CLINICAL FEATURES OF GINGIVITIS AND ITS CORRELATION WITH MICROSCOPIC FINDINGS

2. CLINICAL FEATURESOF
GINGIVITIS
Shilpa Shivanand
I MDS

3. CONTENTS
• Introduction to
inflammation
• Course and duration
• Components of Gingival
Inflammation
• Experimental gingivitis
• Prevalence
• Distribution
• Stages of inflammation
• Bleeding from gingiva
• Color changes in gingiva
• Changes in Gingival
consistency
• Changes in Gingival
Surface texture
• Changes in Gingival
Position
• Changes in Gingival
Contour
• Conclusion
• References
3

4. INTRODUCTION TO INFLAMMATION
• Inflammation is defined as an observable alteration in tissues
associated with changes in vascular permeability and dilation,
often with the infiltration of leukocytes into affected tissues.
(Rushton Parker 1910)
• These changes result in  rubor, tumor, calor, dolor, and loss of
function being the cardinal signs of inflammation
(Celsus 1st centaury AD, Virchow)
• Typically inflammation can progress through three stages:
- Acute
- Sub-Acute and
- Chronic.
4

5. • ACUTE INFLAMMATION: It is a rapid response to injury or
microbes and other foreign substances that is designed to deliver
leukocytes and plasma proteins to sites of injury( Robbins)
• short duration.
• Represents early body reaction , usually followed by repair.
• CHRONIC INFLAMMATION: Is defined as a prolonged process in
which tissue destruction , inflammation & healing occurs at the same
time
• In contrast to acute inflammation, chronic inflammation is
characterized by infiltration of macrophages, lymphocytes , plasma
cells.
5

6. COURSE AND DURATION
• Gingivitis can occur with sudden onset and short duration and can
be painful. A less severe phase of this condition can also occur.
• Recurrent gingivitis reappears after having been eliminated by
treatment or disappearing spontaneously.
• Chronic gingivitis is slow in onset and of long duration.
• Painless, unless complicated by acute/sub acute exacerbations, and
is the type most often encountered
• Fluctuating disease in which inflammation persists or resolves and
normal areas become inflamed. (Hoover DR et al 1965, Larato
DC et al 1969)
6

7. COMPONENTS OF GINGIVAL
INFLAMMATION
• Gingival inflammation has two components:
– the acute inflammatory component,
» with vasodilation,
» edema, and
» polymorphonuclear infiltration, and the
– the chronic inflammatory component,
» with B and T lymphocytes and
» capillary proliferation forming a
granulomatous response.
• Each gingival region can have varying amounts of the
acute or chronic component. 7

8. EXPERIMENTAL GINGIVITIS
• Despite extensive research, we still cannot distinguish definitively
between normal gingival tissue and the initial stage of
gingivitis.
• Most biopsies of clinically normal human gingiva contain
inflammatory cells consisting predominantly of T cells, with very
few B cells or plasma cells.
• In 1965, Loe et al demonstrated that in students with clinically
healthy gingivae.
Clinical symptoms of gingivitis developed within 2 to 3
weeks if dental plaque was allowed to accumulate freely.
 Once adequate tooth cleaning was resumed, the
gingival inflammation subsided within a week
8

9. • The thickness of the gingival plaque gradually increased during
the 3-week experimental period.
• For the first few days:
– gram-positive cocci and
– rods, representing the indigenous micro flora of the tooth
surface.
• After 4 to 5 days:
– filamentous organisms and
– gram-negative cocci as well as rods
• Gradually, non attaching spirochetes appeared in the gingival
sulcus, while the assortment of microorganisms in the gingival
biofilm increased continuously.
EXPERIMENTAL GINGIVITIS
9

10. CHARACTERISTICS OF PLAQUE INDUCED
GINGIVITIS (Mariotti,1999)
1 Plaque present at gingival margin
2 Disease begins at the gingival margin
3 Change in gingival color
4 Change in gingival contour
5 Sulcular temperature change
6 Increased gingival exudate
7 Bleeding upon provocation
8 Absence of attachment loss*
9 Absence of bone loss*
10 Histological changes including an inflammatory lesion
11 Reversible with plaque removal
10

11. PREVALANCE
• The prevalence of gingivitis is evident worldwide.
• Higher prevalence of gingivitis is reported for children and
adolescents. (Albander JM, Brown LJ et al 1996)
• A significant percentage of adults also show signs of gingivitis; more
than half the U.S. adult population estimated to exhibit gingival
bleeding, and other populations show even higher levels of gingival
inflammation. (Albander JM, Kingman A et al 1999)
• In children on average 6% of sites measured showed bleeding on
probing. (Albander JM, Tinoco EM 2002)
11

12. DISTRIBUTION
• Localized gingivitis is confined to the gingiva of a single tooth or
group of teeth, whereas generalized gingivitis involves the entire
mouth.
• Marginal gingivitis involves the gingival margin and may include
a portion of the contiguous attached gingiva.
• Papillary gingivitis involves the interdental papillae and often
extends into the adjacent portion of the gingival margin. Papillae
are involved more frequently than the gingival margin, and the
earliest signs of gingivitis often occur in the papillae.
• Diffuse gingivitis affects the gingival margin, the attached
gingiva, and the interdental papillae. (Glickman 1953)
12

13. GINGIVAL DISEASE IN INDIVIDUAL CASES IS
DESCRIBED BY COMBINING THE PRECEDING
TERMS AS FOLLOWS:
• Localized marginal gingivitis is confined to one or more areas of the
marginal gingiva
• Localized diffuse gingivitis extends from the margin to the
mucobuccal fold in a limited area
• Localized papillary gingivitis is confined to one or more interdental
spaces in a limited area
• Generalized marginal gingivitis involves the gingival margins in
relation to all the teeth. The interdental papillae are usually affected
• Generalized diffuse gingivitis involves the entire gingiva. The
alveolar mucosa and attached gingiva are affected, so the
mucogingival junction is sometimes obliterated.
• Systemic conditions can be involved in the cause of generalized
diffuse gingivitis and should be evaluated if suspected as an etiologic
cofactor.
13

14. 14

15. STAGES OF GINGIVAL
INFLAMMATION
15

16. Gingival alterations which occurred during a 28-day period of
plaque accumulation and gingivitis development in beagles. (a)
Normal gingiva. (b) Day 4. (c) Day 7. (d) Day 14. (e) Day 21. (f)
Day 28 of undisturbed plaque accumulation. Note the gradually
developing plaque on the tooth surfaces and the inflammatory
changes in the gingiva. (Page 1986)
16

17. 17

18. 18

19. Stage I Gingivitis : The Initial Lesion -
SUBCLINICAL GINGIVITIS.
Lindhe , Hamp et al 1973- beagle dogs
• Dilation of capillaries & increase in blood flow.
• Initial inflammatory changes in response to microbial
activation of resident leukocytes, subsequent stimulation of
endothelial cells.
• Clinically- initial response of gingiva to bacterial
plaque(sub clinical gingivitis)- not apparent.
• Changes in JE and perivascular connective tissue-
detected
19

20. •Perivascular connective tissue matrix-altered
•Exudation & deposition of fibrin in affected area
•Accumulation of lymphocytes
•Increase in migration of leukocytes and accumulation within
gingival sulcus corelated with increase in flow of gingival
fluid into sulcus.
STAGE I GINGIVITIS
20

21. •Character and intensity of host response determines whether
initial lesion resolves rapidly with restoration of tissue to
normal state or into chronic inflammatory lesion.
•Inflammatory lesion- infiltrate of macrophages and lymphoid
cells appears within few days.
STAGE I GINGIVITIS
21

22. Changes in blood vessel morphologic features (e.g.,
widening of small capillaries or venules)
Some classic features of acute inflammation seen in
connective tissue beneath the junctional epithelium.
MICROSCOPICALLY
22

23. Adherence of neutrophils to vessel walls (margination) occur
within 1 week and sometimes as early as 2 days after plaque has
been allowed to accumulate.
Leukocytes, mainly polymorphonuclear neutrophils (PMNs),
leave the capillaries by migrating through the walls - increased
quantities in the connective tissue, junctional epithelium, and
the gingival sulcus
Exudation of fluid from gingival sulcus and extravascular
proteins present.
23

24. Human biopsy sample, experimental gingivitis. After 4 days of plaque
accumulation, the blood vessels immediately adjacent to the junctional
epithelium are distended and contain polymorphonuclear leukocytes ( PMNs,
neutrophils). Neutrophils have also migrated between the cells of the
junctional epithelium. OSE, Oral sulcular epithelium.
24

25. STAGE II GINGIVITIS : THE EARLY
LESION
(Payne , Page et al 1975,1991)
•Early lesion evolves from the initial lesion within 1 week after
beginning of plaque accumulation.
•Clinically 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.
25

26. •Bleeding on probing- evident. (Amato R, Caton J, Polson A et
al 1986)
•Gingival fluid flow and numbers of transmigrating leukocytes
reach their maximum between 6 and 12 days after onset of
clinical gingivitis. (Lindhe J, Hamp, Loe H et al 1973)
26

27. 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.
27

28. •PMNs that have left the blood vessels in response to
chemotactic stimuli from plaque components travel to the
epithelium, cross basement lamina, and are found in the
epithelium, emerging in pocket area.
•PMNs are attracted to bacteria and engulf them in the process
of phagocytosis.
•PMNs release their lysosomes in association with ingestion of
bacteria.
• Fibroblasts show cytotoxic alterations, with decreased capacity
for collagen production.
28

29. MICROSCOPIC:
• 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)
(Payne WA, Page RC, Ogilvie AL et al 1975 and Schroeder
HE, Page RC 1973)
• Also composed of some migrating neutrophils, as well as
macrophages, plasma cells, and mast cells.
29

30. All the changes seen in the initial lesion continue to intensify
with the early lesion.
The junctional epithelium- densely infiltrated with neutrophils,
as does the gingival sulcus, and the junctional epithelium may
begin to show development of rete pegs.
30

31. Scanning electron micrograph of leukocyte emerging to pocket wall and covered with
bacteria and extracellular lysosomes. EC, Epithelial cells; B, bacteria; L, lysosomes.
31

32. 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)
32

33. • 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.
• Bluish hue on the reddened gingiva (Hanioka T et al 1991)
• 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.
• The established lesion can be described as moderately to severely
inflamed gingiva.
33

34. • The predominance of plasma cells is thought to be a primary
characteristic of the established lesion.
• Increases in the proportions of plasma cells were evident with
long-standing gingivitis, but 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
34

35. 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.
35

36. 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
36

37. • 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 37

38. Established gingivitis in a human subject. Area of
crevicular epithelium exhibiting enlarged
intercellular spaces with numerous microvilli and
desmosomal junctions.
Several lymphocytes, both small and large, are
seen migrating through the epithelial layer.
(x3000.)
38

39. STAGE IV GINGIVITS : 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.
39

40. MICROSCOPICALLY:
• Fibrosis of the gingiva and widespread manifestations of
inflammatory and immunopathologic tissue damage.
• Plasma cells continue to dominate the connective tissues, and
neutrophils continue to dominate the junctional epithelium
and gingival crevice
40

41. CLINICAL FEATURES
• In evaluating the clinical features it is necessary to be
systematic.
• The clinician should focus on subtle tissue alterations because
these may be of diagnostic significance.
• A systematic clinical approach requires an orderly examination
of the gingiva for
» color,
» contour,
» consistency,
» position, and
» ease and severity of bleeding and
» pain.
41

42. • The two-earliest signs of gingival inflammation preceding
established gingivitis are
» (1) Increased gingival crevicular fluid production rate
and
» (2) Bleeding from the gingival sulcus on gentle
probing
• Raised sulcus temperature has also been shown to be a feature of
plaque induced inflammation (Haffajee et al 1992, Loe et al 1965,
Poison and Goodson 1985)
• Increase in leucocytes seen in gingival fluid associated with
increased GCF (Payne et al 1975, Page and Schroeder 1976)
42

43. 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. 43

44. • 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.
44

45. • 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.
45

46. • 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)
46

47. 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
• 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
47

48. 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.
48

49. • MODIFIED PMA Muhlemann and Mazor
• Modification – discarded A unit
49

50. • 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.
50

51. • 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
51

52. • 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
52

53. • 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 bertwwn
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
53

54. 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)
54

55. • 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. 55

56. • 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)
Microscopic view of interdental space in a
human autopsy specimen.Inflammatory
infiltrate and thinned epithelium in area
adjacent to the tooth, as well as collagenous
tissue in outer half of the section.
56

57. 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. 57

58. 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)
58

59. • 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.
59

60. • 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)
• Among pathologic endocrine changes, diabetes is an
endocrine condition with a well-characterized effect on
gingivitis. (Tatakis DN et al 1994)
60

61. • Several medications have also been found to have adverse
effects on the gingiva. For example, anticonvulsants,
antihypertensive calcium channel blockers, and the
immunosuppressant drugs are known to cause gingival
enlargement, which secondarily can cause gingival bleeding.
• The American Heart Association has recommended over the
counter aspirin as a therapeutic agent for cardiovascular
disease, and aspirin is often prescribed for rheumatoid arthritis,
osteoarthritis, rheumatic fever, and other inflammatory joint
diseases. (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
61

62. COLOUR CHANGES IN GINGIVA
• The color of the gingiva is determined by several
factors, including
– the number and size of blood vessels,
– epithelial thickness,
– quantity of keratinization,
– arid pigments within the epithelium
(Tal H, Tal M 2003)
62

63. COLOR CHANGES IN CHRONIC GINGIVITIS
• Change in color 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.
63

64. • 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.
• Proper diagnosis and treatment require an understanding of the
tissue changes that alter the color of the gingiva at the clinical
level.
64

65. 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.
• 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.
65

66. 66

67. 67

68. 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.
• These changes are rare but still should be ruled out in suspected
cases.
• 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.
• This differs from the tattooing produced by the accidental
embedding of amalgam or other metal fragments.
• 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)
68

69. • 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.
• Pigmentation can be eliminated by treating the inflammatory
changes without necessarily discontinuing the metal
containing medication. 69

70. Bismuth gingivitis.linear black
discoloration of the gingiva in a
patient receiving bismuth therapy.
Discoloration of the gingiva
caused by embedded metal
particles (amalgam).
70

71. COLOR CHANGES ASSOCIATED WITH
SYSTEMIC FACTORS
• Many systemic diseases may cause color changes in the oral mucosa,
including the gingiva.
• In general, these abnormal pigmentations are nonspecific and needs
further diagnostic efforts or referral to the appropriate specialist.
• Endogenous oral pigmentations can be caused by melanin, bilirubin,
or iron.
• Melanin oral pigmentations can be normal physiologic pigmentations
and are often found in highly pigmented ethnic groups.
• Diseases that increase melanin pigmentation include the following:
– Addison’s disease is caused by adrenal dysfunction and produces
isolated patches of discoloration varying from bluish black to brown.
– Peutz-Jeghers syndrome produces intestinal polyposis and melanin
pigmentation in the oral mucosa and lips.
– Albright’s syndrome (polyostotic fibrous dysplasia) and Von
Recklinghausen's disease (neurofibromatosis) produce areas of oral
melanin pigmentation.
71

72. • 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.
• Tobacco causes hyperkeratosis of the gingiva and also may induce a
significant increase in melanin pigmentation of the oral mucosa.
• Localized bluish black areas of pigment are often caused by
amalgam implanted in the mucosa
72

73. 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.
• More over color variation may not be uniform and may exists as
unilateral, bilateral, mottled, macular or blotched and may involve
gingival papillae alone or extend throughout the gingiva on to
other soft tissues.
73

74. • 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).74

75. • 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:
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.
75

76. • 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)
76

77. DEPIGMENTATION
• Traditionally, gingival depigmentation has been carried out using
nonsurgical and surgical procedures, such as
– chemical,
– cryosurgical, and
– electrosurgical techniques.
• However, those techniques were met with skepticism because of
varying degrees of success.
• 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.
77

78. CHANGES IN CONSISTENCY OF THE
GINGIVA
• Both chronic and acute inflammations produce changes in the
normal firm and resilient consistency of the gingiva.
• As previously noted, in chronic gingivitis, both destructive
(edematous) and reparative (fibrotic) changes coexist, and the
consistency of the gingiva is determined by their relative
predominance.
In chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes
coexist, and the consistency of the gingiva is determined by their relative predominance
78

79. 79

80. CALCIFIED MASSES IN THE GINGIVA
• Calcified microscopic masses may be found in the gingiva.
(Box HK 1950)
• 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.
• Crystalline foreign bodies have also been described in the
gingiva, but their origin has not been determined.80

81. 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)
81

82. CHANGES IN SURFACE TEXTURE OF
THE GINGIVA
• The surface of normal gingiva usually exhibits numerous small
depressions and elevations, giving the tissue an orange peel
appearance referred as stippling. (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.
82

83. • 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.
83

84. Gingival biopsy demonstrating alternate
elevations and depressions in the attached
gingiva responsible for stippled
appearance.
84

85. TRAUMATIC LESIONS
• One of the unique features of the most recent gingival disease
classification is the recognition of non-plaque induced
traumatic gingival lesions as distinct gingival conditions.
(Armitage GC 1999)
• Traumatic lesions, whether chemical, physical, or thermal, are
among the most common lesions in the mouth.
• Sources of chemical injuries include aspirin, hydrogen
peroxide, silver nitrate, phenol, and endodontic materials.
• Physical injuries can include lip, oral, and tongue piercing,
which can result in gingival recession.
• Thermal injuries can result from hot drinks and foods..
85

86. • 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)
86

87. POSITION OF GINGIVA
• 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.
87

88.  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,
whereas the apparent position is the level of the crest of the gingival margin.
The severity of recession is determined by the actual position of the gingiva,
not its apparent position.
88

89. 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)
89

90. 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) 90

91. • 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.
• Orthodontic movement in a labial direction in monkeys has
been shown to result in loss of marginal bone and connective91

92. • 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. 92

93. • 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.
93

94. • 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.
94

95. RESTORATIONS AND RECESSION
• The health of the gingival tissue also depends on properly designed
and placed restorative materials.
• Pressure from a poorly designed partial denture, such as ill-fitting
denture clasp, can cause gingival trauma and recession.
• Overhanging dental restorations have long been viewed as a
contributing factor to gingivitis because of plaque retention.
(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)
95

96. 96

97. 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)
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.
97

98. CLASSIFICATION
• 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)
98

99. • 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.
99

100. 100

101. MAHAJAN'S MODIFICATION
An outline of classification system including the above
mentioned changes is presented:
• Class I: GRD not extending to the MGJ.
• Class II: GRD extending to the MGJ/beyond it.
• Class III: GRD with bone or soft-tissue loss in the
interdental area up to cervical 1/3 of the root surface and/or
malpositioning of the teeth.
• Class IV: GRD with severe bone or soft tissue loss in the
interdental area greater than cervical 1/3rd of the root
surface and/or severe malpositioning of the teeth.

102. PROPOSED CLASSIFICATION OF GINGIVAL RECESSION
[ASHISH KUMAR, SUJATA SURENDRA MASAMATTI- 2013]
• This classification can be applied for facial surfaces of
maxillary teeth and facial and lingual surfaces of
mandibular teeth.
• Interdental papilla recession can also be classified according
to this new classification.
• Class I deals with marginal tissue recession with no loss of
interdental bone or soft-tissue.
• Class II and III deal with the loss of interdental bone/soft-
tissue with/ without marginal tissue recession.

103. • Class I: There is no loss of
interdental bone or soft-tissue.
• This is sub-classified into two
categories:
• Class I-A: Gingival margin
on F/L aspect lies apical to
CEJ, but coronal to MGJ with
attached gingiva present
between marginal gingiva and
MGJ.
• Class I-B: Gingival margin
on F/L aspect lies at or apical
to MGJ with an absence of
attached gingiva between
marginal gingiva and MGJ.
• Either of the subdivisions can
be on F or L aspect or both (F
and L)

104. • Class II: The tip of the interdental
papilla is located between the interdental
contact point and the level of the CEJ
midbuccally/ mid-lingually. Interproximal
bone loss is visible on the radiograph.
• This is sub-classified into three categories:
• Class II-A: There is no marginal tissue
recession on F/L aspect.
• Class II-B: Gingival margin on F/L
aspect lies apical to CEJ but coronal to
MGJ with attached gingiva present
between marginal gingiva and MGJ.
• Class II-C: Gingival margin on F/L
aspect lies at or apical to MGJ with an
absence of attached gingiva between
marginal gingiva and MGJ
• Either of the subdivisions can be on F or L
aspect or both (F and L).

105. • Class III: The tip of the interdental
papilla is located at or apical to the level
of the CEJ mid-buccally/mid-lingually.
Interproximal bone loss is visible on the
radiograph.
• This is sub-classified into two
categories:
• Class III-A: Gingival margin on F/L
aspect lies apical to CEJ, but coronal to
MGJ with attached gingiva present
between marginal gingiva and MGJ.
• Class III-B: Gingival margin on F/L
aspect lies at or apical to MGJ with an
absence of attached gingiva between
marginal gingiva and MGJ.
• Either of the subdivisions can be on F or
L aspect or both (F and L).

106. CLASSIFICATION OF PALATAL GINGIVAL RECESSION
The position of interdental papilla remains the basis of
classifying gingival recession on palatal aspect.
• The criteria of sub-classifications have been modified to
compensate for the absence of MGJ.
• PR-I deals with marginal tissue recession on palatal aspect
with no loss of interdental bone or soft-tissue.
• PR-II and PR-III deal with the loss of interdental bone/soft
tissue with marginal tissue recession on palatal aspect.

107. Palatal recession-I
• There is no loss of interdental
bone or soft-tissue.
• This is sub-classified into two
categories:
• PR-I-A: Marginal tissue
recession ≤3 mm from CEJ.
• PR-I-B: Marginal tissue
recession of >3 mm from CEJ.

108. Palatal recession-II
• The tip of the interdental
papilla is located between the
interdental contact point and
the level of the CEJ mid-
palatally. Interproximal bone
loss is visible on the
radiograph.
• This is sub-classified into two
categories:
• PR-II-A: Marginal tissue
recession ≤3 mm from CEJ.
• PR-II-B: Marginal tissue
recession of >3 mm from CEJ

109. Palatal recession-III
• The tip of the interdental
papilla is located at or apical to
the level of the CEJ mid-
palatally. Interproximal bone
loss is visible on the
radiograph.
• This is sub-classified into two
categories:
• PR-III-A: Marginal tissue
recession ≤3 mm from CEJ.
• PR-III-B: Marginal tissue
recession of >3 mm from CEJ.

110. LIST OF DIFFERENT SURGICAL TECHNIQUES USED IN ROOT COVERAGE
PROCEDURES.
110

111. CHANGES IN GINGIVAL CONTOUR
• Changes in gingival contour are primarily associated with
gingival enlargement, but such changes may also occur in
other conditions.
• Of historical interest are the descriptions of indentations of the
gingival margin referred to as Stillman's clefts and the McCall
festoons.
111

112. 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.
112

113. • 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.
• Their association with trauma from occlusion has not been
substantiated.
113

114. • The clefts are divided into
• simple clefts: in which cleavage occurs in a single direction
(the most common type), and
• compound clefts: in which cleavage occurs in more than one
direction.
• The clefts vary in length from a slight break in the gingival
margin to a depth of 5 to 6 mm or more.
114

115. 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.
115

116. 116

117. 117

118. CONCLUSION
• Establish a proper diagnosis based on clinical
findings…..
• Proper management…phase I…
• Prevention of periodontitis….
118

119. REFERENCES
• Clinical Periodontology- Carranza’s 10th edition
• Clinical Periodontalogy and implant dentistry- Jan Lindhe 5th
edition.
• Oral history- Antonio Nanci Ten Cate’s
• Essential Pathology – Harsh Mohan 3rd edition
• The gingival tissues: the architecture of periodontal protection.
Periodontology 2000, vol. 13, 1997, 91-120.
119

120. • Page RC, Gingivitis. J Clin Periodontol 1986;13: 345-355.
• Richard R. Ranney, Discussion: Pathogenesis of gingivitis. J Clin
Periodontol 1986;13: 356-359.
• William, Roy et al, Histopathologic features of the initial and early
stages of experimental gingivitis in man. J. Periodonlal
Res1975;10:51-64.
• Monitoring disease during supportive periodontal treatment by
bleeding on probing. Periodontology 2000, vol. 12, 1996, 4448
120

121. 121