the nasal mucosa that is covered by a serosanguineous exudate forming
crusts and obliterating the nasal cavity. Swallowing is rather difficult.
Erosive syphilides affect the oral cavity and the larynx.
Late congenital syphilis occurs in children aged between 6 and 15.
The most frequently met malformations interest:

ogival palate

saddle nose

frontal bossing

Hutchinsons triad is characterized by:

interstitial keratitis

labyrinthine deafness

dental dysplasia or hypoplasia

From a clinical point of view, the permanent upper central incisors

have a conical shape, while the margin is peg-shaped. Lateral incisors can
present the same abnormalities, although less severe.
The orientation on the arcade is also abnormal and the longitudinal
axis is convergent towards the free margin.
Hypoplasia of the enamel can equally interest the permanent molars,
especially the first inferior molars that present multiple cusps and thus
resulting a mulberry-like aspect (Moon molars).
Positive diagnosis is based on the clinical examination and serologic
testing.
Treatment: penicillin is the treatment of choice in all stages of
syphilis. When there is a case of allergy to penicillin, other types of
antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline,
and doxycycline).

TUBERCULOSIS: it is caused by an aerobic bacillus, Mycobacterium

tuberculosis (Koch bacillus). The most frequent and well known form of the
disease interests the lungs.
The disease spreads through air from one person to another.
The primary from of tuberculosis is usually asymptomatic. In most
cases, granular lung lesions heal with fibrosis and calcified nodules that will
show on radiography examination.
Rarely enough, the disease could spread to cause pleurisy or
pericarditis.
After the primary infection, the disease can remain latent for a
variable period of time.
Reactivation usually happens later on in life, causing pulmonary
manifestations (secondary tuberculosis) or systemic ones.
Tubercular bacilli from granular lesions can disseminate (miliary
tuberculosis) affecting the liver, kidneys, vertebral bodies (Potts syndrome),
gastrointestinal tract and the meninges.
Secondary tuberculosis is accompanied by remittent fever, malaise,
anorexia, weight loss and night sweats. The progression of the pulmonary
condition causes productive cough, haemoptysis, chest pain and dyspnoea.
Oral manifestations in tuberculosis are rare, occurring in 0.5 1.5%
of cases.
It is not common or rare to diagnose pulmonary tuberculosis when
investigations are conducted for an oral lesion.
Primary

tuberculosis

manifests

with

primary

complex

of

ulcerations and lymphadenopathy.

Koch bacilli can pass through post-extraction sores, extended
ulcerations of the mucosa, apical infections or during teething.
Ulceration appears as a little deep lesion with thin borders, redpurple surface and painful.
It is mainly located on the:
-

gingiva

vestibular cavities

sore mucosa surrounding the teeth

post-extraction area

Lymphadenopathy occurs early, at first it is singular and then

multiple. Initially, lymph nods are mobile and painless, then they get fixed
(by reaction of periadenitis), skin becomes adhered to the mass and may
rupture. Suppuration may last for several months and the resulting scar
appears keloid.
Submandibular tuberculosis lymphadenopathy may be, in many cases,
the only clinical manifestation of the primary infection.
Diagnosis is based on clinical data, biopsy, and puncture and, if
necessary, guinea pig inoculation.
Tuberculin intradermal test turns out positive after 20 days of disease
evolution.
The affected lymph nodes can be incised and the purulent collection is
drained.
General treatment contains anti inflammatory drugs, painkillers and
tuberculostatic medication.
Secondary tuberculosis: it occurs in patients who have been
infected with the bacillus. Oral manifestations of secondary tuberculosis
have three clinical aspects:
-

ulceration

gumma

tuberculosis lupus

Ulceration occurs once the infection has spread through saliva. The
most frequent location is on the dorsal part of the tongue, followed by the
palate, jugal mucosa, gingiva and lips.
Typical lesions have 1 -5 cm diameter, irregular borders and granular
surface and are covered by a yellow deposit. Sometimes, at the border of
the lesions small yellow nodules are visible (representing calcified
tubercles) and are called Trlat granulations.
The lesion is very painful and it causes discomfort while eating,
speaking or swallowing.

Complementary examinations which are useful in establishing

diagnosis:
- histopathologic examination shows a granular inflammation formed
of epithelial histocytes, lymphocytes, giant multinucleated cells and a
central area with cazeos necrosis.
In order to identify the micro-organism several staining methods are
used (Ziehl-Neelsen) since other infectious or noninfectious diseases could
cause

similar

granulomatous

reactions

9syphilis,

histoplasmosis,

blastomycosis, sarcoidosis and reaction to foreign body).

-

tuberculin I.D.R.

inoculation on culture media

thoracic radiography showing pulmonary lesions

Differential diagnosis includes:

-

primary syphilis lesions

epidermoid carcinoma

giant aphthae

traumatic ulcerations

deep fungal infections

Treatment
General treatment is specific for tuberculosis. Local treatment
consists of:
-

hygiene of oral cavity

anti inflammatory drugs

painkillers

Tuberculosis gumma is mainly located on the anterior half of the

tongue.
As in syphilitic gumma there are four stages: rawness, softening,
ulceration and healing.
During the first stage it can be shallow or profound and it may have a
tumor like aspect.
Later, it shows on the dorsal part of the tongue. After the softening
stage it ulcerates and it eliminates the yellow-green purulent content. This

abscess contains numerous Koch bacilli.

Treatment is surgical during the first stage and it consists of excision
and suture; during the cold abscess stage it is preferred to drain the
content of the lesion and to undergo a specific anti tuberculostatic
medication.
Tuberculosis lupus with oral localization is a secondary form of the
lupus affecting the nasal fossa or the face.
Infection is spread by contiguity or by lymphatic ways. It is most
frequently met on the veil, the upper gingiva and the inside lip.
Lupoma represents the elementary lesion that appears as a small, soft
tubercle (1-2 mm) located under the mucosa. It becomes yellow when
pressured.
Lupen placard consists of a multitude of small tubercles located on a
congested mucosa.
Tubercles get soft and ulcerate into lesions with bold borders and
granular surface.
Lesions heal leaving keloid, retractable scars and synechiae of the
mucosa.
Treatment is specific to a bacterial infection.
ACTINOMYCOSIS
Although this terminology seems to suggest a fungal infection, the
causative agent of the disease is an air-transmitted filamentous grampositive bacterium.
Etiopathogenesis: actinomycetes are part of the saprophytic flora
that is normally found in the oral cavity. The places for colonization are
represented by:
-

tonsil crypts

dental plaque

carious lesions

tartar

gingival sulcus

periodontal pockets

Although Actinomyces israelli is most commonly involved in the

clinical

infection,

Actinomyces

naeslundii,

Actinomyces

viscosus,

Actinomyces odontolyticus, Actinomyces meyeri and Actinomyces bovis as

well as Arachnia propionica, can also cause actinomycosis. Furthermore, in
most cases, the presence of some bacteria (staphylococcus, streptococcus,
fusobacteria, etc) demonstrates the synergetic pathogenic participation of
these alongside actinomycetes.
The most frequently affected areas are:
-

cervical-facial area

abdominal area

thoracic area

skin

genital area

More than 50% of cases are located on the cervical-facial part of the
body. The soft parts of this area are penetrated through caries, gingival
pockets or continuity osteo-mucotic solutions. Actinomycetes penetrate
through one of these places inside the bone together with common pyogenic
germs and reach the soft cervical-facial parts where they initially produce
uncharacteristic lesions.
Exceptionally, there can appear condensed osteomyelitis lesions at the
bone level that are possible to diagnose only by biopsy. Lymphatic system is
not invaded.
Symptoms: from a clinical point of view, actinomycosis may present
and progress in varied forms, from a small circumscribed nodule to
swellings that affect large areas of tissue and even pseudo-tumoral
forms.
The debut of the disease can start as a nodular tumefaction, not very
painful, with a slow evolution that softens in the centre ulcerating
spontaneously. In other cases the disease can debut with an acute perimaxillary suppuration that becomes chronic after spontaneous ulceration or
surgical treatment (including the removal of the causative factor).
During the state period there will appear a hard tumefaction covered

by small abscesses in various stages of evolution. Teguments become purple

and thinner, the abscesses break open spontaneously into fistula and the
skin looks like a sprinkler
Fistula leaks a serous secretion containing white-yellow granules
similar to pollen.
In an advanced stage there can be seen emerging or ulcerating
abscesses next to fistula and scars.
General wellbeing is not affected by the disease.
Positive diagnosis includes clinical and laboratory findings.
Any peri-maxillary fistula that cannot be attached to a precise cause
(suppurative cysts, osteomyelitis, fistulated nonspecific adenitis, peri-apical
dental process, etc) or any other peri-maxillary suppuration that do not
react to treatment should be considered as a sign of actinomycosis.
When

the

clinical

picture

is

specific

and

the

microbiologic

examination turns out negative, actinomycosis is not excluded, although

successive probes and microbiologic and histological examination are
necessary.
Furthermore, the presence of actinomycotic granules in the leak is not
pathognomonic when the clinical aspect is not characteristic since similar
granules are also visible in botryomycosis.
Histopathologic examination shows the characteristic microscopic
lesion represented by the actinomycetic nodule formed of three parts:
-

central area presenting pus with free or fixed granules formed of a

network of filaments disposed as a star and with slightly swollen
borders

the layer consisting of plasma epithelioid cells

the peripheral layer formed of mononuclear cells that turn fibrotic

during long time evolution and will give the specific sclerotic
aspect.

Actinomycetes are best seen on direct examination of the oral cavity

of granules from pus collections. The culture of actinomycetes in
different media in controlled atmosphere of CO at 37 0 C and the
identification of the species through immunofluorescence method provide a

certain diagnosis.
Differential diagnosis
From a clinical point of view, actinomycosis should be differentiated
from:
-

acute peri-maxillary inflammatory conditions

fistulizing osteitis and ostemyelitis

specific infections (TBC)

infected tumors of the skin and the soft cervical-facial parts

Evolution and complications: the evolution of the disease has many

possibilities. Thus, depending on the precocity of diagnosis and the
therapeutic scheme, the condition can heal within 2 3 weeks, although 2
months period can be required for healing.
In severe forms of the disease where no proper treatment has been
instituted long evolution of up to 10 20 years have been documented; also,
the disease has spread to temporal fossa, meninges and cervical spine and
then invading the medular, mediastinal cavity.
Treatment
Since actinomycosis is a sub-acute or chronic infection characterized
by the formation of fibrosis tissue resistant to antibiotics, treatment consists
of antibiotic therapy associated with surgical intervention.
Surgical treatment consists in the incision and drainage of the content
of abscesses, the removal of the causative factor and the excision of
fistulous tracts and scars. Nodular formations that have been found will also
be removed.
Antibiotic therapy consists of high doses of intramuscular or
intravenous penicillin G administrated for a period of 4 6 weeks
(depending on the severity of the infection), followed by fractioned
administration of penicillin V (2 4g/day).
In cases of allergy to penicillin, the treatment consists of tetracycline
2g/day in 4 doses for a period of 2 weeks.
When microscopic examination shows the involvement of anaerobic
bacteria, antibiotic therapy will be accompanied by metronidazole (1g/day
for 14 days).

When teguments restore and the inflammatory processes have ceased,

the disease is considered healed.
NOMA

(cancrum

oris,

gangrenous

stomatitis,

necrotic

stomatitis): it is a rapidly progressive infection causing destructive lesions

of the oral-facial tissues.
Causative agents, Fusobacterium necrophorum or Fusobacterium
nucleatum and Spirocheta Borrelia vincentii are part of the saprophytic
flora commonly found in the oral cavity, although they can become
pathogenic when immunity is compromised.
Predisposing factors are:
-

malnutrition

dehydration

recent infectious conditions (herpes simplex, varicella, scarlet

fever, tuberculosis, malaria, gastroenteritis, bronchopneumonia)

malign conditions (leukemia)

immunologic deficiencies, including AIDS

poor oral hygiene

The disease is frequently met in underdeveloped countries, in children

aged between 1 and 10, although rarely it can be seen in adults.
From a clinical point of view, the disease can start as an acute
ulcerative-necrotic gingivitis that affects the vestibule and/or tongue,
interesting the adjacent tissues and causing the mucosa to be ulcerativenecrotic.
Necrotic areas could also occur on the soft areas as a consequence of
traumatic lesions without any continuity to the gingiva. Gangrenous
ulcerations present sphacelus and are covered by fibrinoid white-grey
deposits. Denudation and the invasion of maxillaries and mandible cause
necrosis and sequestration.
Pain, fever, hyper-salivation, fetid, halitosis and lymphadenopathy
constantly accompany the other manifestations.
Treatment and prognosis
In the absence of any treatment, mortality rate reaches 95%, although

nowadays less than 10% of patients die from complications of the disease
(pneumonia, diarrhea and septicemia).
Treatment consists of preventing and eliminating the predisposing
factors, diet rebalancing, hydration and antibiotic therapy (penicillin and
metronidazole).

Locally,

the

necrotic

tissue

will

reconstructive surgery will be performed one year later.

be

removed

and