Clinical Features Of Gingivitis.ppt

it describes the various clinical features seen in Gingivitis Condition

1. Clinical Features of Gingivitis

2. CONTENTS
Introduction
Prevalence
Distribution
Bleeding from gingiva
Colour changes in gingiva
Changes in Gingival consistency
Changes in Gingival Surface texture
Changes in Gingival Position
Changes in Gingival Contour
Conclusion
References

3. Introduction
Inflammationisdefinedasanobservablealterationintissues
associatedwithchangesinvascularpermeabilityand
dilation,oftenwiththeinfiltrationofleukocytesintoaffected
tissues.
Thesechangesresultinerythema,Edema,Heat,Pain,and
lossoffunctionbeingthecardinalsignsofinflammation

4. 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

5. Prevalence:
The prevalence of gingivitis is evident worldwide.
For example, epidemiologic studies indicate that more
than 82% of U.S. adolescents have overt gingivitis and
signs of gingival bleeding.
A similar or higher prevalence of gingivitis is reported for
children and adolescents in other parts of the world.
In children on average 6% of sites measured showed
bleeding on probing

6. Course and Duration
Gingivitis can occur with sudden onset and short
duration and can be painful. A less severe phase of this
condition can also occur.
Recurrent gingivitisreappears after having been
eliminated by treatment or disappearing spontaneously.
Chronic gingivitisis 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 gingivitisis a fluctuating disease in which
inflammation persists or resolves and normal areas
become inflamed.

7. Chronic gingivitis. The marginal and
interdental gingivae are smooth,
edematous, and discolored.
Localized, diffuse, intensely red
area irt 12 and
dark-pink marginal changes in
remaining anterior teeth.

8. Distribution
Localized gingivitisis confined to the gingiva of a single
tooth or group of teeth, whereas generalized gingivitis
involves the entire mouth.
Marginal gingivitisinvolves the gingival margin and may
include a portion of the contiguous attached gingiva.
Papillary gingivitisinvolves theinterdental 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 gingivitisaffects the gingival margin, the attached
gingiva, & the interdental papillae.

9. Gingival disease in individual cases is described by combining
the preceding terms as follows:
Localized marginal gingivitisis confined to one or more
areas of the marginal gingiva
Localized diffuse gingivitisextends from the margin to
the mucobuccal fold in a limited area
Localized papillary gingivitisis confined to one or more
interdental spaces in a limited area
Generalized marginal gingivitisinvolves the gingival
margins in relation to all the teeth. The interdental
papillae are usually unaffected
Generalized diffuse gingivitisinvolves the entire gingiva.

10. Generalized marginal gingivitis in
the upper jaw.
Generalized marginal and papillary
gingivitis
Generalized diffuse gingivitis involves the
marginal, papillary, and attached gingivae

11. Clinical features:
Inevaluatingtheclinicalfeaturesitisnecessarytobe
systematic.
Theclinicianshouldfocusonsubtletissuealterations
becausethesemaybeofdiagnosticsignificance.
Asystematicclinicalapproachrequiresanorderly
examinationofthegingivafor
color,
contour,
consistency,
position, and
ease and severity of bleeding and
pain.

12. 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

13. Bleeding on Probing
Itisdetectedclinicallyandthereforeisofvalueforthe
earlydiagnosisandpreventionofmoreadvanced
gingivitis.
Ithasbeenshownthatbleedingonprobingappears
earlierthanachangeincolororothervisualsignsof
inflammation;
Inaddition,theuseofbleedingratherthancolorchanges
todiagnoseearlygingivalinflammationisadvantageous
inthatbleedingisamoreobjectivesignthatrequires
lesssubjectiveestimationbytheexaminer.

14. Gingival bleeding on probing is an important diagnostic
factor –as it is associated with inflammation and
ulceration of the epithelium lining the gingival sulcus.
The presence of plaque for only 2 days can 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.
The 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.

15. Ingeneral,gingivalbleedingonprobingindicatesan
inflammatorylesionbothintheepitheliumandinthe
connectivetissuethatexhibitsspecifichistologicdifferences
comparedwithhealthygingiva.
Eventhoughgingivalbleedingonprobingmaynotbeagood
diagnosticindicatorforclinicalattachmentloss,itsabsenceis
anexcellentnegativepredictoroffutureattachmentloss.

16. 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).
In addition, recent research reveals an increase in
gingival bleeding on probing in patients who quit
smoking.

17. Chronic and Recurrent Bleeding:
The most common cause of abnormal gingival bleeding
on probing is chronic inflammation.
The bleeding is chronic and 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 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.

18. 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, histopathologic alterations that
result in abnormal gingival bleeding include dilation and
engorgement of the capillaries and thinning or ulceration
of the sulcular epithelium.

19. Because the capillaries are engorged and closer to the
surface, and 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 (a characteristic of
stage II, or early, gingivitis).

20. 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 toothbrushing 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.

21. 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.

22. Hemorrhagic disorders in which abnormal gingival bleeding is
encountered include
Vascular abnormalities:
Vitamin C deficiency or
Allergy
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
Post rubella purpura.

23. The effects of hormonal replacement therapy, oral
contraceptives, pregnancy, and the menstrual cycle are
also reported to affect gingival bleeding.
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.
Diabetes is another endocrine condition with a well-
characterized effect on gingivitis.

24. 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 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

25. 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,
and pigments within the epithelium

26. Color Changes in Chronic Gingivitis:
Changeincolorisanimportantclinicalsignofgingival
disease.
Thenormalgingivalcoloris"coralpink"andisproduced
bythetissue'svascularityandmodifiedbytheoverlying
epitheliallayers.
Forthisreason,thegingivabecomesredwhen
vascularizationincreasesorthedegreeofepithelial
keratinizationisreducedordisappears.
Thecolorbecomespalewhenvascularizationisreduced
(inassociationwithfibrosisofthecorium)orepithelial
keratinizationincreases.

27. 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.

28. Color Changes in Acute Gingivitis:
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 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 increase in erythema.

29. 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.

30. Metallic Pigmentation.
Heavymetals(bismuth,arsenic,mercury,leadand
silver)absorbedsystemicallyfromtherapeuticuseor
occupationalorhouseholdenvironmentsmaydiscolor
thegingivaandotherareasoftheoralmucosa.
Typically,metalsproduceablackorbluishlineinthe
gingivathatfollowsthecontourofthemargin.The
pigmentationmayalsoappearasisolatedblackblotches
involvingtheinterdentalmarginalandattachedgingiva.

31. Lead Produces a bluish red or deep blue linear
pigmentation of the gingival margin(Burtonian line)
Exposure to silver produces a violet line accompanied by
a difuse bluish grey discoloration throughout the oral
mucosa(Argyria)
Gingival pigmentation from systemically absorbed metals
results from perivascular precipitation of metallic sulfides
in the subepithelial connective tissue.

32. 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., inner surface of
lips, cheek at level of occlusal line, lateral border of
tongue) are common sites of pigmentation.
Pigmentation can be eliminated by treating the
inflammatory changes without necessarily discontinuing
the metal containing medication.

33. Bismuth gingivitis.linear black
discoloration of the gingiva in a
patient receiving bismuth therapy.
Discoloration of the gingiva
caused by embedded metal
particles (amalgam).

34. Color Changes Associated with Systemic Factors
Endogenous oral pigmentations can be caused by melanin,
bilirubin, or iron.
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’sdisease 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’ssyndrome (polyostotic fibrous dysplasia) and von Recklinghausen's
disease (neurofibromatosis) produce areas of oral melanin pigmentation.

35. Skin and mucous membranes can also be stained by
bile pigments.
The deposition of ironin 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.

36. 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.

37. Changes in Consistency of the Gingiva
Bothchronicandacuteinflammationsproducechangesin
thenormalfirmandresilientconsistencyofthegingiva.
In chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes
coexist, and the consistency of the gingiva is determined by their relative predominance

39. 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.
Chronic inflammation and fibrosis, and occasionally foreign
body, 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.
Calcified Masses in the Gingiva:

40. 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.
In animal studies, mechanical stimulation by tooth-
brushing was found to increase the proliferative
activity.

41. 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.
 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.

42. 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.

43. 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.
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..

44. 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.

45. 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.
Position 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 and apparent positions of the gingiva:
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.

46. 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.
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.

47. Gingival recession increases with age; the incidence varies
from 8% in children to 100% after age 50 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.
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.
Etiologic Factors:

48. The following etiologic factors have been implicated in
gingival recession: faulty toothbrushing technique
(gingival abrasion), tooth malposition, friction from 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.

49. Standardoralhygieneprocedures,whethertooth-
brushingorflossing,mayleadtoafrequenttransientand
minimalgingivalinjury.
Althoughtoothbrushingisimportantforgingivalhealth,
faultytoothbrushingtechniqueorbrushingwithhard
bristlesmaycausesignificantinjury.
Thistypeofinjurymaypresentaslacerations,abrasions,
keratosisandrecession,withthefacialmarginalgingiva
mostaffected.
Thus,inthesecases,recessiontendstobemore
frequentandsevereinpatientswithclinicallyhealthy
gingiva,littlebacterialplaque,andgoodoralhygiene.

50. Susceptibilitytorecessionisalsoinfluencedbythe
•positionofteethinthearch,
•theroot-boneangle,andthe
•mesiodistalcurvatureofthetoothsurface.
Onrotated,tilted,orfaciallydisplacedteeth,thebony
plateisthinnedorreducedinheight.Pressurefrom
masticationormoderatetoothbrushingdamagesthe
unsupportedgingivaandproducesrecession.

51. The effect of the angle of the root in the bone on
recession is often observed in the maxillary molar area.
If the lingual inclination of the palatal root is prominent or
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.

52. Restorations and Recession:
The health of the gingival tissue also depends on
properly designed and placed restorative materials.
Pressure from a poorly designed partial denture, such as
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.

53. 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, or gingival recession.

55. Smoking and Recession:
A relationship may exist between smoking and gingival recession. The
multifactorial mechanisms may include reduced gingival blood flow
and altered immune response .
Clinical Significance:
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 excessive exposure of the root surface.

56. Changes in gingival Contour
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.

57. Stillman's clefts: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.

58. Originally described by Stillman and considered to be the
result of occlusal trauma
These clefts were subsequently described by Box 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 into the supporting tissues.
Their association with trauma from occlusion has not
been substantiated.

59. The clefts are divided into
simple clefts: in which cleavage occurs in a single
direction (the most common type), and
compound clefts: in which cleavage occurs in more than
one direction.
The clefts vary in length from a slight break in the
gingival margin to a depth of 5 to 6 mm or more.

60. McCall festoons: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.
However, this association was never proved, and these indentations
merely represent peculiar inflammatory changes of the marginal
gingiva.

61. Mccall’s Festoons

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