INFECTION -The lodgment and multiplication of a
parasite in or on the tissue of a host constitute infection. It
does not invariably results in disease. In fact, disease is but a
rare consequences of infection, which is a common natural
Gingival disease are a diverse family of complex & distinct
pathological entities which are the result of variety of
The inflammatory response initiated in gingival disease
appears to be prerequisite for destruction of connective tissue
attachment apical to CEJ. (Page et al 1997)
The identification & treatment of gingival disease is important
step in preventing more serious periodontal ailments.
Acute lesions have a rapid onset & is accompanied by pain.
Acute lesions are by definition, of sudden onset, limited
duration & with well defined features in contrast with
An abscess is a cavity containing pus and surrounded by
inflammed tissue, formed as a result of a localized
The formation of pus is termed suppuration.
Classification: Meng 1999
It has been classified into three diagnostic groups:
Involves the marginal gingival and interdental tissues.
Is an infection located contiguous to the periodontal pocket and
may result in destruction of the PDL & alveolar bone.
Is associated with the crown of incompletely erupted tooth.
A localized purulent infection that involves the
marginal gingiva or interdental papilla
Acute inflammatory response to foreign substances
forced into the gingiva
Localized swelling of marginal gingiva or papilla
A red, smooth, shiny surface
May be painful and appear pointed
Purulent exudate may be present
No previous periodontal disease
Treatment of gingival abscess is aimed at
reversal of the acute phase and removal of
1. Topical or local anaesthesia by infiltration
2. When possible, SRP are completed to
establish drainage and remove microbial
3. In acute cases, the fluctuant area is incised
with a #15 scalpel blade and exudate may
be expressed by gentle digital pressure.
4. Any foreign material is removed.
5. The area is irrigated with warm saline water and covered with
moist gauze under light pressure.
6. Once bleeding has stopped, patient is dismissed with
instructions to rinse with warm saline water every 2 hrs.
7. After 24 hrs, the area is reassessed, and if resolution is
sufficient, scaling not previously completed is undertaken.
8. If the lesion is large or poorly accessible, surgical access may
• A periodontal abscess is defined as a localized purulent infection
affecting the tissues surrounding a periodontal pocket that can lead to the
destruction of supporting structures (Meng 1999).
• It is also known as a lateral abscess or parietal abscess.
• It is the third most frequent dental emergency, representing 7–14% of all
dental emergencies, and affecting 6–7‰ of all patients seen in a dental
• It is typically found in patients with untreated periodontitis and in
association with moderate to deep periodontal pockets. (Takei HH 2002)
• Depending on the etiology
• Periodontitis- related abscess
• Non periodontitis- related abscess
• Depending on the course of the lesion (Galego-Feal 1995).
• Depending on the number (Topoll et al. 1990).
• The existence of deep, tortuous pockets, with cul-de-sac, which eventually
become isolated, may favour the formation of abscesses (Carranza 1990).
• The marginal closure of a periodontal pocket, may lead to an extension of the
infection into the surrounding periodontal tissues due to the pressure of the
suppuration inside the closed pocket( DeWitt. 1985).
• Fibrin secretions, leading to the local accumulation of pus may favour the
closure of the gingival margin to the tooth surface (Galego-Feal 1995).
• Changes in the composition of the microflora, bacterial virulence, or in host
defenses (Kareha 1981) could also make the pocket lumen inefficient to drain
the increased suppuration.
Smooth, shiny swelling of the
Painful, tender to palpation
Increased probing depth
Mobile and/or percussion sensitive
Tooth usually vital
Via sulcus is the preferred method
Surgical access for debridement
Incision and drainage
Antibiotic options AAP 2004
Antibiotic of choice:
Loading dose- 1gm
then 500mg tds for 3 days
Reevaluation after 3 days to determine the need for continued or
adjusted antibiotic therapy.
Cephalexin or clindamycin can be used if the infection is not
responding in 24 to 48 hours.
Loading dose- 600mg
then 300mg qid for 3 days.
- Drug of choice in case of rapid local spread
• Azithromycin ( or clarithromycin)
Loading dose- 1gm
then 500mg qid for 3 days
200 - 400 mg tds 5-7 days
A localized purulent
infection within the tissue
surrounding the crown of
a partially erupted tooth.
Most common adjacent to
mandibular third molars in
young adults; usually
caused by impaction of
debris under the soft tissue
Operculum (soft tissue flap)
Localized red, swollen tissue
Area painful to touch
Tissue trauma from opposing tooth common
Purulent exudate, trismus, lymphadenopathy, fever, and
malaise may be present
Debride/irrigate under pericoronal flap
Tissue recontouring (removing tissue flap)
Extraction of involved and/or opposing tooth
Antimicrobials (local and/or systemic as needed)
Culture and sensitivity
Necrotizing ulcerative gingivitis , necrotizing periodontitis,
necrotizing stomatitis are the most severe inflammatory
periodontal disorders caused by plaque bacteria.
They are rapidly destructive & debilitating & represents
various stages of same disease process (Horing & Cohen
They are also referred to as ulceromembraneous gingivitis,
necrotizing gingivostomatitis, vincent’s gingivostomatitis,&
trench mouth( Pickard 1973, Johnson & Engle 1986, Horing
& Cohen 1995).
It is characterized by death & sloughing of gingival tissue &
presents with characteristics signs & symptoms.
EPIDEMIOLOGY & PREVALENCE
NUG often occurs in groups in an epidemic form.
During world war I & II “ epidemics “ broke out among the allied
troops. Epidemic like outbreaks have also occurred among civilian
In developing countries, the prevalence of NPD is higher than in the
industrialized countries, & the disease frequently affects the
In India, 54- 64 % of NPD cases occurred in children below 10 yrs
of age.( Migliani& Sharma 1965; Pindborg et al 1996).
NUG occurs at all ages, with the highest incidence reported between
ages 20 & 30 yrs & ages 15 -20 yrs.
The disease seems to occur slightly more among HIV infected
individuals. Studies among groups of HIV infected individuals
have revealed prevalence of NPD between 0 & 27.7%.
(Reichart et al 2003).
NP was found in 1% of 200 HIV seropositive individuals
(Riley et al 1992) & the prevalence may not in fact, differ from
much of the general population ( Drinkard et al 1991 );This is
particularly true after introduction of antiretroviral therapy.
Role of microorganism
Role of host response
Predisposing factors includes
1. Local predisposing factor
2. Systemic predisposing factor
ROLE OF BACTERIA
Plaut & Vincent introduced the concept that NUG is caused by
specific bacteria ; fusiform bacillus & spirochetal organism.
Loesche et al described a predominant constant flora & a variable
flora associated with NUG. The constant flora is composed of
prevotella intermedia, treponema sp, selenomonas sp, &
fusobacterium sp. The variable flora consists of heterogeneous
array of bacterial types.
The bacteriologic findings have been supported by immunologic
data from Chung et al. - reported increased antibody titers for
spirochetes & P.intermedia in NUG patients compared with titers in
those with chronic gingivitis & healthy controls.
Borrelia, gram positive cocci, b-hemolytic streptococci &
Candida albicans have been isolated from the lesions of HIV
associated NUP.(Reichart & Schiodt 1989).
It has also been proposed that human cytomegalovirus may
play a role in the pathogenesis of NPD. (Sabiston 1986).
Pathogenic potential of microorganism
An important aspects in the pathogenesis of periodontitis is the
capacity of the microorganism to invade the host tissues.
Among the bacteria isolated from necrotizing lesions, spirochetes &
fusobacterium can in fact invade the epithelium. (Heylings 1967).
The spirochetes can also invade the vital connective tissue
The pathogenic potential is further substantiated by the fact that both
fusobacterium & spirochetes can liberate endotoxins
(Kristoffersen et al).
Gram negative bacteria liberate endotoxins in close contact with
connective tissue. Endotoxins may produce tissue destruction both
by direct toxic effects & indirectly by activating & modifying
tissue responses of the host.(Wilton & Lehner 1980)
Through a direct effect, endotoxins may lead to damage of cells &
vessels. Necrosis is a prominent feature so-called Schwartzman
reaction which is caused by endotoxins.
Indirectly endotoxins contribute to tissue damage in several ways;
They can function as antigens & elicit immune reactions.
They can activate compliment directly through the alternative
pathway & thereby liberate chemotoxins.
They can also activate macrophages, T & B lymphocytes &
influence the host immune reactions by interfering with
cytokines produced by these cells.
Studies have shown that endotoxins can stimulate catabolic
processes with degradation of both connective tissue & bone
induced by the released cytokines.
The extent to which such reactions contribute to the host
defense or tissue damage is not yet known.
Fusobacterium & Spirochetes are found in moderate numbers of
other oral diseases, as well as in apparently healthy mouths suggests
that predisposing factors are essential to the development of ANUG.
The disease has never been produced experimentally in either human
beings or animals simply by oral inoculation of materials from lesion
in patients with disease. (Schwartz & Grossman).
King also attempted to produce disease in his own mouth by
inoculation of infected material but he was unsuccessful even after
traumatizing gingiva & the organism promptly disappeared.
But he did show characteristic signs of ANUG however after he
became ill with several colds, a short time later.
ROLE OF HOST RESPONSE
Regardless of whether specific bacteria are implicated in the
etiology of NUG, the presence of these organism is insufficient
to cause the disease.
The role of an impaired host response in NUG has long been
It is particularly evident for HIV-infected patients that the
disease is associated with diminished host resistance; among
other predisposing factors, the basic mechanism may include
altered host immunity.
Changes in leukocyte function & the immune system have been
observed.(Johnson & Engle et al)
NUG is not found in well nourished individuals with a fully
functional immune system. All the predisposing factor for NUG
is associated with immunosuppresion.
Cohen et al described a depression in host defense mechanism
particularly in PMN.
Total leukocyte count have been found to be similar for patients
& controls. Patients with NG shows marked depression in
polymorphonuclear leukocyte chemotaxis & phagocytosis as
compared with control individuals.
Reduced proliferation of peripheral blood lymphocytes has also
been found in those patients.
It was also suggested that elevated levels of blood steroids may
account for the reduced chemotactic & phagocytic responses.
LOCAL PREDISPOSING FACTORS
It includes poor oral hygiene, preexisting gingivitis , injury to
gingiva, & smoking
It may also occur in disease free mouth, it most often occurs
superimposed on preexisting chronic gingival disease &
Areas of gingiva traumatized by opposing teeth in malocclusion –
may predispose to NUG.
Pindborg et al – 98% of his patients with NUG were smokers &
that the frequency of disease increases with an increase exposure
Systemic predisposing factors
nutritional deficiency (malnutrition),
fatigue caused by chronic sleep deficiency,
other health habits like alcohol & drug abuse.
Malnutrition results in lowered tissue resistance - most common
public health problem affecting children who are most often
affected by NPD. (Enwonwu 1985, 1994).
In response to periodontal pathogens phagocytes elaborate
destructive oxidants, proteinases & other factors.
Periodontal damage may often occur as a result of the balance
between these two factors, antioxidants & host derived anti
Malnutrition is characterized by marked tissue depletion of the
key antioxidant nutrients, & impaired acute phase reactions to
the infections. This is due to impairment in the production &
cellular action of cytokines.
Malnutrition – defective mucosal integrity, hormonal
Malnutrition usually involves concomitant deficiencies of
several essential macro & micronutrients, & therefore has the
potential to adversely influence the prognosis of periodontal
infections. (Enwonwu 1994).
It also accentuates the severity of the pathologic changes when
fusospirocheal complex is injected to the animals.
(Smith DT et al)
Debilitating systemic disease may predispose the patient to the
development of NUG.
It includes chronic disease ( eg. Syphilis, cancer), severe
gastrointestinal disorders such as ulcerative colitis, blood
dyscracias (anemia , leukemia) & acquired immunodeficiency
Nutritional deficiency resulting from debilitating disease may be
an additional pre disposing factor.
Ulceronecrotic lesions appear in the gingival margins of hamsters
exposed to total body irradiation.(Mayo J et al)
Psychological factors appear to be important in the etiology of
The disease often occur with association with stressful situation
(Induction in to armed forces, examination periods, emotional disorders, patients
feeling inadequate at handling life situations).
Cohen – Cole et al – psychiatric disturbance and the impact of
negative life events may lead to activation of hypothalamic-
pituitary adrenal axis resulting in elevation of cortisol levels.
This may reduce gingival microcirculation & salivary flow &
enhance nutrition to prevotella intermedia, but also depresses
neutrophil & lymphocyte functions which facilitate bacterial
invasion & damage.(Johnson et al)
Significant correlation between the disease incidence & two
personality traits – dominance & abasement – suggests the
presence of an ANUG prone personality.(Formicola AJ et al).
The mechanisms whereby psychological factors create or
predispose to gingival damage have not been established, but
alterations in digital & gingival capillary response suggestive
of increased autonomic nervous activity have been
demonstrated in patients with ANUG.
The relationship between tobacco usage & NPD appears to be
Smokers in general poorer oral hygiene than the non smokers.
Smoking could lead to increased disease activity by influencing
host response & tissue reactions. As examples, smokers have
depressed numbers of T- helper lymphocytes, & tobacco smoke
can also impair chemotaxis and phagocytosis of oral & peripheral
phagocytes.( Lannan et al 1992, Selby et al 1992)
Nicotine- induced secretion of epinephrine resulting in gingival
vasoconstriction – possible mechanism by which smoking may
influence tissue susceptibility.( Bergstrom & Preber 1986)
HIV infection attacks the T- helper cells of the body, causing
drastic change in the T-helper (CD4+)/T-suppressor(CD8+) ratio
with severe impairment of the host resistance to infection.
Depleted T- helper lymphocyte counts correlate closely with the
occurrence of NG as demonstrated in the study of 390 US HIV
seropositive soldiers (Thompson et al 1992).
A complete absence of T cells in gingival tissue of HIV infected
patients with periodontitis. (Steidley et al 1992).
The lack of local immune effectors & regulatory cells in the HIV
seropositive individuals could explain the characteristic &
rapidly progressive nature of periodontitis in these patients.
Moreover, a protective effect has been encountered with
antiviral treatment of the HIV infection against NPD (Tappuni
& Flemming et al 2001) as well as against HIV-associated
gingivitis & periodontitis. (Masouredis et al 1992).
Clinical features - Oral signs
NG – an inflammatory destructive gingival condition,
characterized by punched out crater like depressions at the crest
of the interdental papillae, subsequently extending to the marginal
gingiva and rarely to the attached gingiva & oral mucosa.
The surface of the craters is covered by a gray pseudomembranous
slough, demarcated from the remainder of the gingival mucosa by
a pronounced linear erythema.
In some cases the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin which is red,
shiny, & hemorrhagic. The characteristic lesion may progressively
destroy the gingiva & underlying periodontal tissues.
Spontaneous gingival hemorrhage or pronounced bleeding
after the slight stimulation are characteristic clinical signs.
A characteristic & pronounced foetor ex ore is often associated
with this disease & also there is increased salivation.
The lesion is extremely sensitive to touch, & the patient may
often complains of a constant radiating, gnawing pain that is
often intensified by eating spicy or hot foods & chewing.
There is metallic foul taste & an excessive amount of pasty
Extra oral & systemic signs & symptoms
In mild & moderate stages of disease
Local lymphadenopathy & slight elevation in temperature.
In severe cases
High fever, increased pulse rate, leucocytois, loss of appetite &
Systemic reactions are more severe in children.
Insomnia, constipation, gastro-intestinal disorders, headache, &
mental depression sometimes accompany the condition.
In very rare cases, severe squeal such as gangrenous stomatitis
& noma have been described.
Stages in the progress of NUG BY PINDBORG et al
Stages of oral necrotizing disease – by
Horning & Cohen
Stage 1- necrosis of the top of the interdental papilla.
Stage 2- necrosis of entire papilla
Stage 3- necrosis extending to the gingival margin.
Stage 4- necrosis extending to the attached gingiva.
Stage 5– necrosis extending to labial & buccal mucosa.
Stage 6- necrosis exposing alveolar bone.
Stage 7– necrosis perforating skin of cheek.
The lesion are seldom associated with deep pocket formation, -
extensive gingival necrosis coincides with rapid loss of crestal
The gingival necrosis develops rapidly & within a few days the
involved papillae is often separated into one facial & one lingual
portion with an interposed necrotic depression.
The central necrosis produces considerable tissue destruction &
regular crater is formed.
At this stage of disease, the disease process usually involves the
periodontal ligament & alveolar bone.(NECROTIZING
Further progression of disease leads to involvement of
underlying bone resulting in sequestrum formation (necrosis
of small or large parts of alveolar bone).
Also the necrotic process progress beyond the mucogingival
junction , the condition is referred to as Necrotizing
Histopathologically, NG lesions is characterized by ulceration
with necrosis of epithelium & superficial layers of the connective
tissue & an non specific inflammatory reaction.
The histological findings demonstrate the formation of regular
layers with certain characteristics (Lisgarten 1965) but there may
be variations in regularity.
The surface epithelium is destroyed & replaced by a meshwork of
fibrin, necrotic epithelium, PMNs & various types of
microorganism. This appears clinically as the surface
Below this necrotic pseudomembrane, the epithelium is
edematous, & the individual cells exhibit varying degrees of
The underlying connective
tissue is extremely hyperemic
with numerous engorged
capillaries & dense infiltration
of PMNs. This acutely inflamed
zone appears clinically as the
Numerous plasma cells may
appear in the periphery of the
infiltrate. This is interpreted as
an area of established chronic
gingivitis on which acute lesion
RELATION OF BACTERIA TO THE
The light microscope & the electron microscope have been used
to study the relationship of bacteria to the characteristic lesion
LISGARTEN described the following four zones which blend
with each other & may not all be present in every case;
Zone1 – bacterial zone
Zone 2 – neutrophil rich zone
Zone 3 – necrotic zone
Zone 4 – zone of spirochetal infiltration
Electron micrograph demonstrating phagocytosing (N)neutrophil close
to the surface of a sequestrum, numerous spirochetes and rods.
The diagnosis of NG, NP, NS is based on clinical findings as
The histopathology of the necrotizing disease is not
pathognomonic of NG & biopsy is not certainly indicated.
Bacterial studies are useful in the differential diagnosis of NUG
& specific infections of oral cavity.
Diagnostic essentials for NUG
Lesions are painful.
Lesions are gingival ulcers, punched out crater like of
interdental papilla & may involve marginal gingiva.
Non essential clinical features of NUG the
absence which does not preclude the
diagnosis of NUG
Pseudomembrane of sloughed necrotic debris & bacteria
covering the ulcerated area.
Foetor ex ore.
Fever, malaise & lymphadenopathy
Important characteristics for differential
diagnosis between NPD & PHG
Etiology Bacteria Herpes simplex virus
Age 15-30 Frequently children
Site Interdental papilla. Rarely outside
Gingiva and entire oral mucosa
Symptoms •Ulcerations and necrotic tissue
and a yellowish –white plaque
•Fetor ex ore
•Moderate Fever may occur
•Multiple vesicles which disrupt,
leaving small round fibrin covered
•Fetor ex ore
Duration 1-2 days if treated 1-2weeks
Contagious - +
Immunity - Partial
Healing Destruction of periodontal tissue
No permanent destruction
The treatment of necrotizing periodontal disease is divided into
1)acute phase treatment
2)maintenance phase treatment
ACUTE PHASE TREATMENT
The aim is to eliminate the disease activity as manifest by ongoing
tissue necrosis developing laterally & apically.
It is also to avoid pain & general discomfort which may severely
compromise food intake.
General examination of the patient
The oral cavity is examined for the characteristic feature of
NUG, its distribution,& possible involvement of oropharyngeal
Oral hygiene is evaluated with special attention to the presence
of pericoronal flaps, periodontal pockets & local factors.
Treatment during initial visits includes,
It is mainly confined to the acutely involved areas
After application of topical anesthetics, the pseudomembrane
& non attached surface debris is removed using a moistened
After the area is cleansed with warm water supragingival calculus
is removed using ultrasonic scalers.
Subgingival scaling & curettage is contraindicated at this time.
Procedures such as extractions or periodontal surgery are
postponed until the patient has been symptom free for 4 weeks, to
minimize the likelihood of exacerbating the acute symptoms.
Patients with moderate or severe NUG & local lymphadenopathy
or systemic signs or symptoms are placed on an antibiotic
regimen of amoxicillin, 500mg orally every 6 hrs for 10 days.
Other antibiotics such as erythromycin (500mg every 6 hrs) or
metronidazole (500mg twice daily for 7 days) are used.
Metronidazole three times daily has been found effective against
spirochetes & appears to be the first choice treatment of NPD.
(Loesche et al).
The adjunctive use of metronidazole in HIV associated NPD is
reported to be extremely effective in reducing acute pain &
promoting rapid healing.(Scully et al).
Topical application of antibiotics is not indicated in the treatment
of NPD because intralesional bacteria are frequent &topical
application does not results in sufficient intralesional
concentration of antibiotics.
Hydrogen peroxide & other oxygen releasing agents also have
a long standing tradition in the treatment of NPD.
Hydrogen peroxide (3%) is used for debridement in necrotic
areas & as a mouth rinse (equal portions 3% H2O2 & warm
Favorable effects of hydrogen peroxide may be due to
mechanical cleaning,& the influence on anaerobic bacterial
flora of the liberated oxygen. (Macphee & Cowley 1981).
Further adjunctive local therapy of NPD showed a more rapid
clinical restitution with less periodontal destruction than in a
group without oxygen therapy. (Gaggl et al 2006)
Twice daily rinsing with a 0.2% chlorhexidine solution is a very
effective adjunct to reduce plaque formation, when particularly
tooth brushing is not performed. It also assists self performed oral
hygiene during the first weeks of treatment.
Appropriate treatment alleviates symptoms with in few days.(5
Systematic subgingival scaling should be continued with
increasing intensity as the symptoms subside.
Correction of restoration margins & polishing of restorations &
root surfaces should be completed after healing of ulcers.
When ulcerated areas are healed local treatment is supplemented
with oral hygiene & patient motivation.
Supportive systemic treatment
In addition to systemic antibiotics, supportive treatment
consists of copious fluid consumption & administration of
analgesics for relief of pain.
Bed rest is necessary for the patients with systemic
complication such as high fever, malaise, anorexia & general
The rationale for the nutritional supplements in the treatment of
ANUG is based on the following;
1) lesions resembling those of the ANUG have been produced
experimentally in animals with nutritional deficiencies.
2) isolated clinical studies report fewer recurrences when local
treatment of ANUG is supplemented with vitamin B & vitamin C.
(Linghorne WJ et al)
And hence nutritional supplements may be indicated along with
local treatment to ward off deficiencies of these vitamins.
MAINTENANCE PHASE TREATMENT
On further visits,
When the acute phase treatment has been completed, necrosis &
acute symptoms in NPD have disappeared.
The formerly necrotic areas are healed & the gingival craters are
reduced in size, although some defects usually persists.
Bacterial plaque accumulates & therefore may predispose to
recurrences of NPD or to further destruction because of a
persisting chronic inflammatory process or both.
These sites therefore requires surgical correction.
Shallow craters can be removed by simple gingivectomy, while
the elimination of deep defects may require flap surgery.
Treatment of NG is not completed until all gingival defects
have been eliminated & optimal conditions for future plaque
control have been established.
Elimination of predisposing factors is also very important to
Gingival changes with healing
The characteristic lesion of NUG undergoes the following changes in
the course of healing in response to treatment,
Removal of pseudomembrane exposes the underlying red
haemorrhagic crater like depression in the gingiva.
In the next stage, the bulk & redness of the crater margins are
Followed by the early signs of restoration of normal gingival
contour & colour.
In the final stage the normal gingival consistency, surface texture,
& contour may be restored. Portion of the root exposed by the
acute disease may be covered by healthy gingiva.
Persistent or recurrent cases
Adequate local therapy with optimal home care will resolve most
cases of NUG. If it persists despite therapy or recurs , the patient
should be revaluated with the focus on the following factors,
Reassessment of differential diagnosis to rule out the disease that
Underlying systemic disease that cause immunosuppresion.
Inadequate local therapy.
Herpetic gingivostomatitis is acute infection that can involve the
gingiva, other oral tissues, the lips, & occasionally the face
Primary infection with herpes virus leads to acute herpetic
gingivostomatitis. The primary attack is believed to confer
It is caused by herpes simplex virus type-1 (HSV-1). It occurs
most often in the children younger than 6 years of age, but it is
also seen in adolescents & adults.
It occurs with equal frequency in male & female patients. In most
patients, the primary infection is asymptomatic.
HERPES SIMPLEX VIRUS
Herpes simplex Virus is a DNA virus & is a member of the human
herpes virus family (HHV) family known as herpetoviridae.
Type 1 – HSV 1 or HHV 2
Type 2 – HSV 2 or HHV 2
Other members of HHV family includes
Varicella zoster virus ( HHV 3)
Epstein barr virus ( HHV 4)
Cytomegalo virus ( HHV 5)
Others – HHV 6, HHV 7, HHV 8
Humans are the only natural reservoirs and all the HHVs have
the ability to reside for life within the infected host.
After the initial infection variable periods of latency &
reactivation with viral shedding are seen.
The two types of HSV are structurally similar structurally but
HSV -1 is spread predominantly through infected saliva or
active perioral lesions. HSV-1 - responsible for oral, facial,
and ocular lesions.
Clinically evident infections with HSV -1 exhibit two patterns.
The initial exposure to an individual without antibodies to the
virus is called the primary infection.
Occurs at an young age & often is asymptomatic.
The virus is then taken up by the sensory nerves & transported to
the associated sensory or less frequently, the autonomic ganglia.
With oral HSV 1 infection the trigeminal ganglion is colonized
and the virus remains at this site in a latent state.
The viruses uses the axons of the sensory neurons to travel back &
froth to the peripheral skin or mucosa.
SECONDARY , RECURRENT OR RECRUDESENT HSV 1
INFECTION occurs with reactivation of the virus although
many patients may show only asymptomatic viral shedding in
Symptomatic recurrences are fairly common & affect the
epithelium fairly supplied by the sensory ganglion.
Spread to an uninfected host can occur easily during periods of
asymptomatic viral shedding or from symptomatic active
Numerous conditions such as old age, ultraviolet light,
emotional stress, pregnancy, allergy, trauma, respiratory
illness, systemic disease or malignancy are associated with
reactivation of virus.
HSV does not survive in the external environment & almost all
the primary infections occur from contact with an infected
person who is releasing the virus.
The usual incubation period is 3 to 9 days.
HSV -1 is acquired from contact with contaminated saliva or
active perioral lesions, poor hygiene promote exposure.
Most cases of acute herpetic gingivostomatitis arise between the
ages of 6 months & 5 years.
The onset is abrupt & accompanied by anterior cervical
lymphadenopathy, fever, anorexia, irritability, and sore mouth
Initially the affected mucosa develops numerous pinhead vesicles,
which rapidly collapse to form numerous small red lesions.
These initial lesions enlarge slightly & develop central areas of
ulceration which are covered by yellow fibrin.
Both the movable & attached oral mucosa can be affected,& the
number of lesions is highly variable.
In all the cases the gingiva is enlarged, painful, & extremely
In addition the affected gingiva often exhibits distinctive punched
out erosions along the mid facial free gingival margins.
An important diagnostic criteria in this disease is the appearance
of a generalized acute marginal gingivitis. The entire gingiva is
edematous & inflamed. Several small gingival ulcers are also
There is inflammation in the posterior pharynx & the
submandibular & cervical lymph nodes are enlarged & tender.
Satellite vesicles of the perioral skin are fairly common.
Mild cases usually resolve within 5 to 7 days; severe cases may
extend to 2 weeks.
Primary HSV in other wise healthy children is a self limiting
The fever ordinarily disappears within 3 or 4 days & the lesion
begin healing in a week to 10 days, although to continue to be
present in the saliva for up to a 10 month after the onset of
Secondary herpes labialis
A patient who has suffered an attack of HGS carries humoral &
possibly cellular antibodies throughout life.
After infection has taken place some virus survives in a latent stage
in the nerve ganglion & may on provocation produce a recurrence.
(secondary herpes labialis, fever blister, cold sore)
The fever blister is a single vesicle or a group of vesicles on the
vermilion border of the lip before an eruption occurs there is often a
prodromal period of burning & tingling in the area.
The blisters break after a few days & form a crust. The lesion heals
after about 2 weeks.
Recurrences can also affect the oral mucosa. In the
immunocompetent patient, involvement is almost always
limited to keratinized mucosa, which is bound to bone
(attached gingiva and hard palate).
The lesion begins as 1 to 3 mm vesicles, which rapidly collapse
to form a cluster of erythematous macules.
The damaged epithelium is lost & a central area of ulceration
develops. Healing takes place within 7 to 10 days.
TRANSFER OF INFECTIONS
Transfer of the herpes virus may be by direct contact or by
contact with contaminated materials or surfaces.
The dental professional is at risk & an infection occasionally
affects on the hand or finger ( HERPETIC WHITLOW). From
such sites the virus may be transferred to the patients.
Each infected individual serves as a permanent carrier who is
The virus exerts its main effects on
the epithelial cells. infected epithelial
cells exhibits acantholysis , nuclear
clearing,& nuclear enlargement –
The acantholytic epithelial cells are
termed as TZANCK CELLS. There is
presence of intranuclear inclusion
bodies – lipschutz bodies.
Nucleolar fragmentation occurs with
the condensation of chromatin around
the periphery of the nucleus. -peri
Intracellular edema leads
to the development of
The vesicle ruptures & the
demonstrate a surface
There is secondary
inflammatory cells in
Patients are easily diagnosed - who present with atypical clinical
picture of generalized symptoms followed by an eruption of oral
vesicles, round shallow symmetrical oral ulcers & acute
marginal gingivitis & who do not have a history of recurrent
Materials may be obtained from the lesions & submitted to the
laboratory for confirmatory tests, including virus culture and
immunologic tests using monoclonal antibodies or DNA
Most commonly used diagnostic procedures - cytological
smear & tissue biopsy
Serological tests for HSV antibodies are positive 4 to 8 days
after initial exposure.
These antibody titers are useful in documenting past exposure
& are used primarily in epidemiologic studies.
Necrotizing ulcerative gingivitis
Stevens – Johnson syndrome
Bullous lichen planus
Lesions of recurrent aphthous stomatitis
Treatment of primary HSV infection is usually palliative. Milder
cases can be managed by supportive care only, since primary
HSV in otherwise healthy individuals is a self limiting disease.
It is important to instruct patient to avoid contact with active
lesions to prevent the spread to other sites and people.
Systemic use of systemic antiviral drugs is indicated in severe
cases of primary HSV , recurrent disease & in
Amir et al demonstrated that antiviral therapy with 15mg/kg of an
acyclovir suspension given five times daily for 7 days substantially
changes the course of disease without significant side effects.
Acyclovir has shown to decrease symptoms of primary HSV infection
in children, including days of fever & viral shedding.
Newer antiherpes drugs are available, including valacyclovir &
famciclovir. The newer drugs have increased bioavailability allowing
effective treatment with fewer daily doses.
Acyclovir – 200mg 5 times daily for 10 days.
Valacyclovir – 100mg 2 times daily for 10 days.
Studies comparing topical antiviral medications for treating recurrent
herpes labialis have been published.
Topical pencyclovir reduces the duration & pain of RHL by 1 to 2 days.
Acyclovir as well as N –Docosanol cream also available for topical use.
Topical acyclovir has been reported to decrease duration of RHL lesions
by 12 hrs & found to be more effective than N-docosanol in treating
Immunosuppressed patients with HSV infection respond well to acyclovir
administered orally or intravenously.
Foscarnet, another antiviral drug has been effective therapy for these
A healthy ,fully erupted tooth is surrounded by a gingival tissue that
typically extends not more than 2 to 3mm coronally.
For a variety of anatomical reasons- partial eruption, malposition,
the immediate proximity of the ramus – the crowns of the third
molars & occasionally other teeth may covered with gingiva &
The potential space between the crown & the soft tissue is of
considerable depth & volume.
A diverse & extensive microflora colonizes these pockets &
gingival inflammation is almost always present.
These sites may acutely infected & may produce symptoms
then they are defined as Pericoronitis.
It was first described by GUNNELL in1844.
It is defined as “ an inflammatory condition of the gingiva &
other supporting tissues that surround the crown of an
incompletely or completely erupted tooth, especially distal
tooth in the arch.( kay 1966)
It is an inflammation of gingiva & contiguous tissues about
crown of an incompletely erupted tooth. (Orban)
Common sites of involvement
In decreasing order of frequency
Mandibular third molars
Mandibular second molars
Mandibular first molars
Maxillary third molars.
LOCAL FACTORS includes
Impacted third molars, more with vertical & distoagular
impactions (taehan, chikkwa, uesa)
Third molars favoring deep distal or distobuccal pocket
Opposing teeth impinging on operculum.
Poor oral hygiene
SYSTEMIC FACTORS includes
Upper respiratory tract infections
General debilitating disease
MULTIFACTORIAL .it includes
Incomplete eruption due to anatomical limitation.
Food impaction & poor oral hygiene.
The occlusal surface of an involved tooth may be partly
covered by a flap of tissue, the operculum, which exists during
the eruption of the tooth & may persist afterward.
The operculum is ideal area for accumulation of food debris
and bacterial growth, since the performance of adequate oral
hygiene in this area is difficult.
It is more vulnerable for irritation & is often directly
traumatized when it is caught between the crown that it covers
& the antagonist tooth during closure.
These factors predisposes to acute infection of the pericoronal
RISK PREDICTORS OF PREICORONITIS
Based on the criteria;
- Vertical or distal tipping of third molars
- Follicular space more than 3mm, the incidence of
getting pericoronitis is 44 times more.
Based on the duration , pericoronitis may be
Also there is an acute exacerbation in chronically inflamed
It is identified by varying degrees of inflammatory involvement
of the pericoronal flap & adjacent structures as well as by
The inflammatory fluid & cellular exudate increases the bulk of
the flap, which may interferes with complete closure of the jaw &
traumatized by contact with the opposing jaw.
There is red, swollen, suppurating lesion that is tender, with
severe throbbing intermittent pain, exaggerated by chewing &
interfering with sleep.
Pain radiates to ear, throat & floor of mouth.
Foul taste, halitosis, & inability to close the mouth.
Swelling of the cheek in the angle of the jaw & lymphadenitis
Systemic complications includes, fever, malaise, leucocytois ,
increased pulse & respiratory rate.
Submandibular lymph nodes may be enlarged & tender on
Sub acute stage
Continuous dull ache, radiates infrequently
Stiffness of jaws, intraoral swelling, unpleasant taste.
Causes less systemic upset
Trismus might be present
Dull pain or mild discomfort lasting for only a day or so,
interspersed with remissions lasting for several months.
Can be made by
Careful history taking
Treatment of pericoronitis focuses on infection control.
It depends on initial assessment of two issues.
1. The severity of infection & the extent to which it has
disseminated from the primary site.
2. The relative importance of the affected tooth & whether the
pericoronal tissue can be returned to & maintained in healthy
Well localized mild to moderate pericoronitis affecting a tooth that is
to be retained is managed conservatively.
Consists of debridement & drainage of the pocket by gentle
curettage & external pressure.
During & after curettage the pocket should be irrigated with sterile
saline solution. Irrigation can also be done with antimicrobial
solution such as 10%providone iodine.
In case of fluctuant abscess drainage should be accomplished by
The patient should be instructed to rinse the area with warm water or
saline solution at frequent intervals until symptoms subside.
Post treatment monitoring is necessary to ensure the resolution of the
When signs & symptoms have regressed the need for
corrective surgery should be considered.
Resection of some or all pericoronal tissue (operculectomy)
depending on tooth position in the jaw & soft tissue
relationships, reduces the chances of recurrent infection.
Operculectomy – surgical removal of operculum. It can be
done using hand instruments, or electrosurgery or LASER.
Operculectomy using electrosurgical
scalpel or radiosurgical loop.
If an opposing third molar is hyper erupted or will require
removal in the near future & is in contact with the inflamed
tissue over the third molar, it can be removed to help decrease
pain & hasten recovery from pericoronitis.
If the affected tooth is non functional or considered
unsalvageable because of malposition or other reasons
extraction is usually appropriate.
If pericoronitis is localized with no evidence of abscess,
extraction may be proceeded or delayed until the acute
inflammation is subsided.
If pus is present , the drainage should be accomplished &
resolution of acute phase before elective extraction.
If immediate extraction is necessary, perioperative and
systemic antimicrobial therapy is used.
Most severe pericoronitis with evidence of regional
dissemination should be treated as described previously. In
addition, antimicrobial chemotherapy should be started
Close monitoring of the outcomes is necessary. Extraction
should be postponed until the infection shows definite signs of
localization or has completely resolved.
ANTIMICROBIALS- IN TREATMENT OF
Commonly used antibiotics includes,
Alternative drugs includes,
Doxycyline 200mg once daily for the first day followed by
100mg twice daily
The involvement may be localized in the form of a pericoronal
It may spread posteriorly into oropharngeal area & medially to
the base of the tongue, making it difficult for the patient to
Depending on the severity & extent of the infection there is
involvement of submaxillary, posterior cervical, & the
retropharyngeal lymph nodes.
Untreated pericoronitis may develop into ANUG. Since
pericoronal flaps are one of the primary incubation zones.
Cyst formation (craig)
Sinus & fistula formation
Root resorption of second molar (kielley & kay)
Migratory abscess of buccal sulcus
Buccal space infection
Retropharyngeal & submandibular space infection.
SERIOUS LIFE- THREATENING COMPLICATION
Cavernous sinus thrombosis
These complications are infrequent but potent squeal of acute
Other acute infections of bacterial
origin- in gingiva
Infection with Neisseria gonorrhea (Scully et al 1995)
Treponema pallidum ( Ramirez –Amador et al 1996)
Streptococci, mycobacterium chelonae (Pedersson et
al 1989) or other micro organism.
It is a rare condition characterized by a diffuse erythema of the
posterior areas of the oral mucosa, sometimes including the gingiva.
Necrosis of the gingival margin is not seen & also there is no
notably fetid odor.
The oral mucosa is covered with a grayish membrane that
sloughs off in areas to expose an underlying bleeding area.
It is most common in newborns & is caused by transmission of
infection from the maternal passages & in adults it results from
Biopsy supplemented by microbiologic examination reveals
the background of the lesions.
Once diagnosed, it is then treated with appropriate
antimicrobials & by conventional means.
CARRANZA’S CLINICAL PERIODONTOLOGTY
CLINICALPERIODONTOLOGY & IMPLANT DENTISTRY –JAN LINDHE
PERIODONTAL & GINGIVAL HEALTH & DISEASE
DECISION MAKING IN PERIODONTOLOGY - WALTER B. HALL
PERIODONTICS – GRANT
PERIODONTICS- ROSE & MALLEY
ORAL & MAXILLOFACIAL PATHOLOGY – ALLEN
TEXT BOOK OF ORAL PATHOLOGY - SHAFER
BURKET’S ORAL MEDICINE
ORAL & MAXILLOFACIAL INFECTIONS – TOPAZIAN.
ORAL & MAXILLOFACIAL SURGERY – HARRY ARCHER
OUTLINE OF PERIODONTICS – MANSON & ELLEY
PERIODONTOLOGY 2OOO – 2002 VOL 30.
THE DENTAL CLINICS OF NORTH AMERICA – 2005 – 49, 15-29.
THE PERIODONTAL ABSCESS: A REVIEW HERRERA D, ROLDA´N S, SANZ
M: JOURNAL OF CLINICAL PERIODONTOLOGY2000
PERIODONTAL ABSCESS: HUAN XIN MENG : ANNALS OF
DIAGNOSIS OF ACUTE PERIODONTAL LESIONS ESMONDE F CORBETT
2004 PERIODONTOLGY 2000