gingival disease...pptx

GINGIVAL DISEASES
AND
THEIR MANAGEMENT
BY- ANAMIKA SINGH
PG 1ST YEAR (2019)
DEPT. OF PERIODONTOLOGY
IPDC

INTRODUCTION
• The gingiva or commonly referred to as gums surround and protect the teeth.
• Gingival diseases refer to the diseases affecting the gingival tissues.
• Gingivitis is a non-specific inflammatory condition and is therefore a consequence
of sustained plaque biofilm accumulation at and apical to the gingival margin.
• Gingival disease if left untreated can progress to periodontal tissues and result in
periodontal disease which is easier to diagnose probably due to its chronic and
severe nature as compared to gingival disease.
HEALTHY GINGIVA INFLAMED GINGIVA

CLASSIFICATION OF GINGIVAL DISEASES

Chapple
ILC,
Mealey
BL,
et
al.
Periodontal
health
and
gingival
diseases
and
conditions
on
an
intact
and
a
reduced
periodontium:
Consensus
report
of
workgroup
1
of
the
2017
World
Workshop
on
the
Classification
of
Periodontal
and
Peri-Implant
Diseases
and
Conditions.
J
Periodontol.
2018;89(Suppl
1):S74–S84.
Conditions marked with an “a” have associated systemic involvement or are oral manifestations of systemic conditions; therefore,
other health-care providers may be involved in diagnosis and treatment.

COURSE AND DURATION
5
• Gingivitis can occur with sudden onset and short duration and can be painful. A
less severe phase of this condition can alsooccur.
• Recurrent gingivitis reappears after having been eliminated by treatment or
disappearing spontaneously.
• Chronic gingivitis is slow in onset and of long duration.
o Painless, unless complicated by acute/sub acute exacerbations, and is the
type most often encountered.
o Fluctuating disease in which inflammation persists or resolves and normal
areas become inflamed. (Hoover DR et al 1965, Larato DC et al 1969)

COMPONENTS OF GINGIVAL
INFLAMMATION
6
• Gingival inflammation has two components:
– the acute inflammatory component,
» withvasodilation,
» edema,and
» polymorphonuclear infiltration
– the chronic inflammatory component,
» with B and T lymphocytesand
» capillary proliferation forminga granulomatous response.
• Each gingival region can have varying amounts of the acute or chronic
component.

EXPERIMENTALGINGIVITIS
7
• Despite extensive research, we still cannot distinguish definitively between
normal gingival tissue and the initial stage of gingivitis.
• Most biopsies of clinically normal human gingiva contain inflammatory cells
consisting predominantly of T cells, withvery few B cells or plasma cells.
• In 1965, Loe et al demonstrated that in students with clinically healthy
gingivae.
Clinical symptoms of gingivitis developed within 2 to 3 weeks if
dental plaque was allowed to accumulate freely.
 Once adequate tooth cleaning was resumed, the gingival
inflammation subsided within a week

• The thickness of the gingival plaque gradually increased during the 3-week
experimental period.
• For the first few days:
– gram-positive cocci and
– rods, representing the indigenous micro flora of the tooth surface.
• After 4 to 5 days:
– filamentous organisms and
– gram-negative cocci as well as rods
• Gradually, non attaching spirochetes appeared in the gingival sulcus, while the
assortment of microorganisms in the gingival biofilm increased continuously.
EXPERIMENTAL GINGIVITIS
9

CHARACTERISTICS OF PLAQUE INDUCED
GINGIVITIS (MARIOTTI,1999)
1 Plaque present at gingival margin
2 Disease begins at the gingival margin
3 Change in gingival color
4 Change in gingival contour
5 Sulcular temperature change
6 Increased gingival exudate
7 Bleeding upon provocation
8 Absence of attachment loss*
9 Absence of bone loss*
10 Histological changes including an inflammatory lesion
11 Reversible with plaque removal

PREV
ALANCE
• The prevalence of gingivitis is evident worldwide.
• Higher prevalence of gingivitis is reported for children and
adolescents. (Albander JM, Brown LJ et al 1996)
• A significant percentage of adults also show signs of gingivitis; more than half the
U.S. adult population estimated to exhibit gingival bleeding, and other populations
show even higher levels of gingival inflammation. (Albander JM, Kingman A et al
1999)
• In children on average 6% of sites measured showed bleeding on probing.
(Albander JM, Tinoco EM 2002)

DISTRIBUTION
• Localized gingivitis is confined to the gingiva of a single tooth or group of teeth,
whereas generalized gingivitis involves the entire mouth.
• Marginal gingivitis involves the gingival margin and may include a portion of the
contiguous attached gingiva.
• Papillary gingivitis involves the interdental papillae and often extends into the
adjacent portion of the gingival margin. Papillae are involved more frequently
than the gingival margin, and the earliest signs of gingivitis often occur in the
papillae.
• Diffuse gingivitis affects the gingival margin, the attached gingiva, and
the interdental papillae. (Glickman 1953)

GINGIVAL DISEASE IN INDIVIDUAL CASES IS DESCRIBED
BY COMBINING THE PRECEDING TERMS AS FOLLOWS:
• Localized marginal gingivitis is confined to one or more areas of the marginal
gingiva.
• Localized diffuse gingivitis extends from the margin to the
mucobuccal fold in a limited area.
• Localized papillary gingivitis is confined to one or more interdental spaces in a
limited area.
• Generalized marginal gingivitis involves the gingival margins in relation to all
the teeth. The interdental papillae are usuallyaffected.
• Generalized diffuse gingivitis involves the entire gingiva. The alveolar
mucosa and attached gingiva are affected, so the mucogingival junction is
sometimes obliterated.
• Systemic conditions can be involved in the cause of generalized diffuse gingivitis
and should be evaluated if suspected as an etiologic cofactor.

STAGES OF GINGIVAL
INFLAMMATION

Stage I Gingivitis : The Initial Lesion - SUBCLINICALGINGIVITIS.
Lindhe , Hamp et al 1973- beagle dogs
• Dilation of capillaries & increase in blood flow.
• Initial inflammatory changes in response to microbial activation of
resident leukocytes, subsequent stimulation of endothelial cells.
• Clinically- initial response of gingiva to bacterial plaque (sub clinical
gingivitis)- not apparent.
• Changes in JE and perivascular connective tissue- detected.

•Perivascular connective tissue matrix-altered
•Exudation & deposition of fibrin in affected area
•Accumulation of lymphocytes
•Increase in migration of leukocytes and accumulation within
gingival sulcus correlated with increase in flow of gingival
fluid into sulcus.
STAGE I GINGIVITIS

•Character and intensity of host response determines whether initial
lesion resolves rapidly with restoration of tissue to normal state or into
chronic inflammatory lesion.
•Inflammatory lesion- infiltrate of macrophages and lymphoid cells
appears within few days.
STAGE I GINGIVITIS

Changes in blood vessel morphologic features (e.g., widening of
small capillaries or venules)
Some classic features of acute inflammation seen in connective
tissue beneath the junctional epithelium.
MICROSCOPICALLY

Adherence of neutrophils to vessel walls (margination) occur within 1 week
and sometimes as early as 2 days after plaque has been allowed to
accumulate.
Leukocytes, mainly polymorphonuclear neutrophils (PMNs), leave the
capillaries by migrating through the walls - increased quantities in the
connective tissue, junctional epithelium, and the gingival sulcus
Exudation of fluid from gingival sulcus and extravascular proteins present.

STAGE II GINGIVITIS : THE EARLY LESION
(PAYNE , PAGE ET AL 1975,1991)
•Early lesion evolves from the initial lesion within 1 week after beginning of
plaque accumulation.
•Clinically may appear as early gingivitis & overlaps with and evolves from the
initial lesion with no clear-cut dividingline.
•As time goes, clinical signs of erythema may appear, mainly because of
proliferation of capillaries and increased formation of capillary loops between rete
pegs.

•Bleeding on probing- evident. (Amato R, Caton J, Polson Aet al 1986)
•Gingival fluid flow and numbers of transmigrating leukocytes reach their
maximum between 6 and 12 days after onset of clinical gingivitis. (Lindhe J,
Hamp, Loe H et al 1973)

Amount of collagen destruction increases;
• 70% - collagen is destroyed around the cellular infiltrate.
• The main fiber groups affected appear to be the circular and dentogingival
fiber assemblies.
• Alterations in blood vessel morphologic features and vascular bed patterns.

• PMNs that have left the blood vessels in response to
chemotactic stimuli from plaque components travel to the
epithelium, cross basement lamina, and are found in the
epithelium, emerging in pocket area.
• PMNs are attracted to bacteria and engulf them in the process
of phagocytosis.
• PMNs release their lysosomes in association with ingestion
bacteria.
• Fibroblasts show cytotoxic alterations, with decreased capacity
for collagen production.

MICROSCOPIC:
• Microscopic examination of the gingiva reveals a leukocyte infiltration
in the connective tissue beneath the junctional epithelium, consisting
mainly of lymphocytes (75% with the majority T cells)
(Payne WA, Page RC, Ogilvie AL et al 1975 and Schroeder HE, Page
RC 1973)
• Also composed of some migrating neutrophils, as well as
macrophages, plasma cells, and mast cells.

• All the changes seen in the initial lesion continue to intensify with the
early lesion.
• The junctional epithelium- densely infiltrated with neutrophils, as does
the gingival sulcus, and the junctional epithelium may begin to show
development of rete pegs.

STAGE III GINGIVITIS : THE ESTABLISHED LESION
•Over time, the established lesion evolves.
•Characterized by a predominance of plasma cells B lymphocytes in
conjunction with the creation of a small gingival pocket lined with a pocket
epithelium (Schroeder HE et al 1975)
•The B cells - predominantly of immunoglobulin G1 (IgG1) and G3 (IgG3)
subclasses (Page RC 1986)

• In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of
plaque accumulation, blood vessels- engorged and congested,
venous return- impaired,
blood flow - sluggish.
• Bluish hue on the reddened gingiva (Hanioka T et al1991)
• Extravasation of erythrocytes into the connective tissue and
breakdown of hemoglobin into its component pigments can also
deepen the color of the chronically inflamed gingiva.
• The established lesion can be described as moderately to severely
inflamed gingiva.

• The predominance of plasma cells is thought to be a primary characteristic
of the established lesion.
• Increase in the proportions of plasma cells were evident with long-
standing gingivitis, but the time for the development of the classic
"established lesion" may exceed 6 months.
• Inverse relationship exist between the number of intact collagen
bundles and the number of inflammatory cells.
• Collagenolytic activity is increased in inflamed gingival tissue

TWO TYPES :
(Lovdal A et al 1958, Mori M et al 1961,Sumoi JD, Smith LW et al 1971)
• Some remain stable and do not progress for months or years
• Others become more active and convert to progressively destructive
lesions.

HISTOLOGIC SECTIONS
• Intense, chronic inflammatory reaction.
• A key feature that differentiates the established lesion is the increased
number of plasma cells, which become the preponderant inflammatory
cell type.
• Plasma cells invade the connective tissue not only immediately below the
junctional epithelium, but also deep into the connective tissue, around
blood vessels, andbetween bundles of collagen fibers

• The junctional epithelium reveals widened intercellular spaces filled with
granular cellular debris, including lysosomes derived from disrupted
neutrophils, lymphocytes, and monocytes.
• Lysosomes contain acid hydrolases - destroy tissue
components.
• The junctional epithelium develops rete pegs or ridges that protrude into
the connective tissue, and the basal lamina is destroyed in some areas.
• In the connective tissue, collagen fibers are destroyed around the infiltrate
of intact and disrupted plasma cells, neutrophils, lymphocytes, monocytes,
and mast cells
37

STAGE IV GINGIVITS : THE ADVANCED LESION
• Extension of the lesion into alveolar bone characterizes a fourth stage
known as the advanced lesion.
• Gingivitis-> periodontitis only in individuals who are susceptible.

MICROSCOPICALLY:
• Fibrosis of the gingiva and widespread manifestations of
inflammatory and immunopathologic tissue damage.
• Plasma cells continue to dominate the connective tissues, and neutrophils
continue to dominate the junctional epithelium and gingival crevice

CLINICAL FEATURES
• In evaluating the clinical features it is necessary to be systematic.
• The clinician should focus on subtle tissue alterations because these may be
of diagnostic significance.
• A systematic clinical approach requires an orderly examination of the gingiva
for
» color,
» contour,
» consistency,
» position,
» ease and severity of bleeding and
» pain.

• The two-earliest signs of gingival inflammation preceding
established gingivitis are
(1) Increased gingival crevicular fluid productionrate and
(2) Bleeding from the gingival sulcus ongentle probing
• Raised sulcus temperature has also been shown to be a feature of plaque
induced inflammation (Haffajee et al 1992, Loe et al 1965, Poison and
Goodson 1985)
• Increase in leucocytes seen in gingival fluid associated with increased
GCF (Payne et al 1975, Page and Schroeder 1976)

BLEEDING ON PROBING
• It is detected clinically and therefore is of value for the early diagnosis and
prevention of more advanced gingivitis.
• It has been shown that bleeding on probing appears earlier than a change in color
or other visual signs of inflammation;
– in addition, the use of bleeding rather than color changes to diagnose
early gingival inflammation is advantageous in that bleeding is a
more objective sign that requires less subjective estimation by the
examiner.
• Therefore, bleeding on probing is widely used by clinicians and epidemiologists
to measure
– disease prevalence and
– progression,
– to measure outcomes of treatment, and – to motivate patients with their home
care.
. 43

• Gingival bleeding on probing is an important diagnostic factor – as it is associated
with inflammation and ulceration of the epithelium lining the gingival sulcus.
• Presence of plaque for only 2 days  initiate gingival bleeding on probing,
whereas once established, it may take 7 days or more after continued plaque
control and treatment to eliminate gingival bleeding.
• Absence of plaque and presence of gingival bleeding may indicate improvement
in plaque control that may have occurred immediately before the examination.
• Presence of bleeding is an indication of active gingival inflammation, and until
it is controlled, the patient is at a risk of continuing periodontal disease and tissue
destruction.

• In general, gingival bleeding on probing indicates an inflammatory lesion both
in the epithelium and in the connective tissue that exhibits specific histologic
differences compared with healthy gingiva.
• Even though gingival bleeding on probing may not be a good diagnostic
indicator for clinical attachment loss, its absence is an excellent negative
predictor of future attachment loss.(Lang et al 1990)
• Therefore the absence of gingival bleeding on probing is desirable and implies
a low risk of future clinical attachment loss.

• Numerous studies show that current cigarette smoking suppresses the gingival
inflammatory response, and smoking was found to exert a strong, chronic,
dose dependent suppressive effect on gingival bleeding on probing in the
third National Health and Nutrition Examination Survey (NHANES III)
(Dietrich et al 2004)
• In addition, recent research reveals an increase in gingival bleeding on probing
in patients who quit smoking. (Nair P
,Palmer RM et al2003)

EXAMINATION FOR BOP
• Walking probe technique
• Done with short upward and downward movement
• A tooth is probed at 6sites- MB, mid B, DB, and corresponding lingual sites.
• Working force should not be more than 20gms.
• Pain during probing is indicative of too heavy probing force

CHRONIC AND RECURRENT BLEEDING:
• The most common cause of abnormal gingival bleeding on probing is chronic
inflammation. (Milne AM 1967)
• The bleeding is chronic and recurrent and is provoked by mechanical trauma
(eg. from tooth brushing, toothpicks, or food impaction) or by biting into solid
foods such as apples.
• The severity of the bleeding and the ease of its provocation depend on the
intensity of the inflammation.
• After the vessels are damaged and ruptured, interrelated mechanisms induce
hemostasis. (Stefanini M, Dameshek W 1962)

• The vessel walls contract, and blood flow is diminished; blood platelets adhere
to the edges of the tissue; and a fibrous clot is formed, which contracts and
results in approximation of the edges of the injured area.
• Bleeding recurs when the area is irritated. In cases of moderate or advanced
periodontitis, the presence of bleeding on probing is considered a sign of active
tissue destruction.
• In gingival inflammation, histopathology alterations that result in abnormal
gingival bleeding include dilation and engorgement of the capillaries and
thinning or ulceration of the sulcular epithelium.
55

Microscopic view of interdental space in a
human autopsy specimen. Inflammatory
infiltrate and thinned epithelium in area
adjacent to the tooth, as well as collagenous
tissue in outer half of the section.
• Sites that bleed on probing have a greater area of inflamed connective tissue (i.e.,
cell-rich, collagen-poor tissue)than sites that do not bleed.
• In most cases the cellular infiltrate of sites that bleed on probing is predominantly
lymphocytic (a characteristic of stage II, or early, gingivitis). (Amato, Catson,
Polson 1986)
56

ACUTE BLEEDING
• Acute episodes of gingival bleeding are caused by injury and can occur
spontaneously in gingival disease.
• Laceration of the gingiva by toothbrush bristles during aggressive tooth
brushing or by sharp pieces of hard food can cause gingival bleeding even in
the absence of gingival disease.
• Gingival burns from hot foods or chemicals increase the ease of gingival
bleeding.
• Spontaneous bleeding or bleeding on slight provocation can occur in acute
necrotizing ulcerative gingivitis.
• In this condition, engorged blood vessels in the inflamed connective tissue
are exposed by ulceration of the necrotic surface epithelium.
. 57

GINGIVAL BLEEDING ASSOCIATED WITH SYSTEMIC
CHANGES
• In some systemic disorders, gingival hemorrhage occurs spontaneously or after
irritation and is excessive and difficult to control.
• These hemorrhagic diseases represent a wide variety of conditions that
vary in etiologic factors and clinical manifestations.
• Such conditions have the common feature of a hemostatic mechanism failure and
result in abnormal bleeding in the skin, internal organs, and other tissues,
including the oral mucosa. (Sodeman WA 1985)

• The effects of hormonal replacement therapy, oral contraceptives,
pregnancy, and the menstrual cycle are also reported to affect gingival
bleeding. (Payne, Maze 1999)
• In addition, changes in androgenic hormones have long been established as
significant modifying factors in gingivitis, especially among adolescents.
• Several reports have shown notable effects of fluctuating
estrogen/progesterone levels on the periodontium, starting as early as puberty.
(Addy M et al 1994)
• Among pathologic endocrine changes, diabetes is an endocrine
condition with a well-characterized effect on gingivitis. (Tatakis DN et
al 1994)

• Several medications have also been found to have adverse effects on the
gingiva. For example, anticonvulsants, antihypertensive calcium channel
blockers, and the immunosuppressant drugs are known to cause gingival
enlargement, which secondarily can cause gingivalbleeding.
• The American Heart Association has recommended over the counter aspirin
as a therapeutic agent for cardiovascular disease, and aspirin is often
prescribed for rheumatoid arthritis, osteoarthritis, rheumatic fever, and other
inflammatory joint diseases. (Hennekens CH et al 1997)
• Thus it is important to consider aspirin's effect on bleeding during a
routine dental examination to avoid false-positive readings, which could
result in an inaccurate patient diagnosis

COLOUR CHANGES IN GINGIVA
• The color of the gingiva is determined by several factors, including
– the number and size of blood vessels,
– epithelial thickness,
– quantity of keratinization,
– arid pigments within the epithelium
(Tal H, Tal M 2003)

COLOR CHANGES IN CHRONIC GINGIVITIS
• Change in color is an important clinical signof gingival disease.
• The normal gingival color is "coral pink" and is produced by the tissue's
vascularity and modified by the overlying epithelial layers.
• For this reason, the gingiva becomes red when vascularization increases or
the degree of epithelial keratinization is reduced or disappears.
• The color becomes pale when vascularization is reduced (in association
with fibrosis of the corium) or epithelial keratinization increases.

• Chronic inflammation intensifies the red or bluish red color because of
vascular proliferation and reduction of keratinization.
• Venous stasis will contribute a bluish hue. The gingival color changes
with increasing chronicity of the inflammatory process.
• The changes start in the interdental papillae and gingival margin
and spread to the attached gingiva.
• Proper diagnosis and treatment require an understanding of the tissue
changes that alter the color of the gingiva at the clinical level.

METALLIC PIGMENTATION
• Heavy metals (i.e., bismuth, arsenic, mercury, lead, and silver) that are
absorbed systemically as a result of therapeutic use or occupational or
household exposures can discolor the gingiva and other areas of the oral
mucosa.
• Gingival pigmentation from systemically absorbed metals results from the
perivascular precipitation of metallic sulfides in the subepithelial
connective tissue.
• Gingival pigmentation is not a result of systemic toxicity. It occurs only in
areas of inflammation in which the increased permeability of irritated blood
vessels permits the seepage of metal into the surrounding tissue.
• In addition to inflamed gingiva, mucosal areas that are irritated by biting or
abnormal chewing habits (e.g., inner surface of lips, cheek at the level of
the occlusal line, lateral border of the tongue) are common sites of
pigmentation.
• Pigmentation can be eliminated by treating the inflammatory changes
without necessarily discontinuing the metal-containing medication.

COLOR CHANGES IN ACUTE GINGIVITIS
• Color changes in acute gingival inflammation differ in both nature and
distribution from those in chronic gingivitis.
• Color changes may be marginal, diffuse, or patch like, depending on the
underlying acute condition. In ANUG, the involvement is marginal; in herpetic
gingivostomatitis, it is diffuse; and in acute reactions to chemical irritation, it is
patch like or diffuse.
• Color changes vary with the intensity of the inflammation. Initially, there is an
increase in erythema.
• If the condition does not worsen, this is the only color change until the gingiva
reverts to normal.
• In severe acute inflammation, the red color gradually becomes a dull, whitish
gray.
• The gray discoloration produced by tissue necrosis is demarcated from the
adjacent gingiva by a thin, sharply defined erythematous zone.

CHANGES IN CONSISTENCY OF THE GINGIVA
• Both chronic and acute inflammations produce changes in the normal firm
and resilient consistency of the gingiva.
• As previously noted, in chronic gingivitis, both destructive (edematous) and
reparative (fibrotic) changes coexist, and the consistency of the gingiva is
determined by their relative predominance.
In chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes
coexist, and the consistency of the gingiva is determined by their relative predominance

CHANGES IN SURFACE TEXTURE OF THE GINGIVA
• The surface of normal gingiva usually exhibits numerous small depressions and
elevations, giving the tissue an orange peel appearance referred as stippling.
(Bergstrom J 1984)
• Stippling is restricted to the attached gingiva and is predominantly
localized to the sub-papillary area, but it extends to a variable degree into
the interdentalpapilla. (Orban B 1948)
• Although the biologic significance of gingival stippling is not known, some
investigators conclude that loss of stippling is an early sign of gingivitis.

• However, its pattern and extent vary in different mouth areas, among patients, and
with age.
• In chronic inflammation the gingival surface is either smooth and shiny or firm
and nodular, depending on whether the dominant changes are exudative or fibrotic.
• Smooth surface texture is also produced by epithelial atrophy in atrophic
gingivitis, and peeling of the surface occurs in chronic desquamative gingivitis.
• Hyperkeratosis results in a leathery texture, and drug-induced gingival overgrowth
produces a nodular surface.

Gingival biopsy demonstrating alternate elevations and
depressions in the attached gingiva responsible for
stippled appearance.

TRAUMATIC LESIONS
• One of the unique features of the most recent gingival disease classification is the
recognition of non-plaque induced traumatic gingival lesions as distinct gingival
conditions. (Armitage GC 1999)
• Traumatic lesions, whether chemical, physical, or thermal, are among the most
common lesions in the mouth.
• Sources of chemical injuries include aspirin, hydrogen peroxide, silver
nitrate, phenol, and endodonticmaterials.
• Physical injuries can include lip, oral, and tongue piercing, which can result
in gingival recession.
• Thermal injuries can result from hot drinks and foods..

• In acute cases, the appearance of slough (necrotizing epithelium), erosion,
or ulceration and the accompanying erythema are common features.
• In chronic cases, permanent gingival defects are usually present in the
form of gingival recession.
• Typically, the localized nature of the lesions and the lack of symptoms
readily eliminate them from the differential diagnosis of systemic
conditions that may be present with erosive or ulcerative oral lesions.
(Rawal SY et al 2004)

POSITION OF GINGIVA
• Gingival recession is a common finding. The prevalence, extent, and severity of
gingival recession increase with age and are more prevalent in males. (Albander
JM, Kingman A 1999)
• By clinical definition, recession is exposure of the root surface by an apical shift
in the position of the gingiva.
• Gingival recession is defined as the apical migration of the junctional epithelium
with exposure of root surfaces.(Kassab MM, Cohen RE 2003)
• Gingival recession is the apical shift of the marginal gingiva from its normal position
on the crown of the tooth to levels on the root surface beyond the cemento enamel
junction (Loe H 1992)
• To understand recession, it helps to distinguish between the actual and apparent
positions of the gingiva.

 In periodontal disease, the inflamed
pocket wall covers part of the denuded
root; thus some of the recession is
hidden, and some may be visible. The
total amount of recession is the sum of
the two.
Recession refers to the location of the
gingiva, not its condition.
 Receded gingiva can be inflamed but
may be normal except for its position.
Recession may be localized to one
tooth or a group of teeth, or it may be
generalized throughout the mouth.
The actual position is the level of the epithelial attachment on the tooth,
whereas the apparent position is the level of the crest of the gingival margin.
The severity of recession is determined by the actual position of the gingiva,
not its apparent position.

CHANGES IN GINGIVAL CONTOUR
66
• Changes in gingival contour are primarily associated with gingival
enlargement, but such changes may also occur in other conditions.
• Of historical interest are the descriptions of indentations of the gingival
margin referred to as Stillman's clefts and the McCall festoons.

STILLMAN'S CLEFTS
• Used to describe a specific type
of gingival recession consisting
of a narrow, triangular shaped
gingival recession.
• As the recession progresses
apically, the cleft becomes
broader, exposing the cementum
of the root surface.
• When the lesion reaches the
mucogingival junction, the apical
border of oral mucosa is usually
inflamed because of the difficulty
in maintaining adequate plaque
control at this site.
67

• Originally described by Stillman PR 1921 and considered to be the result of
occlusal trauma.
• These clefts were subsequently described by Box HK 1950 as pathologic
pockets in which the ulcerative process had extended to the facial surface of
the gingiva.
• The clefts may repair spontaneously or persist as surface lesions of deep
periodontal pockets that penetrate intothe supporting tissues.
• Their association with trauma from occlusion has not been substantiated.
68

MC CALL
’S FESTOONS (JOHN OPPIE MC CALL 1922)
• Used to describe a rolled, thickened
band of gingiva usually seen adjacent to
the cuspids when recession approaches
the muco-gingival junction.
• Initially, Stillman's clefts and McCall
festoons were attributed to traumatic
occlusion, and the recommended
treatment was occlusal adjustment.
• However, this association was never
proved, and these indentations merely
represent peculiar inflammatory changes
of the marginal gingiva.
69

DENTAL PLAQUE–INDUCED
GINGIVAL DISEASES
• Gingivitis that is associated with retained dental plaque is the most common
form of gingival disease. These diseases may occur on a periodontium with no
attachment loss or on a periodontium with attachment loss that is stable and not
progressing (i.e., reduced periodontium).
• As such, gingivitis is not associated with progressive attachment loss. This is not
to say that gingivitis is solely associated with teeth showing no attachment loss.
• Gingivitis can also be diagnosed in the gingiva of periodontitis-affected teeth
that have previously lost attachment but that have been successfully treated with
periodontal therapy to prevent any further attachment loss.
• In these treated cases, where gingival inflammation recurs around teeth with
existing attachment loss due to a history of treated periodontitis, the appropriate
diagnosis would be gingivitis on a reduced periodontium.

Gingivitis Associated With Dental Plaque
Only
• Plaque-induced gingival disease is the result of an interaction
between the microorganisms found in the dental plaque biofilm and
the inflammatory host response.
• A cause-and-effect relationship between microbial plaque and
gingivitis has been elegantly demonstrated by a classic experiment
demonstrating that the cessation of oral hygiene consistently leads
to the manifestation of gingivitis within 2 to 3 weeks in healthy
adults. [Loe H, Theilade E, Jensen SB: Experimental gingivitis in man, J Periodontol 36:177–187,
1965.]

• Clinical gingivitis is histologically characterized by a dense infiltrate
of lymphocytes and other mononuclear cells, fibroblast alterations,
increased vascular permeability, and continuing loss of collagen in
response to the microbial challenge. However, the alveolar bone is
not affected.
• Microbial plaque is thus considered to be the primary etiologic
factor for gingivitis.
• Gingivitis is fully reversible in otherwise healthy persons within
weeks following the removal of local factors and reduction of the
microbial load around the teeth.

Gingival Diseases Modified By Systemic
Factors
• Systemic factors that contribute to gingivitis—such as the
endocrine changes associated with puberty, the menstrual cycle,
pregnancy, and diabetes—may exacerbate the gingival
inflammatory response to plaque.
• This altered response appears to result from the effects of systemic
conditions on the host’s cellular and immunologic functions, but
the primary etiologic factor is still considered to be microbial
plaque.

In blood dyscrasias (e.g., leukemia), the reduced number of
immunocompetent lymphocytes in the periodontal tissues is associated
with increased edema, erythema, and bleeding of the gingiva as well as
gingival enlargement that may be associated with the swollen, spongy
gingival tissues caused by the excessive infiltration of malignant blood
cells.
 One example of altered host response due to systemic factors is apparent
during pregnancy when the incidence and severity of gingival
inflammation may increase even in the presence of low levels of plaque.
Plaque induced pregnancy gingivitis.
Additionally, the upper right central incisor
presents with a pregnancy epulis.
Leukemic Gingival Infiltration. Mani A, Lee D. N Engl J Med 2008;

Gingival Diseases Modified By
Medications
• Gingival diseases that are modified by medications include gingival
overgrowth due to anticonvulsant drugs such as phenytoin,
immunosuppressive drugs such as cyclosporine, and calcium channel blockers
such as nifedipine, verapamil, diltiazem and sodium valproate.
• The increased use of oral contraceptives by premenopausal women has also
been previously associated with a higher incidence of gingival inflammation
and gingival enlargement. Although this fact stood true for earlier
contraceptive formulations, existing contraceptives that include more modest
doses of active ingredients are not commonly associated with gingival
inflammation.
Drug induced gingival enlargement. Zahra Zohri et al. J. Chem. Pharm. Res., 2016,
8(1):439-446

Gingival Diseases Modified By
Malnutrition
• Gingival diseases modified by malnutrition have received
attention because of clinical descriptions of bright red,
swollen, and bleeding gingiva associated with severe ascorbic
acid (vitamin C) deficiency or scurvy. [Mariotti A: Dental plaque-induced
gingival diseases, Ann Periodontol 4:7, 1999.]
• Nonetheless, the available evidence to support a clinically
impactful role for mild nutritional deficiencies in the
development or severity of gingival inflammation in humans is
limited.

NON–PLAQUE-INDUCED
GINGIVAL LESIONS
• Oral manifestations of systemic conditions that produce
lesions in the tissues of the periodontium are less common
than plaque-induced gingivitis.
• This category mainly encompasses lesions of autoimmune or
idiopathic etiology that can manifest in the gingiva.

Gingival Diseases Of Specific Bacterial
Origin
• Gingival diseases of this category are attributed to
specific bacteria that cause characteristic lesions in
the gingiva.
• Neisseria gonorrhoeae and Treponema pallidum that
can be transferred as a result of sexually transmitted
diseases such as gonorrhea and syphilis, respectively,
cause characteristic lesions in the gingiva.
Neisseria Gonorrhea associated
lesions of the oropharynx
Primary chancre of
syphilis.
Streptococcal Species
associated lesions

Gingival Diseases Of Viral
Origin
• Gingival diseases of viral origin may be caused by a variety of
deoxyribonucleic acid and ribonucleic acid viruses, with the
most common being the herpesviruses.
• Viral gingival diseases are treated with topical or systemic
antiviral drugs.
Primary (acute) Herpetic
Gingivostomatitis

Gingival Diseases Of Fungal
Origin
• Gingival diseases of fungal origin are relatively
uncommon in immunocompetent individuals, but
they occur more frequently in immunocompromised
individuals and in those with disturbed microbiota
by the long-term use of broad-spectrum antibiotics.
• Candidiasis can also be seen under prosthetic
devices, in individuals using topical steroids, and in
individuals with decreased salivary low, increased
salivary glucose, or decreased salivary pH.
• In human immunodeficiency virus (HIV) seropositive
persons, candidal infection may present as
continuous erythematous stripe of the attached
gingiva; this has been referred to as linear gingival
erythema or HIV-associated gingivitis.
Linear Gingival erythema in an HIV infected
Oral thrush along the line of
denture

Gingival Diseases Of Genetic
Origin
• One of the most clinically evident conditions is hereditary
gingival fibromatosis, which exhibits autosomal-dominant or
(rarely) autosomal-recessive modes of inheritance.
• The gingival enlargement may completely cover the teeth, delay
eruption, and present as an isolated finding; alternatively, it may
be associated with several more generalized syndromes.
Hereditary Gingival Fibromatosis
in a 37 year-old white mother.
Gummy smile: could it be genetic? Hereditary gingival fibromatosis. Livada R,
Shiloah J. The Journal of the Tennessee Dental Association 92(1):23-6.

Gingival Manifestations Of Systemic
Conditions
• Gingival manifestations of systemic conditions may appear
as desquamative lesions, ulcerations of the gingiva, or
both.
• Allergic reactions that manifest with gingival changes are
uncommon but have been observed in association with
several restorative materials, toothpastes, mouthwashes,
chewing gums, and foods.

Foreign-body
Reactions
• Foreign-body reactions lead to localized inflammatory conditions
of the gingiva and are caused by the introduction of foreign
material into the gingival connective tissues through breaks in the
epithelium.
• Common examples are the introduction of amalgam into the
gingiva during the placement of a restoration, the extraction of a
tooth, or an endodontic apicoectomy with retrofill leaving an
amalgam tattoo, with resultant metal fragments observed during
biopsies; abrasives may also be introduced during polishing
procedures.

TREATMENT OF GINGIVAL DISEASE
• The treatment of gingival disease is based on resolving the
etiologic factors and maintaining the systemic status of the
individual.
• In the case of plaque-induced gingivitis, the main treatment plan
involves removal of plaque and calculus by scaling and root
planning, followed by oral hygiene instruction which includes
modified bass method of brushing and the use of chemical plaque
control agents like 0.2% or 0.02% chlorhexidine gluconate or
essential oil mouthwash.
• In cases of gingival enlargement, initial therapy is focused on
removing plaque and calculus, followed by a review on the gingival
condition; only if the condition does not improve the drug

• Plaque-induced gingival disease influenced by modifying factors is
controlled by reducing the exposure of the modifying factor in
addition to removal of plaque and calculus to maintain oral hygiene.
• Non-plaque-induced gingival diseases are treated depending on the
etiology of the gingival disease. For example, viral lesions are treated
by providing antiviral medications in addition to oral hygiene
instruction.
• Diagnosis is essential for providing the proper treatment plan and
updating recent research which might help prevent undue treatment.

DIAGNOSIS AND TREATMENT OF PLAQUE
INDUCED GINGIVAL DISEASES

DIAGNOSIS AND TREATMENT OF NON-PLAQUE
INDUCED GINGIVAL DISEASES
C, color; Cr, contour; Cs, consistency; T, texture; S, size; P, position; L, lesion; lab and H/P, laboratory procedures and
histopathology; add sym, additional symptoms; D, diagnosis; Rx, treatment; FR, fiery red; G, same as surrounding gingiva; W,
white; PR, pink to reddish; B-Br, black to brown; R-Gy, red to gray; RP, reddish pink; BR, bright red; Pi, pink; Pl, pale pink; Pr,
purple; Bl, blue; OHI, oral hygiene instruction; CHX, chlorhexidine; +, slightly increased; ++, increased; −, slightly decreased; −−,
decreased; −/+, may increase or decrease; =, remains the same

• Clinical Periodontology- Carranza’s 10th edition
• Clinical Periodontology and implant dentistry- Jan Lindhe 5th edition.
• Oral history- Antonio Nanci Ten Cate’s
• Essential Pathology – Harsh Mohan 3rd edition
• The gingival tissues: the architecture of periodontal protection.
Periodontology 2000, vol. 13, 1997, 91-120.
• Page RC, Gingivitis. J Clin Periodontol 1986;13: 345-355.
• Richard R. Ranney, Discussion: Pathogenesis of gingivitis. J Clin
Periodontol 1986;13: 356-359.
• William, Roy et al, Histopathologic features of the initial and early stages
of experimental gingivitis in man. J. Periodontal Res1975;10:51-64.
• Monitoring disease during supportive periodontal treatment by
bleeding on probing. Periodontology 2000, vol. 12, 1996, 4448.
REFERENCES

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