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1. 2-Mar-21
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“If you want it, you can fly, you just have to
trust you a lot …”
-Stevejobs

2. CORRELATION OF GINGIVA
IN HEALTH & DISEASE
2-Mar-21
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Guided by:
Dr. Monica Mahajani
Dr. Chandrahas Goud
Dr. Anup Shelke
Dr. Subodh Gaikwad
Dr. Anup Gore
Dr. Kuldeep Patil
Presented by:
Dr. Chavan Sneha S.
(1ST Year PG)

3. • A systematic clinical approach requires an orderly examination of
the gingiva :
• Color
• Consistency
• Surface texture
• Position
• Contour(shape)
• BOP
• Size
• Exudate
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4. • CHANGES IN COLOR OF THE GINGIVA
Healthy
Uniformly pale pink or coral pink
Variations in pigmentation related to complexion,
races
Underlying factors:
– the number and size of blood vessels,
– epithelial thickness
– quantity of keratinization
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5. • Chronic inflammation intensifies the red or bluish red color
because of vascular proliferation and reduction of
keratinization.
• Venous stasis will contribute a bluish hue. The gingival
color changes with increasing chronicity of the inflammatory
process.
• The changes start in the interdental papillae and gingival
margin and spread to the attached gingiva.
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6. COLOR CHANGES IN ACUTE GINGIVITIS
• Color changes in acute gingival inflammation differ in both nature
and distribution from those in chronic gingivitis.
• Color changes may be marginal, diffuse, or patch like, depending on
the underlying acute condition. In ANUG, the involvement is marginal;
in herpetic gingivostomatitis, it is diffuse; and in acute reactions to
chemical irritation, it is patch like or diffuse.
• 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.
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7. 2-Mar-21
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ANUG Herpetic gingivostomatitis

8. • METALLIC PIGMENTATION
• 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.
• 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.
• Exposure to silver - a violet line accompanied by a diffuse
bluish grey discoloration in throughout the oral mucosa
(Argyria)
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9. 2-Mar-21
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Burtonian line
Amalgam tatto

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Bismuth gingivitis
linear black discoloration of the gingiva in a patient receiving bismuth therapy.

11. • Gingival pigmentation from systemically absorbed metals results from
perivascular precipitation of metallic sulfides in the sub-epithelial
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., inner surface of lips, cheek at level of
occlusal line, lateral border of tongue) are common sites of
pigmentation.
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12. • 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:
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13. 2-Mar-21
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Peutz-Jeghers syndrome Addison’s disease

14. • Skin and mucous membranes can also be stained by bile pigments.
• 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.
• Localized bluish black areas of pigment are often caused by amalgam
implanted in the mucosa
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• Tobacco causes hyperkeratosis of
the gingiva and also may induce a
significant increase in melanin
pigmentation of the oral mucosa.

16. PHYSIOLOGIC PIGMENTATION:
• Dummet et al 1946 proposed the following explanation for gingival
pigmentation.
• The color of healthy gingiva is variable ranging from a pale pink to a
deep bluish purple hue.
• Between these limits of normalcy are a large number of pigmentation
mosaics which depend primarily upon the intensity of melanogenesis,
depth of epithelial cornification and arrangement of gingival vascularity.
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17. • Most pigmentation is caused by five primary pigments. These include:
melanin, melanoid, oxyhemoglobin, reduced haemoglobin and carotene.
• Others are caused by bilirubin and iron.
• Alex A Farnoosh 1990 said that melanin deposits mainly in basal and
suprabasal cell layers of epithelial.
• The degree of pigmentation is attributed to melanoblastic activity and
density of melanophores in gingiva.
• In gingiva number of melanophores in the epithelium and the
subepithelial connective tissue gradually decreases starting from the free
gingival groove area towards the gingival crest in the free gingiva &
towards the muco-gingival junction in attached gingiva.
• In addition, the total number of melanophores in attached gingiva (3230)
approximately is 16 times greater than in free gingiva (198).
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18. • Melanin is a non-hemoglobin derived brown pigment.
• It is more prominent in the oral cavity of black individuals.
• According to Dummett et al 1946, the distribution of oral
pigmentation in black individuals is as follows: gingiva:- 60% hard
palate:- 61% mucous membrane:- 22% tongue:- 15%
• Gingival pigmentation occurs as a diffuse, deep- purplish
discoloration or as irregularly shaped brown and light brown patches.
• It may appear as early as 3 hours after birth.
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19. • DUMMET PROPOSED THE DUMMET ORAL PIGMENTATION INDEX
(DOPI) ASSESSMENT 1964
• Score 0 : Pink tissue (No clinical pigmentation)
• Score 1 : Mild light brown color (Mild clinical pigmentation)
• Score 2 : Medium brown or blue black tissue (Heavy clinical
pigmentation)
• Score 3 : Deep brown or blue black tissue (Heavy clinical pigmentation)
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20. • DEPIGMENTATION
• Traditionally, gingival depigmentation has been carried out using nonsurgical
and surgical procedures, such as
– chemical,
– cryosurgical, and
– electrosurgical techniques.
• More recently, lasers have been used to ablate cells producing the melanin
pigment; a nonspecific laser beam destroys the epithelial cells, including those
at the basal layer.
• In addition, selective ablation using a laser beam with a wavelength that is
specifically absorbed in melanin effectively destroys the pigmented cells
without damaging the non-pigmented cells.
• In both cases, radiation energy is transformed into ablation energy, resulting
in cellular rupture and vaporization with minimal effect on surrounding tissue
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21. • CHANGES IN CONSISTENCY OF THE GINGIVA
Health
firm and resilient
• Both chronic and acute inflammations produce changes in the normal
firm and resilient consistency of the gingiva.
• in chronic gingivitis, both destructive (edematous) and reparative
(fibrotic) changes coexist, and the consistency of the gingiva is
determined by their relative predominance.
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22. • In chronic gingivitis, both destructive
(edematous) and reparative (fibrotic)
changes coexist, and the
consistency of the gingiva is
determined by their relative
predominance
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23. • TOOTH BRUSHING
• Tooth brushing 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. (Mackenzie
IC et al 1972, Tanaka M et al 1998)
• In animal studies, mechanical stimulation by tooth brushing was
found to increase the proliferative activity of junctional basal cells in
dog gingiva by 2.5 times compared with using a scaler. (Yamamoto T
2002)
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24. • CHANGES IN SURFACE TEXTURE OF THE GINGIVA
Healthy
Stippling present
• The surface of normal gingiva usually exhibits numerous small depressions and
elevations, giving the tissue an orange peel appearance referred as stippling.
(Bergstrom J 1984)
• Stippling is restricted to the attached gingiva and is predominantly localized to the
sub-papillary area, but it extends to a variable degree into the interdental papilla.
(Orban B 1948)
• Although the biologic significance of gingival stippling is not known, some
investigators conclude that loss of stippling is an early sign of gingivitis.
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25. • 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
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26. • Gingival biopsy demonstrating
alternate elevations and
depressions in the attached
gingiva responsible for stippled
appearance.
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27. • In acute cases, the appearance of slough (necrotizing epithelium),
erosion, or ulceration and the accompanying erythema are common
features.
• In chronic cases, permanent gingival defects are usually present in
the form of gingival recession.
• Typically, the localized nature of the lesions and the lack of
symptoms readily eliminate them from the differential diagnosis of
systemic conditions that may be present with erosive or ulcerative oral
lesions. (Rawal SY et al 2004)
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28. CHANGES IN POSITION OF THE GINGIVA
Healthy
1mm above CEJ
• Gingival recession is a common finding. The prevalence, extent, and severity of
gingival recession increase with age and are more prevalent in males. (Albander JM,
Kingman A 1999)
• By clinical definition, recession is exposure of the root surface by an apical shift in
the position of the gingiva.
• Gingival recession is defined as the apical migration of the junctional epithelium with
exposure of root surfaces.(Kassab MM, Cohen RE 2003)
• Gingival recession is the apical shift of the marginal gingiva from its normal position
on the crown of the tooth to levels on the root surface beyond the cemento enamel
junction (Loe H 1992)
• To understand recession, it helps to distinguish between the actual and apparent
positions of the gingiva.
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30. • 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.
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31. • THEORY
• The most accepted theory to explain the origin of gingival recession
is based on inflammation of the connective tissue of free gingiva and
its consequent destruction, where the gingival epithelium migrates into
the connective tissue and gets destroyed, while the gingival epithelial
basement membrane and sulcus epithelium reduce the thickness of
the connective tissue between them, thus reducing the blood flow by
impairing the repair of the initial injury.
• As the lesion progresses, the connective tissue disappears and
fusion occurs between the gingival epithelium and the sulcular and
union epithelia, which will subsequently withdraw due to lack of blood
flow (Susin et al)
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32. • ETIOLOGIC FACTORS
• Gingival recession increases with age; the incidence varies from 8% in children to
100% after age 50 years. (Woofter C 1969)
• 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. (Loe H 1967)
• 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. (Hirschfeld I 1923, Loe H 1967)
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33. • 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.
• 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.
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34. • Standard oral hygiene procedures, whether tooth-brushing or
flossing, may lead to a 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 most affected.
• 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
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35. 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.
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.
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36. • 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.
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37. • RESTORATIONS AND RECESSION
• 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. (Zlataric DK, Celebic A et al 2002)
• 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. (Bjorn et al
1969, Garguilo et al 1961)
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39. • 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 but are not, as yet,
conclusive. (Gunsolley JC, Tew J et al 1998)
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40. 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. (Merritt AA 1993)
• Interproximal recession creates oral hygiene
problems and resulting plaque accumulation.
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41. Classification of Gingival Recession:
• An early study of recession associated with mandibular incisor teeth used
the descriptive terms “narrow,” “wide,” “shallow” and “deep” to classify
recession into four groups (Sullivan HC, Atkins JH-1968)
• Another study classified gingival recession into “shallow-narrow” defects
as less than 3 mm in both dimensions, and “deep-wide” defects as more
than 3 mm in both dimensions (Mlinek A, Smukler H, Buchner A 1973)
• According to PD Miller’s: Class-I ,Class-II, Class III, Class IV.
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43. • The Index of Recession, or IR, was introduced by Smith(1997).
• Recession was described by two digits separated by a dash (for
example, F2-4) and the prefixed letter F or L denotes whether the
recession is on the facial or lingual aspects of the tooth.
• The digits describe the horizontal and vertical components of a recession
site in that order. If an asterisk were present, it would denote involvement
of the mucogingival junction.
• The horizontal component is expressed as a whole number value (from
the range 0-5) depending on what proportion of the CEJ is exposed on
either the facial or lingual aspects of the tooth, between the mesial and
distal midpoints.
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44. • CHANGES IN GINGIVAL CONTOUR
Healthy:
Marginal gingiva: scalloped & knife edge
Intrental papilla:ant.: pyramidal
post.: tent shape
• 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.
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45. • STILLMAN'S CLEFTS
• Used to describe a specific type of gingival
recession consisting of a narrow, triangular shaped
gingival recession. As the recession progresses
apically, the cleft becomes broader, exposing the
cementum of the root surface.
• When the lesion reaches the mucogingival junction,
the apical border of oral mucosa is usually inflamed
because of the difficulty in maintaining adequate
plaque control at this site.
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46. • Originally described by Stillman PR 1921 and considered to be the
result of occlusal trauma
• These clefts were subsequently described by Box HK 1950 as
pathologic pockets in which the ulcerative process had extended to the
facial surface of the gingiva.
• The clefts may repair spontaneously or persist as surface lesions of
deep periodontal pockets that penetrate into the supporting tissues.
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47. • The clefts are divided into
• simple clefts: in which cleavage occurs in a single direction (the most
common type), and
• composed 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.
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48. • Mc CALL’s FESTOONS (John Oppie Mc Call 1922)
• Used to describe a rolled, thickened band of gingiva
usually seen adjacent to the cuspids when recession
approaches the muco- gingival junction.
• Initially, Stillman's clefts and McCall festoons were
attributed to traumatic occlusion, and the
recommended treatment was occlusal adjustment.
• However, this association was never proved, and
these indentations merely represent peculiar
inflammatory changes of the marginal gingiva.
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49. • BLEEDING ON PROBING
• It is detected clinically and therefore is of value for the early
diagnosis and prevention of more advanced gingivitis.
• It has been shown that bleeding on probing appears earlier
than a change in color or other visual signs of inflammation;
– in addition, the use of bleeding rather than color changes to
diagnose early gingival inflammation is advantageous in that
bleeding is a more objective sign that requires less subjective
estimation by the examiner.
• Therefore, bleeding on probing is widely used by clinicians and
epidemiologists to measure
– disease prevalence and progression,
– to measure outcomes of treatment, and
– to motivate patients with their home care.
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50. • Gingival bleeding on probing is an important diagnostic factor – as it is
associated with inflammation and ulceration of the epithelium lining the
gingival sulcus.
• Presence of plaque for only 2 days -initiate gingival bleeding on
probing, whereas once established, it may take 7 days or more after
continued plaque control and treatment to eliminate gingival bleeding.
• Absence of plaque and presence of gingival bleeding may indicate
improvement in plaque control that may have occurred immediately
before the examination.
• Presence of bleeding is an indication of active gingival inflammation,
and until it is controlled, the patient is at a risk of continuing periodontal
disease and tissue destruction.
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51. • In general, gingival bleeding on probing indicates an inflammatory
lesion both in the epithelium and in the connective tissue that
exhibits specific histologic differences compared with healthy
gingiva.
• Even though gingival bleeding on probing may not be a good
diagnostic indicator for clinical attachment loss, its absence is an
excellent negative predictor of future attachment loss.(Lang et al
1990)
• Therefore the absence of gingival bleeding on probing is desirable
and implies a low risk of future clinical attachment loss.
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52. • Numerous studies show that current cigarette smoking suppresses the
gingival inflammatory response, and smoking was found to exert a strong,
chronic, dose dependent suppressive effect on gingival bleeding on probing
in the third National Health and Nutrition Examination Survey (NHANES III)
(Dietrich et al 2004)
• In addition, recent research reveals an increase in gingival bleeding on
probing in patients who quit smoking. (Nair P, Palmer RM et al 2003)
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53. • EXAMINATION FOR BOP
• Walking probe technique
• Done with short upward and downward movement
• A tooth is probed at 6 sites- MB, mid B, DB, and corresponding lingual
sites
• Working force should not be more than 20gms
• Pain during probing is indicative of too heavy probing force
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54. • ERRORs
Histopathologic alterations
abnormal bleeding
dilation and engorgement of capillaries, thinning/ulceration of sulcular epithelium
thus capillaries are closer to surface and thinned
degenerated epithelium is less protective, stimuli that are normally innocuous cause
rupture of capillaries and bleeding
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55. • INDICES USED
• SULCUS BLEEDING INDEX Muhlemann H R ,Son S 1971- locate areas
of gingival sulcus bleeding upon gentle probing and recognize presence of
early gingival inflammation
• 1 => healthy looking papillary and marginal gingiva, bleeding on probing
• 2 => bleeding on probing and color change in gingiva
• 3 => bleeding on probing, color change, slight edema
• 4 => bleeding on probing, color change, obvious edema
• 5 => spontaneous bleeding, color change, marked edema or ulceration.
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56. • PAPILLARY BLEEDING INDEX Muhlemann H R 1977 modification of SBI
This modificadon resulted in the PBI Index based on bleeding following gentle
probing of the interdental papilla
• 0 => no bleeding
• 1 => only one bleeding point present
• 2 = > several isolated bleeding points on a small area of blood
• 3 = > interdental triangle filled with blood
• 4 => profuse bleeding spreading toward the marginal gingiva.
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57. • GINGIVAL BLEEDING INDEX Carter H G, Barnes G P 1974- presence/absence of
gingival inflammation as determined by bleeding from interproximal gingival sulci
• MODIFIED SULCULAR BLEEDING INDEX/MODIFIED SULCUS BLEEDING
INDEX- A Mombelli, M A Van Oosten, E Schurch, N P Land 1987
• EASTMAN INTERDENTAL BLEEDING INDEX- Abrams K, Caton J, Polson A 1984
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58. • BLEEDING POINT INDEX Lenox and Kopczyk
• Determines presence/absence of bleeding interproximally on facial and lingual
surfaces
• Probe is drawn horizontally through crevice and gingiva is examined for bleeding
after 30 sec
• GINGIVAL BLEEDING INDEX Ainamo and Bay
• Presence/absence of bleeding determined by gentle probing of crevice
• Appearance of bleeding within 10 sec indicates a positive score
expressed as a percentage of total no of gingival margins examined
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59. • INTERDENTAL BLEEDING INDEX Catson and Polson
• Utilizes a triangular shaped toothpick made of soft pliable wood to stimulate
interproximal gingival tissue
• Interproximal cleaner :inserted horizontally between teeth from facial surface
depressing papilla by 2mm
• Wooden cleaner: inserted and removed 4 times
• Presence/absence of bleeding within 15 secs is noted
• score = no of bleeding sites/no of sites evaluated
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60. • CHRONIC AND RECURRENT BLEEDING:
• The most common cause of abnormal gingival bleeding on probing is chronic
inflammation. (Milne AM 1967)
• The bleeding is chronic and recurrent and is provoked by mechanical trauma (eg.
from tooth brushing, toothpicks, or food impaction) or by biting into solid foods such
as apples.
• The severity of the bleeding and the ease of its provocation depend on the intensity
of the inflammation.
• After the vessels are damaged and ruptured, interrelated mechanisms induce
hemostasis. (Stefanini M, Dameshek W 1962)
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61. • The vessel walls contract, and blood flow is diminished; blood platelets adhere to the
edges of the tissue; and a fibrous clot is formed, which contracts and results in
approximation of the edges of the injured area.
• Bleeding recurs when the area is irritated. In cases of moderate or advanced
periodontitis, the presence of bleeding on probing is considered a sign of active tissue
destruction.
• In gingival inflammation, histopathology alterations that result in abnormal gingival
bleeding include dilation and engorgement of the capillaries and thinning or ulceration
of the sulcular epithelium.
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62. • Sites that bleed on probing have a greater area of inflamed connective
tissue (i.e., cell-rich, collagen-poor tissue) than sites that do not bleed.
• In most cases the cellular infiltrate of sites that bleed on probing is
predominantly lymphocytic (a characteristic of stage II, or early, gingivitis).
(Amato, Catson, Polson 1986)
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63. • ACUTE BLEEDING
• Acute episodes of gingival bleeding are caused by injury and can occur
spontaneously in gingival disease.
• Laceration of the gingiva by toothbrush bristles during aggressive tooth brushing or
by sharp pieces of hard food can cause gingival bleeding even in the absence of
gingival disease.
• Gingival burns from hot foods or chemicals increase the ease of gingival bleeding.
• Spontaneous bleeding or bleeding on slight provocation can occur in acute
necrotizing ulcerative gingivitis.
• In this condition, engorged blood vessels in the inflamed connective tissue are
exposed by ulceration of the necrotic surface epithelium.
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64. • GINGIVAL BLEEDING ASSOCIATED WITH SYSTEMIC CHANGES
• In some systemic disorders, gingival hemorrhage occurs spontaneously or after
irritation and is excessive and difficult to control.
• These hemorrhagic diseases represent a wide variety of conditions that vary in
etiologic factors and clinical manifestations.
• Such conditions have the common feature of a hemostatic mechanism failure and
result in abnormal bleeding in the skin, internal organs, and other tissues, including
the oral mucosa. (Sodeman WA 1985)
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65. • Hemorrhagic disorders in which abnormal gingival bleeding is encountered include
• Vascular abnormalities: – vitamin C deficiency or allergy, e.g., Schonlein- 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
• Post rubella purpura.
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66. • • The effects of hormonal replacement therapy, oral contraceptives, pregnancy, and
the menstrual cycle are also reported to affect gingival bleeding. (Payne, Maze
1999)
• In addition, changes in androgenic hormones have long been established as
significant modifying factors in gingivitis, especially among adolescents.
• Several reports have shown notable effects of fluctuating estrogen/progesterone
levels on the periodontium, starting as early as puberty. (Addy M et al 1994)
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67. • Among pathologic endocrine changes, diabetes is an endocrine
condition with a well-characterized effect on gingivitis. (Tatakis DN
et al 1994)
• Several medications have also been found to have adverse effects
on the gingiva. For example, anticonvulsants, antihypertensive
calcium channel blockers, and the immunosuppressant drugs are
known to cause gingival enlargement, which secondarily can cause
gingival bleeding.
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68. • The American Heart Association has recommended over the
counter aspirin as a therapeutic agent for cardiovascular disease,
and aspirin is often prescribed for rheumatoid arthritis, osteoarthritis,
rheumatic fever, and other inflammatory joint diseases. (Hennekens
CH et al 1997)
• Thus it is important to consider aspirin's effect on bleeding during a
routine dental examination to avoid false-positive readings, which
could result in an inaccurate patient diagnosis
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70. • CHANGES IN SIZE OF THE GINGIVA
Healthy
Normal (not enlarged)
Fits snugly around the tooth
Underlying factors:
Total of the bulk of cellular & intercellular elements & their vascular supply.
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71. Disease
Increased size
Factors responsible
Edematous: inflammatory fluid
cellular exudate
vascular engourgement
hemorrhage
Fibrotic: new collagen fibers
Disease condition
• Gingival enlargement
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72. • CHANGES IN EXUDATE OF THE GINGIVA
Healthy
No exudate expressed on pressure
Disease
White fluid, pus, visible on digital pressure
Amount not related to pocket depth
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73. • Factors responsible
• Inflammation in the connective tissue
• Excessive accumulation of white blood cells with serum & tissue makes up the
exudate (pus)
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74. • CONCLUSION
• Establish a proper diagnosis based on clinical findings…..
• Proper management…phase I…
• Prevention of periodontitis….
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75. • REFERENCES
• Clinical Periodontology- Carranza’s 13th edition
• Essential Pathology – Harsh Mohan 3rd edition
• Oral history- Antonio Nanci Ten Cate’s
• Clinical Periodontalogy and implant dentistry- Jan Lindhe 5th edition.
• Gingival pigmentation: a review and case report Ruth L., Int J Dent Health Sci
2017; 4(1):173-185
• The gingival tissues: the architecture of periodontal protection. Periodontology
2000, vol. 13, 1997, 91-120. 119
• Monitoring disease during supportive periodontal treatment by bleeding on
probing. Periodontology 2000, vol. 12, 1996, 4448 120
• William, Roy et al, Histopathologic features of the initial and early stages of
experimental gingivitis in man. J. Periodonlal Res1975;10:51-64.
• Page RC, Gingivitis. J Clin Periodontol 1986;13: 345-355.
• Richard R. Ranney, Discussion: Pathogenesis of gingivitis. J Clin Periodontol
1986;13: 356-359.
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