gingival inflammation

1. Lecture by dr marij hameed

2.  Acute gingivitis is of sudden onset and short
duration and can be painful.
 A less severe phase of the acute condition has
been termed subacute.
 Recurrent gingivitis reappears after having
been eliminated by treatment or disappearing
spontaneously.
 Chronic gingivitis is slow in onset and of long
duration, and is painless, unless complicated
by acute or subacute exacerbations.

3.  Chronic gingivitis is the type most commonly
encountered.
 Chronic gingivitis is a fluctuating disease in
which inflammation persists or resolves and
normal areas become inflamed.

6. Generalized marginal and papillary gingivitis.

7. Localized, diffuse, intensely red area on the facial surface of tooth #7
and dark-pink marginal changes in the remaining anterior teeth.

11.  Localized gingivitis is confined to the gingiva of a
sin-gle tooth or group of teeth while 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

12.  The distribution of 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 muco-buccal fold but is limited in area.
 Localized papillary gingivitis is confined to one or
more inter-dental spaces in a limited area.
 Generalized marginal gingivitis involves the gingival
margins in relation to all the teeth. The inter-dental
papillae are usually affected in generalized marginal
gingivitis.

13.  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
co-factor.

14.  In evaluating the clinical features of gingivitis,
it is necessary to be systematic.
 Attention should be focused 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.
 These clinical characteristics and the
microscopic changes responsible

15.  The two earliest symptoms of gingival
inflammation pre-ceding established gingivitis,
are
 (1) increased gingival crevicular fluid
production rate and
 (2) bleeding from the gingival sulcus on gentle
probing

17.  Gingival bleeding varies in severity, duration,
and the ease with which it is provoked.
 Bleeding on probing is easily detectable
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

18.  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.
 Several gingival indices based on bleeding
have been developed

19.  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
tooth brushing, toothpicks, or food impaction)
or by biting into solid foods such as apples

20.  Sites that bleed on probing have a greater area
of inflamed connective tissue (i.e., cell-rich,
collagen-poor tissue) than do sites that do not
bleed.
 In most cases, the cellular infiltrate of sites that
bleed on probing is pre-dominantly
lymphocytic (a characteristic of stage II, or
early gingivitis)

21.  Histologic evaluations of animal specimens revealed
that, during the early stages of gingivitis, the
expression of the cytokines responsible for connective
tissue breakdown matrix metallopro-teinases (MMPs)
is ubiquitous.
 Different MMPs play a role in this breakdown at
different stages (e.g., a decrease of MMP-14 activity at
7 days of inflammation; an immediate increase
inMMP-2, especially with fibroblastic stimulation).
In addition, MMP-9 expression peaked 5 days after
gingivitis occurrence, which was also regulated by
macrophages and neutrophils.
 Thus, extracellular matrix remodeling was regulated
with MMP-2 and MMP-9 production and activation
by the host inflammatory response

22.  The severity of the bleeding and the ease with
which it is provoked depend on the intensity of
the inflammation.
 After the vessels are damaged and rupture, a
complex of mechanisms induce hemostasis

23.  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, however, when the area is
irritated.

24.  In cases of moderate or advanced periodontitis,
the presence of bleeding on probing is
considered a sign of active tissue destruction.

26.  In gingival inflammation, histopathologic alterations
that result in abnormal gingival bleeding include
dilation and engorgement of the capillaries and
thinning or ulceration of the sulcular epithelium
 Because the capillaries are engorged and closer to
the surface and because the thinned, degenerated
epithelium is less protective, stimuli that are
normally innocuous cause rupture of the capillaries
and gingival bleeding.
 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, which
is a characteristic of stage II (early) gingivitis

27.  Acute episodes of gingival bleeding are caused
by injury or occur spontaneously in acute
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.

28.  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

29.  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.

30.  The hemorrhagic tendency may be due to failure
of one or more of the hemostatic mechanisms.
 Hemorrhagic disorders in which abnormal
gingival bleeding is encountered include vascular
abnormalities (vitamin C deficiency or allergy such
as Schonlein-Henoch purpura),
 Platelet disorders (thrombocytopenic purpura),
hypo pro thrombinemia (vitamin K deficiency),
other coagulation defects (hemophilia, leukemia,
Christmas disease), deficient platelet thrombo
plastic factor (PF3) resulting from

31.  uremia, multiple myeloma, and postrubella
purpura.
 The effects of hormonal replacement therapy,
oral contraceptives, pregnancy,and the
menstrual cycle are also reported to affect
gingival bleeding.
 Bleeding may follow the administration of
excessive amounts of drugs such as salicylates
and the administration of anticoagulants such
as dicumarol and heparin.

32.  In addition, in women, long-term
depression-related stress exposure may
increase concentrations of interleukin-6 in
gingival crevicular fluid and worsen
periodontal conditions with elevated gingival
inflammation and increased pocket depths

33.  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 and progesterone levels on
the periodontium, starting as early as
puberty.

34.  Color Changes in Chronic Gingivitis.
 Change
 in color is an important clinical sign o f 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 more red when there is
an increase in vascularization or the degree of epithelial
keratinization becomes reduced or disappears.
 The color becomes more pale when vascularization is
reduced (in association with fibrosis of the corium) or
epithelial keratinization increases.

35.  Thus chronic inflammation intensifies the red or
bluish red color, because of vascular proliferation
and reduction of keratinization due to epithelial
compression by the inflamed tissue.
 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. Proper diagnosis and treatment require an
under-standing of the tissue changes that alter the
color of the gingiva at the clinical level.

36. 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
patch like, depending on the underlying acute
condition.

37.  In acute necrotizing ulcerative gingivitis the
involvement is marginal; in herpetic gingivostomatitis,
it is diffuse; and in acute reactions to chemical
irritation, it is patchlike or diffuse.
 Color changes vary with the intensity of the
inflammation.
 Initially, there is an increasingly red 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.

38.  Heavy metals (bismuth,arsenic, mercury, lead, 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, they 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 inter-dental marginal and
attached gingiva.
 This is different from tattooing produced by the
accidental embedding of amalgam or other metal
fragments

39. Chronic gingivitis. Swelling, loss of stippling, and
discoloration occur when inflammatory exudate and edema are the
predominant microscopic changes. The gingiva is soft and friable,
and it bleeds easily

42.  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, where the increased
permeability of irritated blood vessels permits seepage of
the metal into the surrounding tissue.
 In addition to inflamed gingiva, mucosal areas irritated by
biting or abnormal chewing habits (e.g., the inner surface of
the lips,the cheek at the level of the occlusal line, and the
lateral border of the tongue) are common pigmentation
sites.
 Pigmentation can be eliminated by treating the
inflammatory changes without necessarily discontinuing the
metal-containing medication.

44.  Many systemic diseases may cause color changes
in the oral mucosa, including the gingiva.
 In general, these abnormal pigmentations are
nonspecific in nature and should stimulate further
diagnostic efforts or referral to the appropriate
specialis
 Endogenous oral pigmentations can be due to
melanin, bilirubin, or iron." Melanin oral
pigmentations can be normal physiologic
pigmentations and are commonly found in highly
pigmented ethnic groups

45.  Diseases that increase melanin pigmen-tation
include the following.
 Addison's disease: caused by adrenal
dysfunction and pro-duces 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

46.  Albright’s syndrome (polyostotic fibrous dysplasia)
and von Recklinghausen’s disease (neurofibromatosis)
produce areas of oral melanin pigmentation.
 The skin and the mucous membranes can also be
stained by bile pigments. Jaundice is best detected
via the 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

47.  Exogenous factors that are 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 it may also 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

48.  During recent years, the need for aesthetics in
dentistry has increased, with a growing
demand for a pleasing smile.
 This has made many individuals more aware
of their gingival pigmentation,which may be
apparent during smiling and speech.
 Traditionally, gingival depigmentation has
been carried out with the use of nonsurgical
and surgical procedures, including chemical,
cryosurgical, and electrosurgical techniques.

49.  However, those techniques were met with skepticism
because of their varying degrees of success.
 More recently, lasers have been used to ablate cells that
produce the melanin pigment; a nonspecific laser beam
destroys the epithelial cells, including those at the basal
layer.
 In addition, selective ablation with the use of a laser
beam with a wavelength that is specifically absorbed
in melanin effectively destroys the pigmented cells
without damaging the nonpigmented cells.
 In both cases, radiation energy is transformed into
ablation energy, thereby resulting in cellular rupture
and vaporization with minimal heating of the
surrounding tissue

50.  Both chronic and acute inflammations
produce changes in the normal firm and
resilient consistency of the gingiva.
 As previously noted, in patients with chronic
gingivitis, both destructive (edematous) and
reparative (fibrotic) changes coexist, and the
consistency of the gingiva is determined by
their relative predominance

52.  Calcified microscopic masses may be found in
the gingiva.
 These can occur alone or in groups, and they
vary with regard to size, location, shape, and
structure.
 Such masses may be calcified material that
has been removed from the tooth and
traumatically displaced into the gingiva
during scaling, root remnants, cementum
fragments, or cementicles.

53.  Chronic inflammation and fibrosis, an
occasional foreign body, and giant cell
activity occur in relation to these masses.
 They are sometimes enclosed in an osteoid
like matrix.
 Crystalline foreign bodies have also been
described in the gingiva,but their origin has not
been determined.

54.  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.
 In animal studies, mechanical stimulation by
toothbrushing was found to increase the
proliferative activity of the junctional basal
cells in dog gingiva by 2.5 times as compared
with the use of a scaler.


55.  These findings may indicate that tooth-
brushing 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

56.  The surface of normal gingiva usually exhibits
numerous small depressions and elevations that
give the tissue an orange-peel appearance
referred as stippling
 Stippling is restricted to the attached gingiva and
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 the loss of stippling is an early sign
of gingivitis.

57.  However, clinicians must take into
consideration that its pattern and extent vary in
different mouth areas, among patients, and
with age.
 In patients with chronic inflammation, the
gingival surface is either smooth and shiny or
firm and nodular, depending on whether the
dominant changes are exudative or fibrotic.

58.  Smooth surface texture is also produced by
epithelial atrophy in atrophic gingivitis, and
peeling of the surface occurs with chronic
desquamative gingivitis.
 Hyperkeratosis results in a leathery texture,
and drug-induced gingival overgrowth
produces a nodular surface

59.  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 they are chemical,
physical,or thermal—are among the most
common lesions in the mouth.

60.  Sources of chemical injuries include aspirin,
hydrogen peroxide, silver nitrate, phenol, and
endodontic materials.
 Physical injuries can include lip, oral, and
tongue piercings, which can result in gingival
recession.
 Thermal injuries can result from hot drinks and
foods.

61.  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.

62.  Gingival recession is a common finding.
 The prevalence, extent, and severity of gingival
recession increase with age, and this condition
is more prevalent among males

63.  By clinical definition, recession is the exposure
of the root surface by an apical shift in the
position of the gingiva.
 To understand recession, it helps to
distinguish between the actual and apparent
positions 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

64.  The severity of recession is determined by the
actual position of the gingiva and not by 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

65.  Recession refers to the location of the gingiva
rather than to its condition.
 Receded gingiva can be inflamed, but it may
be normal except for its position.
 Recession may be localized
 to one tooth or to a group of teeth, or it may be
generalized through-out the mouth

68.  Gingival recession increases with age; the
incidence varies from 8% in children to 100%
after the age 50 of years.
 This has led some investigators to assume that
recession may be a physiologic process related
to aging.
 However, no convincing evidence has been
presented for a physiologic shift of the gingival
attachment.

69.  The gradual apical shift is most likely the result
of the cumulative effect of minor pathologic
involvement and repeated minor direct trauma
to the gingiva.
 In some populations without access to dental
care, however, recession may be the result of
increasing periodontal disease.

70.  The following etiologic factors have been
implicated in gingival recession: faulty
toothbrushing technique (gingival abrasion), tooth
malposition, friction from the soft tissues
(gingival ablation),gingival inflammation,
abnormal frenum attachment, and iatrogenic
dentistry.
 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.

71.  Standard oral hygiene procedures, whether
they involve tooth-brushing or flossing, may
lead to frequent transient and minimal gingival
injury.
 Although tooth brushing is important for
gingival health, faulty tooth brushing
technique or brushing with hard bristles may
cause significant injury.
 This type of injury may present as lacerations,
abrasions, keratosis, and recession, with the
facial marginal gingiva being the most affected

72.  Thus, in these cases, recession tends to be more
frequent and severe in patients with clinically
healthy gingiva, little bacterial plaque, and
good oral hygiene.
 Susceptibility to recession is also influenced by
the position of teeth in the arch, the root bone
angle, and the mesio-distal curvature of the
tooth surface.

73.  On rotated, tilted, or facially displaced teeth, the
bony plate is thinned or reduced in height.
Pressure from mastication or moderate tooth
brushing damages the unsupported gingiva and
produces recession.
 The effect of the angle of the root in the bone with
recession is often observed in the maxillary molar
area.
 If the lingual inclination of the palatal root is
prominent or if the buccal roots flare outward,
the bone in the cervical area is thinned or
shortened, and recession results from repeated
trauma of the thin marginal gingiva

74.  The health of the gingival tissue also depends on
properly designed and placed restorative materials.
Pressure from a poorly designed partial denture, such
as an ill-fitting denture clasp, can cause gingival
trauma and recession.
 Overhanging dental restorations have long been
viewed as a contributing factor to gingivitis because of
plaque retention.
 In addition, there is general agreement that placing
restorative margins within the biologic width
frequently leads to gingival inflammation, clinical
attachment loss, and, eventually, bone loss.
 Clinically, the violation of biologic width typically
manifests as gingival inflammation, deepened
periodontal pockets, and gingival recession.

75.  A relationship may exist between smoking and
gingival recession.
 The multi factorial mechanisms may include
reduced gingival blood flow and altered
immune response, but they are not as yet
conclusive.

76.  Several aspects of gingival recession make it
clinically significant. Exposed root surfaces are
susceptible to caries.
 Abrasion or erosion of the cementum exposed
by recession leaves an underlying dentinal
surface that can be sensitive.
 Hyperemia of the pulp and associated
symptoms may also result from the excessive
exposure of the root surface.
 Interproximal recession creates oral hygiene
problems and resulting plaque accumulation.

77.  Changes in gingival contour are primarily
associated with gingival enlargement, but such
changes may also occur with other conditions.
 Of historical interest are the descriptions of
indentations of the gingival margin referred to
as Stillman’s clefts and the McCall festoons.

78.  The term Stillman’s clefts has been used to
describe a specific type of gingival recession that
consists of a narrow, triangular-shaped gingival
recession.
 As the recession progresses apically, the cleft
becomes broader,thereby 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 with
maintaining adequate plaque control at this site.

79.  The term Stillman’s clefts has been used to
describe a specific type of gingival recession that
consists of a narrow, triangular-shaped gingival
recession.
 As the recession progresses apically, the cleft
becomes broader, thereby exposing the
cementum of the root surface.
 When the lesion reaches the muco-gingival
junction, the apical border of oral mucosa is
usually inflamed because of the difficulty with
maintaining adequate plaque control at this site.

87.  The term McCall festoons has been used to describe a
rolled, thickened band of gingiva that is usually
seen adjacent to the cuspids when recession
approaches the mucogingival junction.
 Ini-tially, 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
 These are semilunar enlargements named after John
Opple McCall along with Paul R Stillman, believed
occlusal traumatism to be an etiologic factor.

88.  Thank you