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