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clinical features of gingivitis.pdf
1.
2.
3. INTRODUCTION
Experimental gingivitis studies provide the first empiric evidence that
accumulation of on clean tooth surface result in development of an
inflammatory process around the gingival tissue (Loe H 1965).
Research has shown that local inflammation will persist as long as the
microbial biofilm will persist along the adjacent to the gingival tissue,
and that the inflammation will resolve subsequent to meticulous
removal of the biofilm( Silness J, Loe H 1964).
4. The prevalence of gingivitis is evident worldwide. Epidemiologist studies
indicate more than 82% of US adolescents having overt gingivitis and
sign of gingival bleeding.
In general, clinical feature may be characterize by the presence of
following clinical sign: redness and sponginess of the gingival tissue,
bleeding on provocation , change in contour and presence of calculus or
plaque with no radiographic evidence of crestal bone loss
5. GINGIVITIS CLASSIFICATION
COURSE AND DURATION
Acute Gingivitis: Sudden onset and short duration and can be painful.
Subacute: A less severe form of the acute condition.
Recurrent Gingivitis: It reappears after having been eliminated by
treatment or disappearing spontaneously.
6. Chronic gingivitis: Slow in onset, is of long duration, and is painless
unless complicated by acute or subacute exacarbations.
It is the most commonly encountered.
8. DISTRIBUTION
Localized : Confined to the gingival of a single tooth or group of teeth.
Generalized : It involves the entire mouth.
Marginal : Involves the gingival margin and may include a portion of the
contiguous attached gingival
9. Papillary : Involves the Interdental papillae and often extends into the
adjacent portion of the gingival margin. Papillae are involved more
frequently than the gingival margin, and the earliest signs of gingivitis
often occurs in the papillae.
Diffuse : Affects the gingival margin, the attached gingival and the
interdental papillae.
10. The distribution of gingival disease in individual cases is described by
combining the preceding terms as follows :
Localised marginal gingivitis : confined to one or more areas of
marginal gingival.
Localized diffuse gingivitis : Extends from the margin to the
mucobuccal fold but is limited in the area.
Localized papillary gingivitis : It is confined to one or more
interdental spaces in a limited area.
12. Generalized marginal gingivitis : It involves the gingival margin in
relation to all teeth. The interdental papillae are usually effected in
generalized marginal gingivitis.
Generalized diffuse gingivitis : It involves the entire gingival. The
alveolar mucosa and attached gingival are affected, so the muco gingival
junction is sometimes obliterated.
Systemic condition can be involved in the cause of generalized diffuse
gingivitis and should be evaluated if suspected as an etiology co-factor.
17. GINGIVAL BLEEDING ON PROBING
The two earliest signs of gingival inflammation preceding established
gingivitis are–
Increased gingival crevicular fluid production rate.
Bleeding from the gingival sulcus on gentle probing
18. Gingival bleeding varies in severity, duration, and ease of
provocation.
Bleeding on probing is easily detected clinically and therefore is of
value for the early diagnosis and prevention of more advanced
gingivitis
Bleeding on probing appears earlier than a change in color or other
visual signs of inflammation
20. LOCAL FACTORS :
Contributing factors to plaque retention that may lead to gingivitis include
anatomic and developmental tooth variations, caries, frenum pull,
iatrogenic factors, malpositioned teeth, mouth breathing,
overhangs, partial dentures, lack of attached gingival and recession.
21. Chronic and recurrent bleeding :
The most common cause of abnormal gingival bleeding on probing is
chronic inflammation.
The bleeding is chronic or recurrent and is provoked by mechanical
trauma (eg from tooth brushing, toothpicks, food impaction) or by
biting into solid food such as apples.
22. Acute episodes of gingival bleeding are caused by injury and can occur
spontaneously in gingival disease.
Laceration of the gingiva by tooth brush 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 case of gingival
bleeding.
23. Spontaneous 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.
24. Site that bleed on probing have greater area of inflamed connective
tissue ( cell rich, collagen poor tissue) than site that do not bleed.
The severity of the bleeding and the ease of its provocation and on the
intensity of the inflammation.
After the vessel walls are damaged and ruptured, interrelated
mechanism induce hemostasis, the vessel wall contract, the blood flow
is diminished; blood platelets adhere to the edges of the tissue, and a
fibrous clot is formed, which contracts and result in approximation of
edges of the injured area.
Bleeding recurs when the area is irritated.
25. SYSTEMIC CAUSES
In some systemic disorders gingival harmony occurs spontaneously or
after irritation and is and difficult to control.
Such condition have common feature of a hemostatic mechanism
failure and result in abnormal bleeding in skin, internal organ, tissue
including oral mucosa.
26. 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.
Hemorrhagic disorders
Vascular abnormalities
Vitamin C deficiency.
Platelet disorder
Thrombocytopenia purpura.
28. Anticoagulents
Heparin
Effect of hormonal replacement therapy,oral contraceptive, pregnancy
menstrual cycle.
Hyprothrombinemia
Vitamin K deficiency.
Poor General health
Nutritional status.
29. HISTOPATHOLOGY OF GINGIVAL BLEEDING
Injurious agents - Initiate inflammation
Increase permeability of sulcus epithelium
by degrading inter cellular cementing substance
and widening the intercellular spaces.
As inflammation become chronic:
Sulcus epithelium undergoes ulceration, cellular and fluid exudates and
proliferation of new blood vessels, create pressure upon the epithelium on
the crest and external surface of the marginal and interdental gingiva.
33. Vitimin K: it is fat soluble, dietary principle required for the synthesis
of clotting factors.
Damm ( 1929) produced bleeding disorder in chicken by feeding
deficient diet. This was later found to be due to decrease concentration
of prothrombin in blood that could be cured by taking fat soluble
fraction of hogs liver. That was latter called KOAGULATION
VITAMIN( vit K)
34. Daily requirement: 3-10µg/day
Utilization: vit K is absorbed from intestine via lymph and required bile
salts for absorption while water soluble are absorbed directly into
portal blood.
35. Action of vit K
Vit K acts as co-factor at a late stage in the synthesis by liver of
coagulation protein – prothrombin factor vii, ix and x.
36. Local hemostatics ( STYPTICS)
These agents are used to stop bleeding from local approachable sites.
Thrombin: obtain from bovine plasma , it is applied as dry powder. Used
in haemophillia.
Fibrin: obtain from human plasma and is dried. Sheets or foams for
covering bleeding sites.
Gelatin foam: spongy gelatin available in various shapes. It is moistened
with saline or thrombine. Get absorbe in 1-2 months
37. Russels viper venoms: applied locally it acts as thromboplastin.
Vasoconstriction: like 1% of Adr is used , stops epitaxis and other
bleeding.
38. Astringent :like tannic acid ( 20 % in glycerine) used in bleeding
gums.
Astringents are the substance that precipitate protein but do not
penetrate cells thus affecting superficial layer.
Mineral astringent: heavy metal ions are astringent and antiseptics.
Alum has been used as after shave and local haemostatic on minor cuts
39. Indices used for assessment of
gingival bleeding:
1) Sulcus bleeding index
2) Papillary bleeding index
3) Gingival bleeding index
4) Modified sulcular bleeding index
40. Sulcus Bleeding Index
Given by Muhlemann HR and Son S in 1971
Fourgingival units are scored labial and lingual marginal gingiva(M)
and mesial and distal papilla gingiva (P) unit.
41. Scoring criteria
0 Healthy appearance of P and M. No
bleeding
1 Healthy appearance of P and M, no
change in color, contour and no edema
but bleeding from sulcus
2 Bleeding on probing and color change
cause by inflammation. No edema
3 Bleeding on probing, color change and
slight edema
42. 4 Bleeding on probing, color change,
swelling/ Bleeding on probing,
swelling obvious
5 Spontaneous bleeding on probing,
color change, marked swelling with or
with out ulceration
43. PROCEDURE:
The probe is carefully inserted to the bottom of the pocket and gently
moved laterally along the pocket wall and then wait for 30-60 sec. Then
recheck the area for the presence or absence of bleeding.
Bleeding on probing is widely used by clinicians to measure activity of
disease, progression, to measure outcomes of treatment and to motivate
patients with their home care.
44.
45.
46. Papillary bleeding index:
It was developed by Muhlemann HR in 1977.
Type of modification of sulcus bleeding index.
Performed by sweeping the papillary sulcus on mesial and distal aspect
with periodontal probe. The mouth is divided into quadrant, with
maxillary left and mand right quadrant probe bucally.
47. 0 No bleeding after probing
1 A single discreet bleeding
point appears after probing
2 Several isolated bleeding
points or a single fine line of
blood appears
3 The interdental triangle fills
the blood shortly after
probing
4 Profuse bleeding after
probing
48. Modified sulcular bleeding index
Was developed in 1987 by A. Mombelli, MA Van Oosten, E. Schurch
and N P Land.
Is a modified papillary bleeding index.
49. 0 No bleeding when
periodontal probe passes
along gingival margin
1 Isolated bleeding spot visible
2 Blood forms a confluent red
line on margine
3 Heavy or profuse bleeding
50. COLOR CHANGES IN GINGIVA :
The color of gingiva is determined by visual inspection. It depends
on several factors
number and size of blood vessels
epithelial thickness
degree of keratinization
pigments with in the epithelium
inflammation.
51. Healthy gingival usually has a color that has been
described as “Coral Pink” Other colors like red, white
and blue can signify inflammation (gingivitis).
Normal racial pigmentation makes the gingival appear
darker.
52. In acute gingival inflammation –
In ANUG – the involvement is marginal
gingiva
In herpetic gingivostomatitis – it is diffuse.
In acute reaction to chemical irritation – it is patch like
or diffuse.
53. COLOR CHANGE IN ACUTE
INFLAMMATION:
Color changes vary with intensity of inflammation
Initial bright red erythema
Severe acute Inflammation
Red – Shiny grey
Dull whitest grey
(The grey discoloration is
produced by tissue necrosis.)
54. In Chronic Inflammation
Red or bluish red color, because of vascular proliferation and reduction
of Keratinization. .
The changes start in the interdental papillae and gingival margin and
spread to the attached gingiva.
Color changes vary with the intensity of the inflammation. Initially,
there is an increase in erythema. If the condition does not worsen, the
gingiva reverts to normal.
55. MELANIN PIGMENTATION
It can be normal physiologic pigmentation and is commonly found in
highly pigmented ethic groups.
Melanin is brown black – non hemoglobin – derived pigment normally
present in hair, eye, skin and adrenal medulla: gingiva & Oral mucous
membrane.
56. Melanocytes Melanophores
Melanin is
synthesized is stored in cytoplasm
and present in granules in phagocytic cells.
basal cells of epit
helium
present in underlying dermis
Epidermis and
spinous layers
of gingival epithelium
58. PIGMENTED LESION OF THE ORAL
CAVITY
Classification:
According to cause of endogenous oral and perioral
discolorations:
Source Etiology Example of
associated
lesions
Vascular developmental,
hamartomatous
varix,
hemangioma,
lymphangioma,an
giosarcoma
62. BLUE/ PURPLE VASCULAR LESION:
Hemangioma: vascular lesions presenting as a
proliferation of vascular channels, are tumor like
hemartomas when they arise in childhood; in adult
begnin vascular proliferation is varicosities.
The clinical presentation is quite variable ranging from
flat reddish blue macule to a nodule.
Most of the oral hemangioma are located on the tongue.
63. Varix: pathological dilatation of veins or venules are varices or
varicosities and the chief site is ventral surface of tongue. Lingual
varicosities appears as tortuous serpentine blue , red, and purple
elevations that coarse over the ventrolateral surface of the tongue with
extension anteriorly.
Focal dilatation of vein is called varix.
Varix of the lip and buccal mucosa are common.
Treatment of the varix is interlesional 1% sodium tetra decyl sulfate
64. Angiosarcoma: malignant vascular neoplasm,
distinct from Kaposi sarcoma, not related with HIV.
They arise from blood or lymph or perivascular cells.
They appear red, blue or purple.
65. Hereditary hemorrhagic talangiestic: characterize by
multiple round oval purple papule measuring .5 cm.
It is genetic transmitted disease.
The lesion represent multiple microaneurysm, owing to
the weakening defect in adventitial coat of the venules.
There may be more than 100 purple papule on the
vermillion and on the mucosal surface of the lips as well
on the tongue and buccal mucosa
66. BROWN MELANOTIC LESIONS
Ephelis and oral melanotic macule
The common cutaneous freckle or Ephelis, represent
increase in melanin pigmentation synthesis by basal layer
melanocytes without increase in no of melanocytes. Ephelis
can therefore encounter on the vermillion boarder of the
lip, and lower lip being the favour site.
The intraoral counter part to the ephelis is oral melanotic
macule. This lesion are oval or irregular in out line, brown
or black and tend to occur in gingival, palate, and buccal
mucosa.
67. Once they reach a particular size they do not enlarge.
OMM is innoculous, does not represent melanotic
prolification and does not predispose to melanoma.
68.
69. Navocellular Navus and Blue Navus:
Navi are begnin prolification melanocytes.
Navocelullararise from basal layer melanocytes early in
life. They are flat, brown and have regular round outline.
With the time, the melanocytes form cluster at the
epitheliomesenchymal junction and begin to proliferates
down into connective tissue, although it do not invade
vessels or lymphatic.
70.
71. In oral cavity both navocellularand blue nevi appears
brown and may be macular or nodular.
Seen at any age and common site is palate and gingival.
72. Malignant melanoma:
In oral cavity they occur on labial gingiva and anterior
aspect of hard palate. In the early stage, oral
melanomas are macular brown black plaque with
irregular out line.
73.
74. Drug induce melanosis:
A variety of drugs can induce oral mucosal pigmentation.
The chief drug is quinolones, hydroxyquinoline, and
amodiaquine antimalarials. Minocycline used in the
treatment of acne, can produce oral pigmentation.
The cause is unknown and pigment may remain for quite
some time after with drawal of drug.
75. Café au Lait pigmentation:
In neurofibromatosis, an autosomal dominant inherited
disease, both nodular and diffuse pendulous neurofibroma
occurs on the skin and rarely in the oral cavity.
These lesion have color of coffee with cream.
Microscopically, café au lait spot represent basiler
melanosis without melanocyte prolification.
76. Smokers melanosis:
Diffuse macular melanosis of the buccal mucosa,
lateral border tongue, palate, floor of the mouth is
occasionally seen among cigarette smoker.
Pigmented lichen planus:
LP is the disease that generally present as white lesion
with variants showing red and desquamated lesions.
77.
78. Peutz-jughers syndrome:
Multiple focal melanotic brown macule are
concentrated about lips while the remaining facial skin
is less sticking involved.
The macule appears as freckle or ephelides, usually
measuring <0.5 cm in diameter.
81. Petechia:
Capillary hemorrhages will appear red initially and turn brown in few days
once the extravasated red cells have lysed and have been degraded to
hemosiderin.
Petechiae secondary to platelets deficiencies or aggregation disorder are
usually not limited to the oral mucus but occur on skin also.
82. Depigmentation: Melanin hyperpigmentation usually does not present as
a medical problem , but patients may complain their black gums are
unaesthetic.
This problem is aggravated in patients with a “gummy smile ” or excessive
gingival display while smiling. The first and foremost indication for
depigmentation is patient demand for improved esthetics.
83. Methods aimed at removing the pigment layer
A. Surgical method of de-pigmentation
1. Scalpel surgical technique.
2. Cryosurgery
3.Electrosurgery
4 Lasers
Neodymium;Aluminum-Yitrium-Garnet (Nd- YAG) lasers.
Erbium-YAG lasers.
Carbon-di-oxide CO2 laser
B Chemical methods of de pigmentation
84. Scalpel surgical technique
One of the first, and still popular, techniques to be employed was the
surgical removal of undesirable pigmentation using scalpels.
The procedure essentially involves surgical removal of gingival epithelium
along with a layer of the underlying connective tissue and allowing the
denuded connective tissue to heal by secondary intention.
The new epithelium that forms is devoid of melanin pigmentation.
85. Scraping technique
Scraping technique to remove heavy continuous band of gingival
pigmentation was performed by Manchandia (1979). He observed
repigmentation in the form of spots in 42% of the subjects
Fornoosh A.A in 1990 used a high speed hand piece and surgical
diamond bur to eliminate dark pigmentation in 20 patients.
Slight repigmentation was observed in 2 cases after 20 months post
surgical follow up.
86. He concluded that since this technique is relatively simple, versatile
and requires minimum time and effort, if repigmentation occurs, the
procedure can be repeated in the same area without limitation or
causing any permanent damage.
87. Using gingivectomy procedures
Dummett and Bolden (1963), used gingivectomy to remove pigmented gingiva. They
concluded that gingival resective procedures, if performed solely for cosmetic
reasons, offers no permanent results.
This procedure resulted with prolonged healing by secondary intention, excessive
pain and discomfort caused by exposure caused by underlining bone.
88. Cryosurgery
Cryosurgery is that branch of therapeutics which makes use of local
freezing for the controlled destruction or removal of living tissue.
Use of extreme cold as a therapeutic measure has been documented as
early as 2500 B.C.
89. The biologic effect of physical factors such as cold behave like ionizing
radiation and the maximum lethal effect is obtained when they are
applied to cells undergoing mitosis.
It was not until 1961, that a controllable system was developed to allow
controlled destruction of living tissue by freezing.
90. Cryosurgical technique
Cryosurgical apparatus are used in 2 basic technique.
Open system were, cryogen is directly sprayed on the tissues and the
closed system using cryoprobe for application on the tissues.
91. LASERS
Lasers are devices which produce beams of very high intensity light.
A large number of current and potential uses have been identified
that involves the treatment of soft tissues and modification of hard
tooth structures
The word Laser is an acronym for ‘Light amplification by stimulated
emission of radiation’.
92. A crystal or gas is excited to emit light photons of a characteristic
wavelength that are amplified and filtered to make a coherent light
beam.
The effect of laser depends upon power of the beam and the extent to
which the beam is absorbed.
There are several types available based on wavelengths.
Lasers range from long wavelengths (infrared), through visible
wavelengths, to short wavelength (ultra violet).
93. Eg;- CO2 laser, Nd :YAG, Er :YAG- Infrared, HeNe and Argon- Visible
and Excimers- ultraviolet range.
For any application it is important to select the correct wavelength for
absorption of the energy and prevention of side-effects from heat
generation.
Interaction with the substrate can occur photothermal and
photochemical reaction.
94. At low temperatures, below 100 degrees , thermal effects denature
proteins, produce hemolysis, cause coagulation, and cause
shrinkage.
Above 100 degrees , soft or hard tissues boils, producing explosive
expansion.
Above 400 degrees carbonization of organic materials is completed
with the onset of inorganic changes.
As temperature increases from 400- 1400 degrees, inorganic
constituents change in chemistry, may melt and re-crystallize, and
may vaporize.
95. CHANGE IN GINGIVAL CONTOURS –
Contour or the shape of the gingival varies considerably and depends on the
shape of the teeth and their alignment in the arch ,the location and the size of
the area of proximal contact and dimensions of facial and lingual embrasure.
The marginal gingival envelopes the teeth in collor like fashion and follows a
scalloped out line on facial and lingual surface. On teeth with pronounced
mesiodistal convexity the normal contour is accentuated and gingival is located
apically. On teeth with lingual version, gingival is horizontal and thickened.
96. Altered gingival contours can be the result of a wide range of factors.
They become clinically important if they create esthetic problems, make
plaque control difficult or interfere with function. For example gingival
enlargement is a well-known side effect of certain medication (eg
phenytoin, nifedipine, cyclosporine).
Sometimes the enlargement is due to unusual anatomic variations like
mandibular tori which can become so large that they interfere with chewing
or impede access for plaque control procedures.
97.
98. In some patients with long standing chronic periodontitis, the gingiva become firm and
enlarge in reaction to the chronic inflammation, such tissues are referred as “Fibrotic”.
In contrast to gingival enlargement due to tissue edema, fibrotic enlargements will not
disappear after scaling and root planning.
The best way to confirm that the tissue is fibrotic is to gently press on the gingiva with the
side of the periodontal probe. Unlike, the reaction of edematous tissue to this procedure,
no imprint of the probe will be left behind.
99. CHANGES IN GINGIVAL CONTOUR
Stillman’s clefts :
Apostrophe – shaped indentation extending into the
gingival margin for varying distances, the cleft
generally occurs on the facial surface. The margins of
the cleft are rolled underneath the linear gap in the
gingival and the remainder of the gingival margin is
blunt instead of knife edged.
100. Cleft
Simple Compound
(cleavage occurs in (cleavage occurs
in more
a single direction) than one
direction)
101. Etiology
Stillman in (1921) – Considered it to be a result of
occlusal trauma.
Box in (1950) – Considered to be a result of
pathologic pockets in which ulcerative process
has extended through the facial surface of the
gingiva.
The cleft :May repair spontaneously
Persist as surface lesion of deep periodontal
pockets.
102. McCall’s Festoons:
McCall’s Festoons are life preserver shaped enlargement of
the marginal gingival that occur most frequently in the
canine and PM areas on the facial surface.
In early stages color and consisting of gingival are normal.
With accumulation of food debris, lead to secondary
inflammatory changes
103.
104. CHANGES IN CONSISTENCY OF THE
GINGIVA:
Both acute and chronic inflammation produce
changes in the normal firm and resilient
(capacity of a strained body to recover its size and
shape after deformation) consistency of the
gingiva.
Recognition of gingival swelling or edema
requires that the clinician have a very clear
mental picture of the consistency of gingiva. If
there is presence of gingival edema, it is useful to
gently press the side of a periodontal probe
against the tissue for a few seconds and then
remove it.
105. At edematous site, the imprint of the probe can often
be seen.
106. 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.
In animal studies, mechanical stimulation by tooth
brushing was found to increase the proliferative
activity of the functional basal cells in dog gingiva by
2.5 times compared with using a scalar.
107. These findings may indicate that tooth brushing
causes increased turnover rate and desquamation of
the junctional epithelial surfaces. This process may
repair small breaks in the junctional epithelium and
prevent access to the underlying tissue by periodontal
pathogen.
108. Calcified mass in gingival: calcified microscopic mass
may found in gingival.
They can occur alone or in a group and vary in size,
location and shape and structure.
Such mass may be calcified material removed from tooth
and traumatically displaced into gingival during scaling,
root remnants ,cementum fragments or cementicles
(globular masses of cementum).
They are enclose in osteoid like matrix.
109. CLINICAL AND HISTOPATHOLOGIC CHANGES IN
GINGIVAL CONSISTENCY.
Clinical Changes Underlying microscopic
Features
ACUTE FORMS OF GINGIVITIS
Diffuse puffiness & softening Diffuse edema of acute inflammatory
origin, fatty infiltration in
xanthomatosis (deposition of
yellowish cholesterol-rich material
that can appear anywhere in the body
in various disease state)
Sloughing with grayish, flake like
Particles of debris adhering to eroded
Surface.
Necrosis with formation of
pseudo membrane composed of
Bacteria, PMNs and degenerated
epithelial cells in fibrinous meshwork.
110. Vesicle formation
(small fluid filled bladder,cyst,sac
orvacoule within the body)
Intercellular and intracellular
edema with Degeneration of
nucleus and cytoplasm
and rupture of cell wall.
111. Chronic gingivitis
Soggy Puffiness that pits on pressure Infiltration by fluid and cells of
inflammatory exudates.
Marked softness and friability with
fragmentation on tissue and
exploration with Probe and pinpoint
surface areas of redness and
desquamation
Degeneration of connective and
epithelium associated with injurious
substance that provoke the
inflammation and inflammatory
exudate
Change in CT-epithelium relationship
Fibrosis and epithelium proliferation
associated with long standing chronic
inflammation
112. CHANGES IN SURFACE TEXTURE
OF THE GINGIVA
The surface of normal gingival usually exhibits
numerous small depressions and elevations, giving the
tissue an ORANGE – PEEL APPEARANCE referred as
stippling.
Stippling is restricted to the attached gingival and is
predominantly localized to the sub papillary area, but it
extends to a variable degree into the interdental papilla.
Stippling is a form of adaptive specialization or
reinforcement for function. It is a feature of healthy
gingival, and reduction or loss of stippling is a common
sign of gingival disease. When the gingival is restored to
health, after treatment, the stippled appearance returns.
113. In Chronic inflammation the gingival surface is either
smooth and shiny or firm and nodular depending
on whether the dominant charges are exudative or
fibrotic.
Atrophic Gingivitis – Smooth surface texture is
produced by epithelial atrophy
Chronic Desquamative gingivitis – Peeling of the
surface occurs.
Drug induced gingival – nodular surface overgrowth.
114. Stippling is visible in dry area (gingiva) due to
refraction stippling is always seen in parallel light,
stippling is absent in Infants and older age due to diet
pattern as stippling is adaptive reinforcement for
function of mucosa.
Presence of stippling is indicator of healthy gingival.
Absence of stippling as disease indicator because
stippling may be absent in some individuals , it only
act as indicator of health.
115. CHANGES IN POSITION OF
GINGIVA
Gingival Recession
Recession is progressive exposure of the root surface by
an apical shift in position of the gingiva.
Actual position of the gingiva determines the severity
of recession.
Actual Position
Level of the epithelial attachment on the tooth.
Apparent Position
Level of the crest of gingival margin.
116.
117. Types of Recession
1. a. Visible: Clinically observable.
b. Hidden:
Covered by gingiva and can only be measured by inscribing a
probe to the level of epithelial attachment. Eg. : In periodontal
diseases
Recession = Hidden + visible
(covered by denuded root
inflamed Pocket wall)
Recession refers to the location of the gingiva and not its
condition. Receding gingival is often inflamed but may be
normal except for its position.
118. According to distribution
Localized to a tooth.
Generalized – Throughout the month.
121. PHYSIOLOGICAL
G. recession increases with age, incidence various from
8% in children to 100% after age of 50 years (Woofter
1969).
Thus assumed that recession in physiological process
related to aging.
No convincing evidence of physiological shift (Loc
1967)
122. Gradual shift result of –
Cumulative effects of minor pathological involvement.
Repeated minor trauma to gingival.
Increasing periodontal disease.
124. TFO (Mechanism of action never demonstrated).
Orthodontic movement in labial direction in monkeys.
1. Localized g. recession (children)
2. Position of teeth in arch (children)
3. Tooth in labial position, tilted, rotated.
4. Ant Open bite.
125. Osteoporosis (Risk Indicator)
In (After) Phase 1 therapy.
Self inflicted gingival injuries such as gingival
recession in children and adults
After crown placement.
Smoking and recession may be linked but much
multifunctional.
126. Tooth brushing trauma
➢Faulty tooth brushing technique eg. : horizontal scrub
method.
➢Brushing with hard bristles
➢Recession tends to be more frequent and severe in
patients with comparatively healthy gingival, little
bacterial plaque and good oral hygiene O’leary,Drake
1971.
127. Susceptibility is influenced by
a. Position of teeth in Arch.
b. root – bone angle.
c. mesiodistal curvatures of tooth surface.
128. On rotated, tilted, or faulty displaced teeth, bony
plate is thinned or reduced in height. Pressure from
mastication or moderate tooth brushing damages the
unsupported gingival and produces recession.
Effect of angle of the root in the bone on recession is
often observed in max. molar area.
If lingual inclination of the palatal root is prominent
or buccal roots flare outward, then the bone in
cervical area is thinned or shortened and recession
results from repeated trauma of marginal gingiva.
129.
130. Clinical Appearance
V-shaped or wedge shaped ditch on root side of
Cementoenamal junction in teeth alongwith gingival
recession.
DEGREE OF GINGIVAL RECESSION
During periodontal examination it is necessary to
record the data regarding the amount of gingival
recession. This measurement is taken with the
periodontal probe from cemento enamel junction to
the gingival crest.
131. Gingival Recession – Classifications
Several classification of denuded roots have been
proposed –
In 1960 Sullivan and Atkins classified gingival
recession into four morphologic categories.
❖Shallow – narrow
❖Shallow – wide
❖Deep – narrow
❖Deep – wide
132. Miller (1985)
➢Class – I : Marginal tissue recession that deos not
extend to the mucogingival junction. There is no loss
of bone or soft tissue in the interdental area. It can be
narrow or wide.
➢Class – II : Marginal tissue recession that extends to or
beyond the mucogingival junction. There is no loss of
bone or soft tissue in the interdental area. It can be
wide or narrow.
133.
134.
135. ➢Class – III : Marginal tissue recession that extends to or
beyond the mucogingival junction. In addition there is
bone and soft tissue loss interdentally or malpositioning of
the teeth.
➢Class – IV : Marginal tissue recession that extends to or
beyond the mucogingival junction with swear bone and
soft tissue loss interdentally and / or severe tooth
malpositioning.
136.
137.
138. Clinical Significance of G. Recession
➢Exposed root surfaces are susceptible to caries.
➢Abrasion or erosion of cementum exposed by
recession leaves and underlying dentinal surface
that can be sensitive.
➢Hyperemia of pulp and associated symptoms.
➢Interproximal recession creates oral hygiene
problems and resulting plaque accumulation.
139. PROGNOSIS, PROGNOSTIC FACTORS AND PROGNOSIS
ASSESSMENT
Although the clinical signs of gingivitis are easy to
detect, it is not clear how much inflammation a person
must have to be considered a gingivitis case. A
universally accepted threshold for the amount or
severity of gingival inflammation that must be present
in an individual does not exist. In studies of gingivitis,
a variety of indices have been used. Because different
indices have different clinical criteria for establishing
the presence or absence of gingivitis, the definition of
a gingivitis case varies across studies
140. . In general, however, a gingivitis case is a person with
at least mild inflammation in at least one of the
gingival units that are assessed. Depending on the
study, a gingival unit may be an anatomic structure of
the gingiva, such as the interdental papilla, marginal
gingiva, or attached gingiva, or it may be a gingival site
defined in relation to a tooth, such as the facial,
lingual, mesial, or distal gingiva.
141. HOW IS GINGIVITIS MEASURED?
Gingivitis is measured by gingival indices. Indices are
methods for quantifying the amount and severity of
diseases or conditions in individuals or populations.
Indices are used in clinical practice to assess the
gingival status of patients and follow any changes in
gingival status over time. Gingival indices are used in
epidemiologic studies to compare the prevalence of
gingivitis in population groups. In clinical studies,
gingival indices are used to test the efficacy of
therapeutic agents or devices
142. Gingival Index:
Criteria for the Gingival Index
Score Criteria
0 Normal gingiva
1 Mild inflammation: slight change in color and slight
edema. No bleeding on probing.
2 Moderate inflammation: redness, edema, and glazing.
Bleeding on probing.
3 Severe inflammation: marked redness and edema.
Ulceration, tendency toward
spontaneous bleeding.
{From Loe H: The gingival index, the plaque index, and the
retention index systems. J Periodontol 1967; 38:610(suppl)}
143. Modified Gingival Index
Criteria for the Modified Gingival Index
Score Criteria
0 Absence of inflammation
1 Mild inflammation: slight change in color, little
change in texture of any portion of but not the
entire marginal or papillary gingival unit
2 Mild inflammation: criteria as above but
involving the entire marginal or papillary gingival unit
3 Moderate inflammation: glazing, redness, edema, and/or
hypertrophy of the marginal or papillary gingival unit
4 Severe inflammation: marked redness, edema, and/or
hypertrophy of the marginal or papillary gingival unit;
spontaneous bleeding, congestion, or ulceration
{From Lobene RR, Weatherfor T, Ross NM, et al: A modified gingival
index for use in clinical trials. Clin Prevent Dent 1986; 8(1):3.}
144. MICROORGANISMS ASSOCIATED WITH
GINGIVITIS
The development of gingivitis has been extensively
studied in a model system referred to as experimental
gingivitis and initially described by Harald Loe and
coworkers. Periodontal health is first established in
human subjects by cleaning and rigorous oral hygiene
measures, followed by abstinence from oral hygiene
for 21 days. After 8 hours without oral hygiene,
bacteria may be found at concentrations of 10 3 to 104
per square millimeter of tooth surface and will
increase in number by a factor of 100 to 1000 in the
next 24-hour period
145. The initial microbiota of experimental gingivitis
consists of gram-positive rods, gram-positive cocci, and
gram-negative cocci. The transition to gingivitis is
evident by inflammatory changes observed in the
gingival tissues and is accompanied first by the
appearance of gram-negative rods and filaments, then
by spirochetal and motile microorganisms. The bacteria
found in naturally occurring dental plaque-induced
gingivitis (chronic gingivitis) consist of roughly equal
proportions of gram-positive (56%) and gram-negative
(44%) species, as well as facultative (59%) and
anaerobic (41%) microorganisms.
146. Predominant gram-positive species include S. sanguis, S.
mitis, S. intermedius, S. oralis, A. viscosus, A. naeslundii,
and Peptostreptococcus micros. The gram-negative
microorganisms are predominantly F. nucleatum, P.
intermedia, V. parvula, as well as Hemophilus,
Capnocytophaga and Campylobacter spp.
Pregnancy-associated gingivitis is an acute inflammation of
the gingival tissues associated with pregnancy. This
condition is accompanied by increases in steroid hormones
in crevicular fluid and dramatic increases in the levels of P.
intermedia, which use the steroids as growth factors
147. Fig. Cultivablesubgingival microbiotaassociated with periodontal
health and disease. A, Distributionof gram-positiveand gram-
negative rods and cocci. B, Distributionof anaerobic, facultative,
gram-positiveand gram-negative species. (Adapted from Slots J,
Rams TE: Microbiologyof periodontal disease. I n: Slots J, Taubman
MA (eds): Contemporary Oral Microbiologyand Immunology. St
Louis, Mosby, 1992.)
148. IMMUNOLOGY IN GINGIVAL DISEASES
The most common form of gingivitis is plaque induced
gingivitis. Common clinical findings in
gingivitis include erythema, edema, tissue
enlargement, and bleeding. Two forms of plaque-
induced gingivitis have been investigated: a naturally
occurring gingivitis and experimental gingivitis.
149. The development of experimental gingivitis occurs in parallel
with a tremendous increase in the number of bacteria present in
plaque. A distinct shift in the bacterial composition of the
plaque also occurs, with increasing proportionsof gram-negative
anaerobes. Studies on the microbiology of naturally occurring
gingivitis indicate relatively equal proportionsof gram-positive
facultative and gram-negative anaerobic bacteria, with evidence
of a greater shift as compared with experimental gingivitis. The
host response to plaque bacteria is fundamentally an
inflammatory response involving the processes described
previously. Although gingivitis is not associated with loss of
connective tissue attachment, it is evident histologically that
some loss of collagen occurs within the connective tissues.
150. Experimental gingivitis is a longitudinal clinical model
that has been widely used in human and animal
studies. In humans, experimental gingivitis is induced
through abstinence from oral hygiene measures; in
animal studies a soft diet favoring plaque
accumulation is instituted. The studies of
experimental gingivitis have provided a clear
demonstration that plaque accumulation invariably
causes gingivitis and that gingivitis is reversible with
removal of the plaque deposits.
151. Stages of Gingivitis
Stage
Time
(Days)
Blood
Vessels
Junctional
and Sulcular
Epithelium
Predominant
Immune Cells
Collagen
Clinical
Findings
I. Initial lesion 2-4
Vascular dilation Infiltrated by PMNs PMNs Perivascular
loss
Gingival fluid flow
II. Early
lesion
4-7 Vascular
proliferation
Same as Stage I.
Rete peg formation,
Atrophic areas
Lymphocytes I ncreased
loss
around
infiltrate
Erythema
Bleeding on
Probing
III. Established
Lesion
14-21 Same as Stage II,
plus blood stasis
Same as Stage II but
more advanced
Plasma cells Continued loss Changes in color,
size, texture, etc.
154. TREATMENT
Plaque Control
Plaque control is the removal of dental plaque on a regular basis and the
prevention of its accumulation on the teeth and adjacent gingival surfaces.
It is a critical component of dental practice, permitting long-term success of
periodontal and dental care.
This widely held view is reflected in the following policy statement adopted in
1998 European Workshop on Mechanical Plaque Control: "Forty years of
experimental research, clinical trials, and demonstration projects in different
geographical and social settings have confirmed that effective removal of
dental plaque is essential to dental and periodontal health throughout life.
155. In 1965, Loe and co-workers conducted the classic study
demonstrating the relationship between plaque
accumulation and the development of experimental
gingivitis in humans. Dental plaque was allowed to
accumulate in the absence of any plaque control
procedures, within 7 to 21 days. The composition of
bacteria also shifted so that gram-negative organisms
predominated in dental plaque associated with gingival
inflammation. In addition, it was shown that the gingivitis
was reversible. Daily removal of dental plaque led to
resolution of the gingival inflammation in just a few days.
Good supragingival plaque control has also been shown to
retard calculus formation and affect the growth and
composition of subgingival plaque.
156. The dental profession relies on mechanical plaque
control (i.e., daily cleaning with a toothbrush and other
oral hygiene aids) as the most dependable way of
achieving oral health benefits for all dental patients
including periodontal patients. Plaque growth occurs
within hours and must be completely removed at the
very least every 48 hours in periodontally healthy
subjects to prevent inflammation. Toothbrushing is a
completely accepted part of daily life and good oral
hygiene practice. However, plaque control by
toothbrushing alone is not sufficient to control gingival
and periodontal diseases because periodontal lesions
are predominantly interdental
157. It has been demonstrated in healthy subjects that
plaque formation begins on the interproximal surfaces
where the toothbrush does not reach. Masses of
plaque first develop in the molar and premolar areas,
followed by the proximal surfaces of the anterior teeth
and the facial surfaces of the molars and premolars.
158. The optimal frequency for plaque removal by
periodontal patients has not been determined, but it is
reasonable to expect periodontal patients to
completely remove plaque from the teeth at least once
every 24 hours due to patient susceptibility to disease
and complexity of the task. Taken together, these
findings suggest plaque control efforts must focus on
more than simply improved toothbrushing.
159. Plaque control is one of the key elements of the practice of
dentistry. It permits each patient to assume responsibility
for his or her own oral health on a daily basis. Without it,
optimal oral health through periodontal treatment cannot
be attained or preserved. Every patient in every dental
practice should be educated about plaque control and
encouraged to perform a personalized program on a daily
basis. Good plaque control facilitates the return to health
for patients with gingival and periodontal diseases,
prevents tooth decay, and preserves oral health for a
lifetime.
