Gingivitis is defined as the inflammation of gingival tissue.Gingival inflammation has two components: the acute inflammatory component, with vasodilation, edema, and polymorphonuclear infiltration, and the chronic inflammatory component, with B and T lymphocytes and capillary proliferation forming a granulomatous response.

1. BY- OINAM MONICA DEVI

2.  Clinically Healthy Gingiva
 Gingival Inflammation
 Etiology
 Classification
 Characteristic of Plaque- Induced Gingivitis
 Course and Duration
 Distribution
 Experimental Gingivitis
 Stages of Gingivitis
 Clinical Features of Gingivitis
 Bleeding on Probing
 Color Changes in Gingiva
 Changes in Gingival Consistency
 Changes in Gingival Surface Texture
 Changes in Gingival Position
 Changes in Gingival Contour
 Clinical Relevance of Bleeding on Probing
 Reference

3.  The clinically healthy gingiva
consistently features a small infiltrate
of inflammatory cells that involves both
the junctional epithelium and the
subjacent connective tissue (Page &
Schroeder 1976).
 This inflammatory reaction occurs in
response to the continuous presence of
bacterial products in the crevice region.
 The small inflammatory lesion also
harbors lymphocytes and macrophages.
Carranza 3rd SA Ed

4.  Transudates and exudates of fluid that contains varying amounts of
plasma proteins leave the vessels of the dentogingival plexus and arrive
in the gingival crevice region as the gingival crevicular fluid (GCF).
 Among the leukocytes, neutrophils cells (PMN), predominate in the
crevice region (sulcus) and appear to migrate continuously through the
junctional epithelium into the crevice .

5. Sites with clinically healthy gingiva appear to deal with continuous microbial
challenges without progressing to clinical gingivitis probably because of
several defensive factors that include:
1. The intact barrier provided by the junctional epithelium.
2. The regular shedding of epithelial cells into the oral cavity.
3. The positive flow of fluid to the gingival crevice which may wash away
unattached microorganisms and noxious products.
4. The presence of antibodies in GCF to microbial products.
5. The phagocytic function of neutrophils and macrophages.
6. The detrimental effect of complement on the microbiota.

6.  Gingivitis will follow if there is sufficient plaque accumulation and
retention such that microbial products evoke a more substantive
inflammatory response.
 Lesions characteristic of gingivitis occupy a larger volume and present with
pronounced loss of collagen than those in clinically healthy gingiva.
 Gingival lesions may persist for many years without concomitant loss of
periodontal attachment, destruction of periodontal ligament or evidence of
bone loss.
 Individuals with obvious defects of the inflammatory system, e.g.
neutrophil depletion or dysfunction, may rapidly develop advanced
periodontitis.

7. Definition-
Genco in 1990 stated, “gingivitis is inflammation of the gingiva in which the
junctional epithelium remains attached to the tooth at its original level”.

8.  The most common cause of gingivitis is poor oral hygiene.
 Plaque-induced gingival disease is the result of an interaction between the
microorganisms found in the dental plaque biofilm and the tissues and
inflammatory cells of the host.
Local factors:
Dental calculus
Malocclusions
Faulty dental
restorations
Tooth anatomic
factors
Systemic factors:
Endocrine changes
associated with
puberty
Menstrual cycle
Pregnancy
Diabetes
Medications:
Cyclosporine
Amlodipine
Calcium-channel blocker
Phenytoin
Gingivitis can be altered by the effects of

10. 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
Carranza, 11th Ed

11. Acute gingivitis:
 Sudden onset
 Short duration
 Painful
Chronic gingivitis:
 Fluctuating disease
 Slow onset
 Long duration
 Painless, unless complicated by acute or sub acute exacerbations
Recurrent gingivitis:
 Reappears after having been eliminated by treatment or disappeared
spontaneously

12.  Localized gingivitis is confined to the gingiva of a single tooth or group of
teeth.
 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.
 Diffuse gingivitis affects the gingival margin, the attached gingiva, and the
interdental papillae. (Glickman 1953)

13. Generalized marginal gingivitis
in the upper jaw with areas of
diffuse gingivitis
Localized, diffuse , intensely red area
facial of 12
Generalized papillary gingivitis
Generalized marginal and
papillary gingivitis
Generalized diffuse gingivitis
involves the marginal, papillary, and
attached gingiva
Carranza, 11th Ed

14. SUBJECTS- all healthy individuals living on an adequate diet
Nine first-year clinical students
One teacher in periodontology
Two laboratory technicians
The mean age of the group was twenty-three years

15. Results
PLAQUE INDEX
GINGIVAL INDEX

16. First phase Immediately after the beginning of the
experiment
Drastic increase of the
coccal flora
Second phase Started two to four days after tooth
cleansing had been abolished
Preponderance of filamentous
forms and slender rods,
Last stage Started six to ten days after tooth
cleansing had ceased
Presence of vibrios and
spirochetes

17. In 1976, Page and Schroeder divided the progressing lesion in the
gingival/periodontal tissues into four stages:
1. Initial
2. Early
3. Established
4. Advanced
 Initial and early lesion characterize the histopathology of clinically healthy
gingiva and early stages of gingivitis
 Established lesion featured “chronic” gingivitis.
 Advanced lesion reflect the phase when gingivitis progressed to periodontitis
and consistently associated with attachment and bone loss.

18.  The first manifestations of
gingival inflammation are
vascular changes consisting
essentially of dilation of
capillaries and increased blood
flow.
Clinically:
 This initial response of the
gingiva to bacterial plaque is not
apparent.
Lindhe, 6th Ed

19. Changes in blood vessel morphologic features
Dilation of the arterioles, capillaries, and venules of the vascular network
becomes a prominent feature.
Within 24 hours marked changes are evident in the dentogingival plexus
as more blood is brought to the area.
Classic features of acute inflammation seen in connective tissue beneath
the junctional epithelium.
Inflammation soon develops as plaque is formed on the gingival margin.
Microscopically

21.  Lymphocytes are retained in the connective tissues on contact with
antigens, cytokines or adhesion molecules and are not so readily lost through
the junctional epithelium and into the oral cavity, as are PMNs.
 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 latter occurs, an infiltrate of macrophages and lymphoid cells appears within
a few days.

22. Stage II Gingivitis : The Early
Lesion
 Early lesion evolves from the initial lesion within
1 week after beginning of plaque accumulation.
 Clinically it may appear as early gingivitis &
overlaps with and evolves from the initial lesion
with no clear-cut dividing line.
 As time goes, clinical signs of erythema may
appear, mainly because of proliferation of
capillaries and increased formation of capillary
loops between rete pegs.
 Bleeding on probing may also be evident.
Carranza 3rd SA Ed

23. Microscopic:
 The vessels in the dentogingival plexus remain dilated, but their numbers
increase due to the opening up of previously inactive capillary beds.
 The increased size and enhanced numbers of vascular units are reflected in
increased redness of the marginal gingiva that is a characteristic clinical
symptom during this phase.
 Microscopic examination of the gingiva reveals a leukocyte infiltration in the
connective tissue beneath the junctional epithelium, consisting mainly of
lymphocytes (75% with the majority T cells).
 Also composed of some migrating neutrophils, as well as macrophages, plasma
cells, and mast cells.

24. PMNs in response to chemotactic stimuli from plaque components
• Leave the blood vessels
Travel to the epithelium, cross basement lamina, & emerge into the pocket area
PMNs are attracted to bacteria and engulf them in the process of phagocytosis
Release lysosomes in association with ingestion of bacteria
Fibroblasts show cytotoxic alterations, with decreased capacity for collagen
production
Permits more leukocyte infiltration (Page & Schroeder 1976; Takahashi et al. 1995)

25.  Gingival fluid flow and numbers of transmigrating leukocytes reach their
maximum between 6 and 12 days after onset of clinical gingivitis.
 Amount of collagen destruction increases.
 70% - collagen is destroyed around the cellular infiltrate.
 The main fiber groups affected appear to be the Circular and Dentogingival
fiber assemblies.
 Alterations in blood vessel morphologic features and vascular bed patterns.

26. The junctional epithelium- densely infiltrated with neutrophils, as does the gingival
sulcus
Rete pegs develop and invades the coronal portion of the lesion in the connective
tissue
Represents an attempt by the body to enhance the “mechanical” barrier to plaque
bacteria and their products
A niche between the epithelium and the enamel surface and a subgingival biofilm
may now form
This so-called early lesion may persist for long periods
Variability in time required to produce an established lesion may reflect variance in
susceptibility between subjects

27. The early gingival lesion: a sign of immune recognition? (Schroeder H,
Listgarten et.al, 1997)
1. Post-capillary venules of junctional epithelium assume the characteristics of
high endothelial venules which serve for homing and entry of T-lymphocytes
into the connective tissue.
2. The early gingival lesion may represent a transient lymphoid tissue, rather than
a leukocyte infiltration including various T-cell subsets, high endothelial
venules, antigen-presenting cells such as activated macrophages and possibly
interdigitating cells.
 Consequently, the leukocyte accumulation in junctional epithelium and the
innermost connective tissue of the gingiva in children and young adolescents
should not be regarded unequivocally as a first step toward severe gingivitis
and periodontitis, but rather as a normal constituent of the host defense
system, not associated with a destructive process.

28. Stage III Gingivitis : The
Established Lesion
 Over time, the established lesion evolves
 Characterized by a predominance of
plasma cells B lymphocytes in conjunction
with the creation of a small gingival
pocket lined with a pocket epithelium
(Schroeder HE et al 1975)
 The B cells - predominantly of
immunoglobulin G1 (IgG1) and G3
(IgG3) subclasses (Page RC 1986)
Carranza 3rd SA Ed

29.  In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of
plaque accumulation, blood vessels- engorged and congested,
venous return- impaired
blood flow - sluggish
Localized gingival anoxemia, which superimposes a Bluish hue on the
reddened gingiva
 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.

30. • The predominance of plasma cells is thought to be a primary characteristic
of the established lesion.
• The time for the development of the classic "established lesion" may
exceed 6 months.
• Inverse relationship exist between the number of intact collagen bundles
and the number of inflammatory cells.
• Collagenolytic activity is increased in inflamed gingival tissue.

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

32. • Collagenase is normally present in gingival tissues and is produced by
some oral bacteria and by PMNs.
• Collagen loss continues as the inflammatory cell infiltrate expands,
resulting in collagen-depleted spaces extending deeper into the tissues,
which then become available for infiltration and accumulation of
leukocytes.

33.  Enzyme histochemistry studies have shown that chronically inflamed
gingivae have elevated levels of acid and alkaline phosphatase, ß-
glucuronidase, ß-glucosidase, ß-galactosidase, esterases, aminopeptidase and
cytochrome oxidase.
 Neutral mucopolysaccharide levels are decreased, presumably as a result of
degradation of the ground substances
TWO TYPES :
(Lovdal A et al 1958, Mori M et al 1961,Sumoi JD, Smith LW et al 1971)
 Some remain stable and do not progress for months or years.
 Others become more active and convert to progressively destructive lesions.

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

35.  The junctional epithelium is substituted by a pocket epithelium that is not
attached to the tooth surface.
 This allows for a further apical migration of the biofilm.
 The pocket epithelium harbors large numbers of leukocytes, predominantly
PMNs.
 In comparison to the original junctional epithelium, the pocket epithelium is
more permeable to the passage of substances into and out of the underlying
connective tissue.
 This pocket epithelium may be ulcerated in places.

36. Features of the Established Lesion
1. Persistence of the manifestations of acute inflammation.
2. Predominance of plasma cells but without appreciable bone loss.
3. Persistence of immunoglobulins extravascularly in the connective tissues and
junctional epithelium.
4. Continuing loss of connective tissue substance noted in the early lesion.
5. Proliferation, apical migration, and lateral extension of the junctional
epithelium, early pocket formation may or may not take place.

37. Stage IV Gingivitis : The Advanced Lesion
 Extension of the lesion into alveolar bone characterizes a fourth stage known
as the advanced lesion.
 Gingivitis Periodontitis only in individuals who are susceptible

38. Microscopically:
 Fibrosis of the gingiva
 Widespread manifestations of inflammatory & immunopathologic tissue damage
 Plasma cells continue to dominate the connective tissues
 Neutrophils continue to dominate the junctional epithelium and gingival crevice
 As the pocket deepens, the gingival tissues offer reduced resistance to
periodontal probing
 The advanced lesion has many of the characteristics of the established lesion but
differs importantly in that loss of connective tissue attachment and alveolar bone

39. Features of the Advanced Lesion
1. Persistence of features described for the established lesion.
2. Extension of the lesion into alveolar bone and periodontal ligament, with
significant bone loss.
3. Continued loss of collagen subjacent to the pocket epithelium with fibrosis at
more distant sites.
4. Presence of cytopathically altered plasma cells.
5. Formation of periodontal pockets.
6. Widespread manifestations of inflammatory and immunopathologic tissue
reactions.

40. Clinical signs:
• Redness and sponginess of the gingival tissue
• Bleeding on provocation
• Changes in contour
• Consistency
• Position
• Presence of calculus or plaque with no
radiographic evidence of crestal bone loss.
The two earliest signs of gingival inflammation preceding established gingivitis
are
(1) Increased gingival crevicular fluid production rate
(2) Bleeding from the gingival sulcus on gentle probing
Carranza 11th Ed

41.  Varies in severity, duration, and ease of provocation.
 Easily detected clinically and therefore is of value for the early diagnosis
and prevention of more advanced gingivitis.
 It appears earlier than a change in color or other visual signs of
inflammation
 It is a more objective sign that requires less subjective estimation by the
examiner.
Bleeding on Probing

42.  Longitudinal findings revealed that sites with consistent bleeding (gingival
index [GI] = 2) had 70% more attachment loss than sites that were non-
inflamed over a 26-year .
 Thus persistent gingivitis can be considered as a risk factor for periodontal
attachment loss that may lead to tooth loss.
 Many 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).
 Increase in gingival bleeding is associated with smoking cessation.

43. Contributing factors to plaque retention that may lead to gingivitis include
1. Anatomic and developmental tooth variations
2. Caries
3. Frenum pull
4. Iatrogenic factors
5. Mal-positioned teeth
6. Mouth breathing
7. Overhangs
8. Faulty partial dentures
9. Lack of attached gingiva
10. Gingival recession
11. Orthodontic treatment and fixed retainers were associated with increased
plaque retention and increased bleeding on probing

44.  The most common cause of abnormal gingival bleeding on probing is
chronic inflammation.
 Provoked by mechanical trauma or by biting into solid foods such as
apples.
 Sites that bleed on probing have a greater area of inflamed connective
tissue than sites that do not bleed.
 Histopathologic alterations include dilation and engorgement of the
capillaries and thinning or ulceration of the sulcular epithelium.
 In most cases the cellular infiltrate of sites that bleed on probing is
predominantly lymphocytic.

45. After the vessels are damaged and rupture
A complex of mechanisms induce hemostasis
The vessel walls contract
Blood flow is diminished
Blood platelets adhere to the edges of the tissue
Fibrous clot is formed
Contracts and results in approximation of the edges of the injured area
 Bleeding recurs, however, 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.

46.  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
 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.

47. In some systemic disorders, gingival hemorrhage occurs spontaneously or
after irritation and is excessive and difficult to control.
A. Hemorrhagic disorders
B. Medication
C. Hormonal changes
 These hemorrhagic diseases represent a wide variety of conditions that vary
in etiologic factors and clinical manifestations.

48. Vascular abnormalities
 Vitamin C deficiency
 Allergy e.g., Schonlein-
Henoch purpura
Platelet disorders :
 Thrombocytopenic purpura,
 Hypoprothrombinemia ,
Vitamin K deficiency
Other coagulation defects
• Hemophilia,
• Leukemia,
• Christmas disease,
• Multiple myeloma
A. Hemorrhagic Disorders

49. B. Medications-
Bleeding may follow the administration of excessive amounts of drugs such as
 Salicylates
 Anticoagulants ( dicumarol and heparin)
Aspirin
• Interferes with normal platelet aggregation and can result in prolonged bleeding.
• The effects of aspirin last at least 4 to 7 days.
• Higher doses (>325 mg) may increase bleeding time and predispose the patient to
postoperative bleeding.
• It is important to consider aspirin’s effect on bleeding, during a routine dental
examination to avoid false positive readings.
Kim et.al. 2007 measured the effect of aspirin on gingival crevicular fluid levels
of inflammatory and anti-inflammatory mediators in patients with gingivitis. They
concluded that aspirin can have an affect on BOP in naturally occurring gingivitis
patient

50.  The effects of oral contraceptives, pregnancy, and the menstrual cycle
are also reported to affect gingival bleeding.
 Changes in androgenic hormones are 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
 Among pathologic endocrine changes, diabetes is an endocrine
condition with a well-characterized effect on gingivitis.
C. Hormonal replacement therapy

51.  It 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.
 The color of the gingiva is determined by several factors, including
1. The number and size of blood vessels
2. Epithelial thickness
3. Quantity of keratinization
4. Pigments within the epithelium

52.  Color changes may be marginal, diffuse, or patch like, depending on the
underlying acute condition.
1. In ANUG, the involvement is marginal
2. In herpetic gingivostomatitis, it is diffuse
3. In acute reactions to chemical irritation, it is patch like or diffuse.
 Color changes vary with the intensity of the inflammation.
 Initially, there is an increase in erythema. If the condition does not worsen,
this is the only color change until the gingiva reverts to normal.
 In severe acute inflammation, the red color gradually becomes a dull, whitish
gray.
 The gray discoloration produced by tissue necrosis is demarcated from the
adjacent gingiva by a thin, sharply defined erythematous zone.

53.  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.
 Venous stasis will contribute a bluish hue.
 The changes start in the interdental papillae and gingival margin and spread
to the attached gingiva.
 Proper diagnosis and treatment require an understanding of the tissue
changes that alter the color of the gingiva at the clinical level.
Colour Changes in Chronic Gingivitis

54.  Heavy metals 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.
 Lead Produces a bluish red or deep blue linear pigmentation of the gingival
margin (Burtonian line).
 Exposure to silver - a violet line accompanied by a diffuse bluish grey
discoloration in throughout the oral mucosa (Argyria).

55. Bismuth gingivitis.linear black
discoloration of the gingiva in
apatient receiving bismuth therapy.
Discoloration of the gingiva
caused by embedded metal
particles (amalgam).
Carranza 11th Ed

56.  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.
 Pigmentation can be eliminated by treating the inflammatory changes
without necessarily discontinuing the metal containing medication.
 Mucosal areas irritated by biting or abnormal chewing habits are common
sites of pigmentation

57.  Many systemic diseases may cause color changes in the oral mucosa, including
the gingiva.
 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:
1. Addison’s disease produces isolated patches of discoloration varying from
bluish black to brown.
2. Peutz-Jeghers syndrome produces melanin pigmentation in the oral mucosa and
lips.
3. Albright’s syndrome and Von Recklinghausen's disease produce areas of oral
melanin pigmentation.

58.  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 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.

59.  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.
 Most pigmentation is caused by five primary pigments. These include:
1. Melanin
2. Melanoid
3. Oxyhemoglobin
4. Reduced haemoglobin
5. Carotene
6. Others are caused by bilirubin and iron.

60.  Melanin is a non-hemoglobin derived brown pigment.
 It is responsible for the normal pigmentation of the skin, gingiva and
remainder of the oral mucosa.
 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:
1. Gingiva:- 60%
2. Hard palate:- 61%
3. Mucous membrane:- 22%
4. 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.

61. The Dummet Oral Pigmentation Index (DOPI) Assessment ( Dummet 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)

62.  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
Carranza 11th Ed

63. Acute form of Gingivitis
1. Diffuse puffiness and softening
2. Sloughing with grayish, flaklike particles of debris adhering to eroded
surface
3. Vesicle formation
Chronic Gingivitis
1. Soggy puffiness that pits on pressure
2. Marked softness and friability, with ready fragmentation on exploration
with probe and pinpoint surface areas of redness and desquamation.

64.  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.
 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.

65. Tooth brushing has various effects on the consistency of the gingiva, such as
1. Promote keratinization of the oral epithelium
2. Enhance capillary gingival circulation
3. Thickening of alveolar bone.
• 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.

66.  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 sub-papillary 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.

67.  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.
 Peeling of the surface occurs in chronic desquamative gingivitis.
 Hyperkeratosis results in a leathery texture.
 Drug-induced gingival overgrowth produces a nodular surface.

69.  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.
 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.

70.  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.

71.  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
 The prevalence, extent, and severity of gingival recession increase with age
and are more prevalent in males.
 POSITION OF GINGIVA- By clinical definition, recession is 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.

72. 72
 In periodontal disease, the inflamed
pocket wall covers part of the
denuded root; thus some of the
recession is hidden, and some may
be visible. The total amount of
recession is the sum of the two.
Recession refers to the location of the
gingiva, not its condition.
 Receded gingiva can be inflamed
but may be normal except for its
position. Recession may be
localized to one tooth or a group of
teeth, or it may be generalized
throughout the mouth.
• The actual position is the level of the epithelial attachment on the tooth,
• 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.

73.  Gingival recession increases with age
 Incidence varies from 8% in children to 100% after age 50 years.
 The gradual apical shift may be 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.
 Etiologic factors implicated in gingival recession:
1. Faulty tooth-brushing technique (gingival abrasion)
2. Tooth malposition
3. Friction from soft tissues (gingival ablation)
4. Gingival inflammation
5. Abnormal frenum attachment
6. Iatrogenic dentistry

74. 1. Faulty tooth brushing technique or brushing with hard bristles may cause
significant injury.
 Lacerations, abrasions, keratosis, and recession with the facial marginal
gingiva most affected.
 Amonf these, recession tends to be more frequent and severe in patients with
clinically healthy gingiva, little bacterial plaque, and good oral hygiene.
2. 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.

75. 3. 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.
4.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.
 There is general agreement that placing restorative margins within the
biologic width frequently leads to gingival inflammation, clinical
attachment loss, and eventually, bone loss.

76.  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.

77. Stillman’s Clefts
 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.
 Originally described by Stillman PR
1921 and considered to be the result of
occlusal trauma.
 The clefts may repair spontaneously or
persist as surface lesions of deep
periodontal pockets that penetrate into
the supporting tissues.
Carranza 11th Ed

78.  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.
Carranza 10th Ed

79.  It 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 and implies a low risk of future clinical
attachment loss.
Clinical Relevance of Bleeding on Probing
Carranza 11th Ed
Mild edematous gingivitis; a probe
has been introduced to the bottom of
the gingival sulcus
Bleeding appears after a few
seconds

80.  Probing pocket depth measurements by themselves are of limited value for
the assessment of the extent and severity of gingivitis.
 For example, gingival recession may result in reduction of the probing depth
and thus cause an inaccurate assessment of the periodontal status
 So, bleeding on probing is widely used by clinicians and epidemiologists to
measure
1. Disease prevalence and progression
2. Outcomes of treatment
3. To motivate patients with their home care

81. Bleeding on probing address two different levels of risk for disease progression:
1. The percentage of sites within a dentition for which BOP may provide information on
the subject’s risk for disease progression.
2. The dichotomous evaluation of whether or not a single tooth site BOP may provide
information on the local risk assessment at a given tooth site.
 Both of these are valuable diagnostic tests during supportive periodontal treatment.
The results indicated that pockets with a probing depth of ≥ 5 mm had a significantly
higher incidence of bleeding on probing.
Patients with 16% or more bleeding on probing sites had a higher chance of loosing
attachment than patients with<l6% bleeding on probing.

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 Essential Pathology – Harsh Mohan 3rd edition
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 William, Roy et al, Histopathologic features of the initial and early stages of experimental
gingivitis in man. J. Periodonlal Res.1975;10:51-64.
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