Clinical features and stages of gingivitis

DR.NEHA PRITAM
1ST YEAR MDS PGT
DEPARTMENT OF
PERIODONTICS
HIDSAR
CLINICAL FEATURES AND
STAGES OF GINGIVITIS

CLINICAL FEATURES OF GINGIVA
• COLOR
• PHYSIOLOGIC PIGMENTATION(MELANIN)
• SIZE CONTOUR
• SHAPE
• CONSISTENCY
• SURFACE TEXTURE
• POSITION
STAGES OF GINGIVITIS
• STAGE I
• STAGE II
• STAGE III
• STAGE IV
CLINICAL FEATURES OF GINGIVITIS
CONTENTS

The gingiva is the part of the oral
mucosa that covers the alveolar
processes of the jaws and surrounds
the necks of the teeth.
 In an adult, normal gingiva covers
the alveolar bone and tooth root
to a level just coronal to the
cementoenamel junction.
GINGIVA

The gingiva is divided anatomically into marginal,
attached, and interdental areas.

MARGINAL GINGIVA
 The marginal, or unattached gingiva is the terminal
edge or border of the gingiva surrounding the teeth in
collarlike fashion.
 In about 50% of cases, it is demarcated from the
adjacent attached gingiva by a shallow linear
depression, the free gingival groove.
 Usually about 1 mm wide, the marginal gingiva forms
the soft tissue wall of the gingival sulcus. It may be
separated from the tooth surface with a periodontal
probe.

In clinically healthy human gingiva, a sulcus
of some depth can be found.
The depth of this sulcus, as determined in
histologic sections, has been reported as 1.8
mm, with variations from 0 to 6 mm

ATTACHED GINGIVA
 The attached gingiva is continuous with the marginal gingiva. It is
firm, resilient, and tightly bound to the underlying periosteum of
alveolar bone.The facial aspect of the attached gingiva extends to the
relatively loose and movable alveolar mucosa and is demarcated by
the mucogingival junction.

000
 The width of the attached
gingiva on the facial aspect
differs in different areas of
the mouth. It is generally
greatest in the incisor region
(3.5 to 4.5 mm in maxilla, 3.3
to 3.9 mm in mandible), and
narrower in the posterior
segments (1.9 mm in
maxillary and 1.8 mm in
mandibular first premolars).

INTERDENTAL GINGIVA
The interdental gingiva occupies the
gingival embrasure, which is the
interproximal space beneath the area of
tooth contact.
The interdental gingiva can be pyramidal or
can have a “col” shape. In the former the tip
of one papilla is located immediately
beneath the contact point; the latter
presents a valleylike depression that
connects a facial and lingual papilla and
conforms to the shape of the interproximal
contact.

In the premolar/molar regions of the dentition, the teeth have
approximal contact surfaces rather than contact points. Since the
interdental papilla has a shape in conformity with the outline of the
interdental contact surfaces, a concavity —a col — is established in
the premolar and molar regions.Thus, the interdental papillae in
these areas often have one vestibular (VP) and one lingual/ palatal
portion (LP) separated by the col region.

 COLOR
 PHYSIOLOGIC PIGMENTATION(MELANIN)
 SIZE
 CONTOUR
 SHAPE
 CONSISTENCY
 SURFACE TEXTURE
 POSITION
CLINICAL FEATURES OF GINGIVA

 The color of the attached and marginal gingiva is
generally described as “coral pink” .
 The alveolar mucosa is red, smooth, and shiny
rather than pink and stippled.
COLOR
It is produced by the vascular supply, the thickness
and degree of keratinization of the epithelium, and
the presence of pigment-containing cells.

 Hemoglobin-derived brown pigment.
 Responsible for the normal pigmentation of the skin, gingiva, and
remainder of the oral mucous membrane.
 Melanin pigmentation in the oral cavity is prominent in black
individuals.
 Ascorbic acid directly downregulates melanin pigmentation in gingival
tissues.
PHYSIOLOGIC PIGMENTATION MELANIN

 The size of the gingiva corresponds with the sum total of the bulk of
cellular and intercellular elements and their vascular supply.
 Alteration in size is a common feature of gingival disease.
CONTOUR
 The contour or shape of the gingiva varies considerably and depends on
the shape of the teeth and their alignment in the arch, the location and
size of the area of proximal contact, and the dimensions of the facial
and lingual gingival embrasures.
SIZE

 The marginal gingiva envelops the teeth in collarlike fashion and
follows a scalloped outline on the facial and lingual surfaces.
 On teeth in lingual version, the gingiva is horizontal and thickened .

 The shape of the interdental gingiva is governed by the contour of the
proximal tooth surfaces and the location and shape of gingival
embrasures.
 When the proximal surfaces of the crowns are relatively flat
faciolingually, the roots are close together, the interdental bone is
thin mesiodistally, and the gingival embrasures and interdental
gingiva are narrow mesiodistally.
SHAPE

Conversely, with proximal surfaces that flare away from the
area of contact, the mesiodistal diameter of the interdental
gingiva is broad .
 The height of the interdental gingiva varies with the
location of the proximal contact.Thus, in the anterior region
of the dentition, the interdental papilla is pyramidal in form,
whereas the papilla is more flattened in a buccolingual
direction in the molar region.

The gingiva is firm and resilient and with the exception of
the movable free margin, tightly bound to the underlying
bone.
The collagenous nature of the lamina propria and its
contiguity with the mucoperiosteum of the alveolar bone
determine the firmness of the attached gingiva.
The gingival fibers contribute to the firmness of the gingival
margin.
CONSISTENCY

SURFACE TEXTURE
 The gingiva presents a textured
surface similar to an orange peel
and is referred to as being stippled .
Stippling is best viewed by drying
the gingiva.
 The attached gingiva is stippled; the
marginal gingiva is not.
 The central portion of the
interdental papillae is usually
stippled, but the marginal borders
are smooth.The pattern and extent
of stippling vary among individuals
and different areas of the same
mouth.

 Stippling is less prominent on lingual than facial surfaces and may be
absent in some persons.
 Stippling varies with age. It is absent in infancy, appears in some children
at about 5 years of age, increases until adulthood, and frequently begins
to disappear in old age.
Microscopically, stippling is produced by alternate rounded
protuberances and depressions in the gingival surface. The
papillary layer of the connective tissue projects into the elevations,
and the elevated and depressed areas are covered by stratified
squamous epithelium . The degree of keratinization and the
prominence of stippling appear to be related
STIPPLING

Stippling is a form of adaptive specialization or reinforcement for function.
It is a feature of healthy gingiva, and reduction or loss of stippling is a
common sign of gingival disease. When the gingiva is restored to health
after treatment, the stippled appearance returns.
The surface texture of the gingiva is also related to the presence and degree
of epithelial keratinization. Keratinization is considered a protective
adaptation to function. It increases when the gingiva is stimulated by
toothbrushing. However, research on free gingival grafts has shown that
when connective tissue is transplanted from a keratinized area to a
nonkeratinized area, it becomes covered by a keratinized epithelium.

Gingival biopsy of patient
demonstrating alternate elevations and
depressions(arrows) in the attached
gingiva responsible for stippled
appearance.

 When the tooth erupts into the oral cavity, the margin and sulcus are
at the tip of the crown; as eruption progresses, they are seen closer to
the root.
 During this eruption process, as described earlier, the junctional
epithelium, oral epithelium, and reduced enamel epithelium undergo
extensive alterations and remodeling while maintaining the shallow
physiologic depth of the sulcus.
 Without this remodeling of the epithe-lia, an abnormal anatomic
relationship between the gingiva and the tooth would result.
POSITION

 Pathologic changes in gingivitis are
associated with the presence of oral
microorganisms attached to the
tooth and perhaps in or near the
gingival sulcus.
 The sequence of events cumulating
in clinically apparent gingivitis is
categorized into initial, early, and
established stages, with
periodontitis designated as the
advanced stage.
GINGIVAL INFLAMMATION

 The first manifestations of gingival inflammation are vascular changes
consisting of dilated capillaries and increased blood flow.
 These initial inflammatory changes occur in response to microbial
activation of resident leukocytes and the subsequent stimulation of
endothelial cells. Clinically, this initial response of the gingiva to
bacterial plaque (subclinical gingivitis) is not apparent.
 Subtle changes can also be detected in the junctional epithelium and
perivascular connective tissue at this early stage. For example, the
perivascular connective tissue matrix becomes altered, and there is
exudation and deposition of fibrin in the affected area.Also,
lymphocytes soon begin to accumulate.
STAGE I GINGIVITIS: THE INITIAL LESION

The character and intensity of the host response
determine whether this initial lesion resolves rapidly,
with the restoration of the tissue to a normal state, or
evolves into a chronic inflammatory lesion. If the latter
occurs, an infiltrate of macrophages and lymphoid cells
appears within a few days.

 Classic features of acute inflammation can be seen in the
connective tissue beneath the junctional epithelium.
 Changes in blood vessel morphologic features (e.g., widening of
small capillaries or venules) and 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 (diapedesis,
emigration).
 They can be seen in increased quantities in the connective tissue,
the junctional epithelium, and the gingival sulcus. Exudation of
fluid from the gingival sulcus and extravascular proteins are
present.
MICROSCOPICALLY

Human biopsy sample ,experimental gingivitis. After
4days of plaque accumulation,the blood vessels
immediately adjacent to the junctional epithelium are
distended and contains polymorphonuclear
leukocytes(PMNs,neutrophils). Neutrophils have also
migrated between the cells of the junctional
epithelium(JE).OSE,Oral sulcular epithelium.

 The early lesion evolves from the initial lesion within about 1 week
after the beginning of plaque accumulation.
Clinical signs of erythema may appear, mainly because of the
proliferation of capillaries and increased formation of capillary loops
between rete pegs or ridges.
 Bleeding on probing may also be evident.
 Gingival fluid flow and the numbers of transmigrating leukocytes
reach their maximum between 6 and 12 days after the onset of clinical
gingivitis.
STAGE II GINGIVITIS: THE EARLY LESION

 The amount of collagen destruction increases; 70% of the collagen is
destroyed around the cellular infiltrate.
 Main fiber groups affected- circular and dentogingival fiber assemblies.
Alterations in blood vessel morphologic features and vascular bed
patterns have also been described.

 PMNs that have left the blood vessels in response to chemotactic stimuli from
plaque components travel to the epithelium, cross the basement lamina, and
are found in the epithelium, emerging in the pocket area .PMNs are attracted
to bacteria and engulf them in the process of phagocytosis .
 PMNs release their lysosomes in association with the ingestion of bacteria.
Fibroblasts show cytotoxic alterations, with a decreased capacity for collagen.
 Meanwhile, on the opposite side of molecular events, collagen degradation is
related to matrix metalloproteins (MMPs). Different MMPs are responsible for
extracellular matrix remodeling within 7 days of inflammation, which is
directly related to MMP-2 and MMP-9 production and activation.

 Examination of the gingiva reveals a leukocyte infiltration in the
connective tissue beneath the junctional epithelium, consisting mainly
of lymphocytes (75%, with the majorityT cells) but 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 becomes densely infiltrated with
neutrophils, as does the gingival sulcus, and the junctional epithelium
may begin to show development of rete pegs or ridges.
MICROSCOPICALLY

Human biopsy, experimental gingivitis.
A, Control biopsy specimen from a
patient with good oral hygiene and no
detectable plaque accumulation. The
junctional epithelium is at the left. The
connective tissue (CT) shows few cells
other than fibroblasts, blood vessels,
and a dense background of collagen
fibers. (×500.) B, Biopsy specimen
taken after 8 days of plaque
accumulation. The connective tissue is
infiltrated with inflammatory cells,
which displace the collagen fibers. A
distended blood vessel (V) is seen in
the center. (×500.) C, After 8 days of
plaque accumulation, the connective
tissue next to the junctional epithelium
at the base of the sulcus shows a
mononuclear cell infiltrate and
evidence of collagen degeneration
(clear spaces around cellular infiltrate).
(×500.). D, The inflammatory cell
infiltrate at higher magnification. After
8 days of plaque accumulation,
numerous small (SL) and medium-sized
(ML) lymphocytes are seen within the
connective tissue. Most of the collagen
fibers around these cells have
disappeared, presumably as a result of
enzymatic digestion.

 Over time, the established lesion evolves, characterized by a
predominance of plasma cells and B lymphocytes and probably in
conjunction with the creation of a small gingival pocket lined with a
pocket epithelium.The B cells found in the established lesion are
predominantly of the immunoglobulin G1 (IgG1) and G3
(IgG3)subclasses.
STAGE III GINGIVITIS: THE ESTABLISHED LESION

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.

 In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of
plaque accumulation, the blood vessels become engorged and
congested, venous return is impaired, and the blood flow becomes
sluggish .
 The result is localized gingival anoxemia, which superimposes a
somewhat bluish hue on the reddened gingiva.
Marginal supragingival
plaque and gingivitis

 An intense, chronic inflammatory reaction is observed.
Several detailed cytologic studies have been performed on
chronically inflamed gingiva. 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, and
between bundles of collagen fibers.

MICROSCOPICALLY

 The junctional epithelium reveals widened
intercellular spaces filled with granular cellular
debris, including lysosomes derived from disrupted
neutrophils, lymphocytes, and monocytes .The
lysosomes contain acid hydrolases that can 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 .

 Extension of the lesion into alveolar bone characterizes a
fourth stage known as the advanced lesion or phase of
periodontal breakdown.
 Patients with experimental gingivitis showed significantly
more plaque accumulation, higher IL-1β, and lower IL-8
concentrations at 28 days.
 Gingivitis will progress to periodontitis only in individuals
who are susceptible.
STAGE IV GINGIVITIS: THE ADVANCED LESION

There is fibrosis of the gingiva and widespread
manifestations of inflammatory and immunopathologic
tissue damage. At the advanced stage, plasma cell
presence dominates connective tissue and neutrophils
continue dominating the junctional epithelium.
MICROSCOPICALLY

CLINICAL FEATURES OF
GINGIVITIS

 In general, clinical features of gingivitis may be characterized by the
presence of any of the following clinical signs: redness and sponginess
of the gingival tissue, bleeding on provocation, changes in contour, and
presence of calculus or plaque with no radiographic evidence of crestal
bone loss.
 Histologic examination of inflamed gingival tissue reveals ulcerated
epithelium.The presence of inflammatory mediators negatively affects
epithelial function as a protective barrier. Repair of this ulcerated
epithelium depends on the proliferative or regenerative activity of the
epithelial cells. Removal of the etiologic agents triggering the gingival
breakdown is essential.
CHANGES IN GINGIVAL CONTOUR

 Gingivitis can occur with sudden onset and short duration and can be
painful. A less severe phase of this condition can also occur.
 Recurrent gingivitis reappears after having been eliminated by
treatment or disappeared spontaneously.
 Chronic gingivitis is slow in onset and of long duration. It is painless,
unless complicated by acute or subacute exacerbations, and is the type
most often encountered .
 Chronic gingivitis is a fluctuating disease in which inflammation
persists or resolves and normal areas become inflamed.
COURSE AND DURATION

 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.
DESCRIPTION

 Papillary gingivitis involves the interdental papillae and
often extends into the adjacent portion of the gingival
margin.
 Diffuse gingivitis affects the gingival margin, the
attached gingiva, and the interdental papillae.
 Papillae are involved more frequently than the gingival
margin, and the earliest signs of gingivitis often occur in
the papillae.

 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 usually affected .

 • 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.

GINGIVAL BLEEDING ON PROBING
The two earliest signs of gingival inflammation preceding established
gingivitis are
(1) increased gingival crevicular fluid production rate and
(2) bleeding from the gingival sulcus on gentle probing .
CLINICAL FINDINGS
Bleeding on probing. A, Mild edematous gingivitis; a probe has been
introduced to the bottom of the gingival sulcus. B, Bleeding appears
after a few seconds.

 Gingival bleeding varies in severity, duration, and ease of provocation.
Bleeding on probing is easily 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 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. Therefore the absence of
gingival bleeding on probing is desirable and implies a low risk of future
clinical attachment loss.

Gingival Bleeding Caused By Local Factors
 Contributing factors to plaque retention that may lead to
gingivitis include anatomic and developmental tooth
variations, caries, frenum pull, iatrogenic factors,
malpositioned teeth, mouth breathing, overhangs, partial
dentures, lack of attached gingiva, and recession.
 In addition, orthodontic treatment and fixed retainers were
associated with increased plaque retention and increased
bleeding on probing.

CHRONIC AND RECURRENT BLEEDING
 The most common cause of abnormal gingival bleeding on probing is
chronic inflammation.
 The bleeding is chronic or recurrent and is provoked by mechanical
trauma (e.g., from toothbrushing, toothpicks, or food impaction) or
by biting into solid foods such as apples.
 The severity of bleeding and the ease of its provocation depend on
the intensity of the inflammation

 Hemorrhagic disorders in which abnormal gingival bleeding is
encountered include vascular abnormalities (vitamin C deficiency or
allergy [e.g., Schönlein-Henoch purpura]), platelet
disorders(thrombocytopenic purpura), hypoprothrombinemia (vitamin K
deficiency), other coagulation defects (hemophilia, leukemia, Christmas
disease), deficient platelet thromboplastic factor (PF3) resulting from
uremia, multiple myeloma and postrubella purpura.
GINGIVAL BLEEDING ASSOCIATED WITH
SYSTEMIC CHANGES

 The effects of hormonal replacement therapy, oral contraceptives,
pregnancy, and the menstrual cycle are also reported to affect
gingival bleeding.
 In addition, in women, long-term depression-related stress exposure
may increase concentrations of interleukin-6 (IL-6) in gingival
crevicular fluid and may worsen periodontal conditions with
elevated gingival inflammation and increased pocket depths.

Fluctuating estrogen/progesterone levels on the periodontium, starting as
early as puberty among adolescents.
Among pathologic endocrine changes, diabetes is an endocrine condition
with a well-characterized effect on gingivitis.
Several medications have also been found to have adverse effects on the
gingiva. For example, anticonvulsants, antihypertensive ,calcium channel
blockers, and immunosuppressant drugs are known to cause gingival
enlargement, which secondarily can cause gingival bleeding.

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.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.

 Change in color is an important clinical sign of 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.
COLOR CHANGES IN GINGIVITIS

 Thus chronic inflammation intensifies the red or bluish
red color because of vascular proliferation and reduction
of keratinization. Additionally, 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

 Color changes in acute gingival inflammation differ in both
nature and distribution from those in chronic gingivitis.The
color changes may be marginal, diffuse, or patchlike,
depending on the underlying acute condition.
 In acute necrotizing ulcerativegingivitis, the involvement
is marginal; in herpetic gingivostomatitis, it is diffuse; and
in acute reactions to chemical irritation, it is patchlike or
diffuse.

 Heavy metals (bismuth, arsenic, mercury, lead, and silver) absorbed
systemically from therapeutic use or occupational or household environments
may discolor the gingiva and other areas of the oral mucosa. These changes
are rare but still should be ruled out in suspected cases.
 Typically, metals produce a black or bluish line in the gingiva that follows the
contour of the margin .
 The pigmentation may also appear as isolated black blotches involving the
interdental, marginal and attached gingiva. This differs from the tattooing
produced by the accidental embedding of amalgam or other metal
fragments.
METALLIC PIGMENTATION

 Gingival pigmentation from systemically absorbed metals results from
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 seepage of the metal into the
surrounding tissue.
 Pigmentation can be eliminated by treating the inflammatory changes
without necessarily discontinuing the metal containing medication.

Endogenous oral pigmentations can be caused by
 melanin
 bilirubin
 iron.
COLOR CHANGES ASSOCIATEDWITH
SYSTEMIC FACTORS

Melanin oral pigmentations can be normal physiologic
pigmentations and are often found in highly pigmented ethnic
groups . Diseases that increase melanin pigmentation include
the following:
• Addison’s disease is caused by adrenal dysfunction and produces isolated
patches of discoloration varying from bluish black to brown.
• Peutz-Jeghers syndrome produces intestinal polyposis and melanin
pigmentation in the oral mucosa and lips.
• Albright’s syndrome (polyostotic fibrous dysplasia) and von
Recklinghausen’s disease (neurofibromatosis) produce areas of melanin
pigmentation

 Skin and mucous membranes can be stained by bile
pigments.
 Jaundice is best detected by examination of the sclera, but
the oral mucosa may also acquire a yellowish color.
 The deposition of iron in hemochromatosis may produce a
blue-gray pigmentation of the oral mucosa. Several
endocrine and metabolic disturbances, including diabetes
and pregnancy, may result in color changes.
 Blood dyscrasias, such as anemia, polycythemia, and
leukemia, may also induce color changes.

Exogenous factors capable of producing color changes in the gingiva
include atmospheric irritants, such as coal and metal dust, and coloring
agents in food or lozenges.Tobacco causes hyperkeratosis of the gingiva
and also may induce a significant increase in melanin pigmentation of the
oral mucosa. Localized bluish black areas of pigment are often caused by
amalgam implanted in the mucosa

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.
CHANGES IN CONSISTENCY OFTHE
GINGIVA

Calcified microscopic masses may be found in the gingiva.
They can occur alone or in groups and vary in size, location,
shape, and structure. Such masses may be calcified material
removed from the tooth and traumatically displaced into the
gingiva during scaling,root remnants, cementum fragments,
or cementicles.
CALCIFIED MASSES INTHE GINGIVA
FACTORS AFFECTING THE CONSISENCY OF
GINGIVA

TOOTHBRUSHING
Toothbrushing has various effects on the
consistency of the gingiva such as promoting
keratinization of the oral epithelium, enhancing
capillary gingival circulation, and thickening
alveolar bone.
Toothbrushing causes an increased turnover rate
and desquamation of the junctional epithelial
surfaces.This process may repair small breaks in
the junctional epithelium and prevent direct
access to the underlying tissue by periodontal
pathogens

The surface of normal gingiva usually exhibits numerous
small depressions and elevations, giving the tissue an
orange-peel appearance referred as stippling.
Stippling is restricted to the attached gingiva and is
predominantly localized to the subpapillary area, but it
extends to a variable degree into the interdental papilla.
Although the biologic significance of gingival stippling is not
known, some investigators conclude that loss of stippling is
an early sign of gingivitis.
CHANGES IN SURFACETEXTURE OFTHE
GINGIVA

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.

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.Traumatic lesions, whether chemical,
physical, or thermal, are among the most common lesions in
the mouth.
CHANGES IN POSITION OFTHE
GINGIVA

 Sources of chemical injuries include aspirin, hydrogen peroxide, silver
nitrate, phenol, and endodontic materials.
 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.

 Gingival Recession- Gingival recession is a common finding.The
prevalence, extent, and severity of gingival recession increase with age
and are more prevalent in males.
 Positions of the Gingiva- By clinical definition, recession is exposure of
the root surface by an apical shift in the position of the gingiva.

 The actual position is the level of
the coronal end 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.
 For example, 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.

 The following etiologic factors have been implicated in gingival
recession: faulty tooth brushing technique (gingival abrasion), tooth
malposition, friction from soft tissues (gingival ablation), gingival
inflammation, abnormal frenum attachment, and iatrogenic dentistry.
 Susceptibility to recession is also influenced by the position of teeth in
the arch, the root-bone angle, and the mesiodistal curvature of the
tooth surface.
 Trauma from occlusion has been suggested in the past, but its
mechanism of action has never been demonstrated. For example, a
deep overbite has been associated with gingival inflammation and
recession. Excessive incisal overlap may result in a traumatic injury to
the gingiva.

 CLINICAL SIGNIFICANCE -several aspects of gingival
recession make it clinically significant. Exposed root
surfaces are susceptible to caries.
 Abration or erosion of cementum exposed by recession
leaves an underline dentinal surface which can be
sensitive.
 Hyperemia of the pulp and associated sympotms may also
result from eccessive exposure of root surface.
 Interproximal recession creates oral hygiene problems and
resulting plaque accumulation.

Changes in gingival contour are primarily associated with gingival
enlargement.
Of historical interest are the descriptions of indentations of the gingival
margin referred to as Stillman’s clefts and the McCall festoons.
The term “Stillman’s clefts” has been 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.
CHANGES IN GINGIVAL CONTOUR

The term “McCall festoons” has been used to describe a rolled, thickened
band of gingiva usually seen adjacent to the cuspids when recession
approaches the mucogingival junction. Initially, Stillman’s clefts and
McCall festoons were attributed to traumatic occlusion, and the
recommended treatment was occlusal adjustment.
McCall’s Festoons (right).The attached gingiva consists of nothing more than a
collar-like, fibrous thickening (arrow).This may be a tissue response to further
recession beyond the mucogingival line.StillmanCleft (left)Cleft-like defect of
traumatic etiology. Such clefts may spread laterally, creating an area of gingival
recession.The exposed root surface may be extremely sensitive.Such clefts are
often covered with plaque.

TREATMENT OF PLAQUE INDUCED
GINGIVITIS
I. The treatment of plaque induced gingivitis is primarily self-administered
plaque control. Although mechanical plaque control remains the mainstay for
plaque control, chemical control of plaque is an effective option for those
individuals who, because of physical or mental disability, cannot effectively
apply mechanical means.
II. However, the presence of plaque retaining factors, such as dental calculus or
inadequate restorations, may result in either method being ineffective.
Professional intervention is needed to eliminate these as an adjunct to self-
administered plaque control.

 Wegener's granulomatosis (WG) is an immunologically mediated
inflammatory disease characterized by granulomatous vasculitis of the
upper and lower aerodigestive tracts together with glomerulonephritis.
 Correlation of histopathology with routine hematoxylin and eosin and
special stains [Grocott-Gomori methenamine-silver nitrate and Periodic
Acid Schiff (PAS)], Mantoux test, peripheral blood smear and clinical
presentation were established in diagnosing this rare entity.
 By the above-mentioned procedures and methodology, it was arrived at
the diagnosis of Wegner's granulomatosis limited to the upper
aerodigestive tract.
Strawberry gingivitis: A diagnostic feature of gingivalWegener's
granulomatosis.
R.Heera et al. (2012)
Dental Research Journal 2012 Dec; 9(Suppl 1): S123–S126.

This is the first reported case of WG manifesting as “strawberry gingivitis” in
the Indian population.
A rare case of gingivalWG that presented with erythematous and painful
generalized gingival enlargement.
Therefore, the aim of reporting this case was to emphasize that, the dental surgeon often being
the first person to examine the oral cavity, should be familiar with the typical appearance of
gingival WG as “strawberry gingivitis,” its clinical course as well as diagnostic parameters and
adequate management.

 The decrease in plasminogen level reduces natural fibrinolysis, which causes
fibrin deposits on the membranes.
 This change leads to the formation of pseudomembranous lesions on mucous
membranes which impairs normal tissue and its functions.
 Ligneous conjunctivitis is the most common clinical manifestation of
congenital plasminogen deficiency (CPD). If left untreated, progressive vision
loss and even blindness can occur.
 Ligneous lesions can also be seen in other mucous membranes such as ears,
nose, mouth (as gingivitis), cerebral vascular spaces, tonsils, respiratory,
gastrointestinal and genitourinary tracts.
 Plasminogen deficiency is a rare congenital condition that leads to
pseudomembraneous lesions, such as ligneous conjunctivitis and
ligneous gingivitis. Because of its rarity, ligneous gingivitis is not a pathology
one may easily suspect from its clinical symptoms.
Ligneous gingivitis: Hard to diagnose and treat
Tiraje Celkan (2019)
Pediatric Hematology-Oncology, Cerrahpasa
Medical Faculty, Istanbul University Cerrahpasa, Istanbul,Turkey.

 The efficacy of several variants of essential oil mouthrinses has been studied
extensively.This was the first study to compare the anti-plaque and anti-
gingivitis efficacy of two marketed essential oil mouthrinses: one is an alcohol
containing mouthrinse and the other one is an alcohol-free mouthrinse.
 This examiner randomized subjects to three groups: 1) Mechanical Oral Hygiene
(MOH) only; 2) MOH plus Alcohol-Containing essential oil Mouthrinse (ACM); 3)
MOH plus Alcohol-Free essential oil Mouthrinse (AFM).
 A total of 348 subjects completed the study. After six months, subjects using
essential oil mouthrinses with or without alcohol showed significant reduction (p
< 0.001) in gingivitis (28.2% and 26. 7%, respectively) and significant reduction (p
< 0.001) in plaque (37.8% and 37.0%, respectively), compared to those performing
MOH only.
 No statistically significant differences were observed for all measured indices
between ACM and AFM groups at any time point. Both mouthrinses were well
tolerated.
 Conclusions: No significant differences were observed in the efficacy of ACM and
AFM to reduce plaque and gingivitis, when used in addition to MOH, over six
months.
The effects of essential oil mouthrinses with or without alcohol on plaque
and gingivitis: a randomized controlled clinical study
Michael C. Lynch et al. (2018) BMC Oral Health . 2018 Jan 10;18(1):6.

 This study evaluated the distribution of dental plaque and gingivitis scores within
the dental arches after prophylaxis.
 Enrolled subjects underwent oral examinations for dental plaque (PI) and
gingivitis (GI) using the Turesky modification of the Quigley-Hein and the Lo¨e-
Silness Index, respectively, at the baseline visit, followed by a whole mouth
dental prophylaxis.
 Subjects were given fluoride toothpaste for twice daily oral hygiene for the next
30 days. Subjects were recalled on days 15 and 30 for PI and GI examinations
identical to baseline. Results: Analyses indicated that mean scores for PI and GI
on either arch and the whole mouth were higher than 2 and 1, respectively, during
all examinations. Anterior surfaces consistently exhibited lower PI scores than
posterior regions of either arch, or the entire dentition. Regional GI differences
within the dentition were similar to PI scores, with lower scores on anterior than
posterior teeth.
 Differences observed in PI and GI within the dentition have several practical
implications: (a) there are advantages of whole mouth assessments for oral health
(b) a need for oral hygiene formulations to reduce the larger deposits of dental
plaque in the posterior region and resultant gingival inflammation, and (c) a
requirement for ongoing oral hygiene education.
Distribution of dental plaque and gingivitis within the dental arches.
Prem K. Sreenivasan et al. (2017)
Journal of International Medical Research

 Individuals with altered passive eruption (APE) are assumed to be more
susceptible to periodontal diseases.To date, this hypothesis has not been
sufficiently supported by scientific evidence.
 The aim of this study, using an experimental gingivitis model, was to examine
the development and resolution of gingival inflammation in patients with APE
when compared to patients with normal gingival anatomy.
 Results: During the experimental gingivitis phase (days 0 – 21), the rate of
change in gingival inflammation (GI) was dramatically different between the
APE test group and the control group. On day 21, at the time of maximum
plaque accumulation, the GI of the APE test group was a 109% greater than
the GI of the test group (p≤ 0.001) despite similar plaque levels (p = 0.436).
During the resolution of inflammation phase (days 22 – 42), the APE test
group continued to exhibit statistically higher GI scores than the control
group (p=0.029).
 Conclusion: In the presence of similar amounts of plaque deposits and plaque
accumulation rates, APE patients exhibited differences in the development
and resolution of plaque-induced gingival inflammation when compared to
controls.
Experimental Gingivitis in Patients with and without Altered Passive Eruption
Rustam Aghazada et al. (2019)
Section of Periodontics, Department of Oral and Maxillofacial Sciences,
“Sapienza” University of Rome, Rome, Italy

1.Clinical periodontology-newman,tokei,klokevold 11th edition
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3. Celkan T. Ligneous gingivitis: Hard to diagnose and treat. Haemophilia. 2020
Mar;26(2):e49-e50. doi: 10.1111/hae.13924. Epub 2019 Dec 30. PMID: 31886930.
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Grogan TR, Gleber-Netto FO, WhitemanY, Li F, Lee HJ, Dharia K, Aro K, Martin
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Klokkevold PR, Elashoff D, Barnes VM, Richter R, DeVizio W, Masters JG, Wong DTW.
Salivary exRNA biomarkers to detect gingivitis and monitor disease regression. J Clin
Periodontol. 2018 Jul;45(7):806-817. doi: 10.1111/jcpe.12930. Epub 2018 Jun 15.
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5.Sreenivasan PK, Prasad KVV. Distribution of dental plaque and gingivitis
within the dental arches. J Int Med Res. 2017 Oct;45(5):1585-1596. doi:
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8. Msallem B, Bassetti S, Matter MS, Thieringer FM. Strawberry gingivitis:
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