INFLAMMATION

1. GINGIVAL INFLAMMATION
GROUP B
UNDISA EURO
EMMANUEL KITUZI
KEZIAH MWANGI

2. GINGIVAL
INFLAMMATION

3. Definition
Inflammation:
A response of living tissues to injury due to any foreign agent
Signs of inflammation: rubor, calor, dolor, tumor & loss of
function
Inflammation of the gingiva is called gingivitis
Gingival inflammation results in Pathologic changes that are
associated with the presence of oral microorganisms attached
to the tooth and, in or near the gingival sulcus

4. CLASSIFICATION
i. Based on presence/absence of plaque:
Dental biofilm induced Vs non-biofilm induced

5. ii. According to duration:
 Acute: Sudden onset & of short duration which is
painful, & resolves quickly.
Features: accumulation of fluid & plasma on affected site,
activation of PMNL
Chronic: Slow onset & of long duration. Painless,
unless complicated by acute or sub-acute exacerbations.
It is the most common type of gingivitis.
Features: chronic inflammatory cells, formation of
granulation tissue

6. iii. According to distribution:
Localized: Gingivitis confined to the gingiva of a single tooth
or group of teeth
Generalized: Involves the entire mouth.
Marginal: Involves the gingival margin & may include a
portion of the contiguous attached gingiva
Papillary gingivitis: Involves the interdental papilla & often
extends into the adjacent portion of the gingival margin
Diffuse gingivitis: Affects the gingival margin, attached
gingiva & interdental papillae

8. a) Generalized marginal & papillary gingivitis
b) Generalized diffuse gingivitis

9. STAGES OF GINGIVITIS

10. Stage I: Initial Lesion
Occur 2 to 4 days of plaque accumulation
Vascular changes (dilation of arterioles, capillaries and
venules of the dentogingival plexus & increased blood flow).
Increase in GCF flow-
Increase in PMNL in the connective tissue, JE & gingival
sulcus.
Little or no proliferation of JE
Loss of perivascular collagen within the infiltrated area

11. Stage 2: Early lesion
4 to 7 days after plaque accumulation
Clinical signs of erythema
Proliferation of capillaries & increased formation of capillary
loops between rete pegs & as such, there is bleeding on
probing
Lymphocytes (mainly T lymphocytes) and PMNs are
predominant. Very few plasma cells are present.

12. 70% of the collagen is destroyed around the cellular
infiltrate. Main fiber groups affected are the circular and
dento-gingival fibers
Fibroblasts show decreased capacity for collagen
formation
JE develops widened intracellular spaces that are
infiltrated by neutrophils and some monocytes.

14. Stage 3: Established lesion
2-4weeks after beginning of plaque accumulation
Engorged & congested blood vessels gives gingiva a bluish
hue,
Impaired venous return, blood flow becomes sluggish
Increased fluid exudation & leukocyte migration into tissues
& the gingival crevice
Dominated by plasma cells and B lymphocytes.

15. Collagen loss in lateral & apical directions as the
inflammatory cell infiltrate expands,
The JE continues to proliferate & the rete pegs extend deeper
into CT
JE is not closely attached to the tooth surface
No alveolar bone loss, or of apical migration of JE

16. Stage 4: Advanced lesion
• Final stage
• Inflammatory cell infiltrate extends laterally & further
apically into CT.
• Has all the characteristics of established lesion but has
alveolar bone loss, extensive fiber damage & apical migration
of JE
• Plasma cells are dominant
• Gingivitis progresses to periodontitis

17. CLINICAL FEATURES AND DIAGNOSIS
OF GINGIVAL INFLAMMATION

18. CONTENTS
1. Gingival Bleeding
2. Changes in gingival colour
3. Changes in Gingival Contour
4. Changes in gingival Consistency
5. Changes in Surface Texture of Gingiva
6. Changes in the Position of the Gingiva

19. 1. GINGIVAL BLEEDING

20. • Occurs due to dilation and engorgement of capillaries
• Degradation of intercellular cementing substances increases
permeability of sulcular epithelium
• With chronic inflammation, the sulcular epithelium ulcerates
• Because the epithelium is now less protective, innocuous stimuli
causes rupture of capillaries and gingival bleeding

21. ETIOLOGICAL FACTORS FOR GINGIVAL BLEEDING ARE:
LOCAL FACTORS:
i. Acute:
• Aggressive toothbrushing
• Sharp pieces of hard food
• Gingival burns from hot foods or chemicals
• NUG
ii. Chronic:
• Chronic Gingival Inflammation

22. SYSTEMIC FACTORS:
• Vascular abnormality- Vit C deficiency, Henoch Schonlein purpura
• Vitamin K deficiency
• Platelet disorder- ITP
• Deficient platelet thromboplastic factors- Uremia, Multiple myeloma
• Coagulation defects- Hemophilia
• Malignancy- Leukemia
• Drugs- Salicylates and anticoagulants

23. • Gingival bleeding is an objective sign and appears earlier than other
visual signs of inflammation
• It varies in severity, duration and ease of provocation
• Gingival Bleeding on Probing helps to determine whether a lesion is
active or inactive

24. 2. CHANGES IN GINGIVAL COLOUR
• Normal healthy gingiva is coral pink in colour.
• Due to vascular supply modified by the overlying keratinized layer of
gingival epithelium
• Gingiva becomes red when there is increase in vascularization and
reduction of keratinization
• Colour changes correlated with intensity of the inflammatory process
taking place

25. A. COLOUR CHANGES ASSOCIATED WITH LOCAL FACTORS
i. Acute Gingivitis
 NUG - Marginal bright red erythema. When severe, red colour turns
to dull whitish- gray due to tissue necrosis. Gray discoloration
demarcated from adjacent gingiva by thin sharply defined
erythematous zone
 Herpetic gingivostomatitis - Diffuse erythema
 Chemical irritations - patch-like pattern

26. Necrotizing Ulcerative Gingivitis

27. ii. Chronic gingivitis
 Intensification of red colour because of vascular proliferation and
reduction of keratinization due to epithelial compression by inflamed
tissue
iii. Metallic pigmentation
 Perivascular precipitation of metallic sulfides of systemically absorbed
metals in the subepithelial connective tissue
 Occurs in areas of inflammation (increased permeability)

28.  Bismuth pigmentation - Black line
 Arsenuc - Black
 Mercury - black line
 Lead - Bluish red, deep blue or gray (Burtonian line)
 Silver - Violet marginal line

29. B. COLOUR CHANGES ASSOCIATED WITH SYSTEMIC FACTORS
i. Endogenous factors
 Addison’s disease - increased melanin pigmentation
 Peutz-Jeghers syndrome - increased melanin pigmentation
 Albright’s syndrome - increased melanin pigmentation
 Jaundice
 Hemochromatosis
 Diabetes
 Pregnancy
 Blood dyscrasias
 Drugs - Zidovudine, Minocycline,Ketoconazole, Methyldopa

30. ii. Exogenous factors
 Tobacco - Grayish discoloration
 Amalgam - Localized bluish-black
 Coloring agents in food
Amalgam tattoo

31. 3. Changes in GINGIVAL CONTOUR
• Normal gingival contour is scalloped and knife-edged.
• Disease conditions where there are changes in gingival contour are:
Acute and Chronic Gingivitis - Rounded/ rolled marginal gingiva
Gingival enlargement - Bulbous papilla

32.  Stillman’s clefts - Apostrophe shaped indentations extending from
and into gingival margin along root surface mostly on labial surfaces.
Margins of the cleft are rolled underneath the linear gap in gingiva
and remaining margin is blunt.
It may be simple - cleavage in 1 direction
Compound - cleavage in more than 1 direction

33.  McCall’s festoons - Enlargement of the marginal gingiva with
formation of ‘lifesaver’ like gingival prominence usually on canine and
premolar facial surfaces
NUG - Cratered papillae
McCall’s
Festoons

34. 4. Changes in GINGIVAL CONSISTENCY
• In acute gingivitis - puffiness and softening of the gingiva
• In chronic gingivitis - Soggy puffiness that pits on pressure or firm,
leathery consistency.
• Both destructive (edematous) and reparative (fibrotic) changes
coexist in chronic gingivitis hence consistency is determined by their
relative predominance

35. • A gingival lump (s) is seen in the following conditions:
• Erupting third molars
• Pregnancy gingivitis
• Fibroepithelial polyp
• Malignant conditions such as Kaposi’s sarcoma or lymphomas

36. 5. Changes in GINGIVAL SURFACE TEXTURE
i. Loss of stippling (smooth, shiny surface) seen in chronic gingivitis,
atrophic gingivitis and chronic desquamative gingivitis
ii. Leathery texture seen in hyperkeratosis
iii. Nodular surface in drug induced gingival overgrowth
Loss of Stippling

37. Nodular Surface in drug
induced gingival overgrowth

38. 6. Changes in GINGIVAL POSITION
• In a fully erupted normal tooth, position of the gingival margin is 1-
2mm above the CEJ or slightly below the enamel contour
• The junctional epithelium is at the CEJ
• The actual position is the level of epithelial attachment on the tooth
while the apparent position is the level of the crest of gingival margin
• Actual position determined by probing

39. CHANGES IN THE POSITION OF THE GINGIVA INCLUDE:
i. Enlargement
• Gingival margin becomes high on the enamel; partly or nearly covering the
anatomic crown
ii. Recession
• Exposure of the root surface by an apical shift of the gingival attachment
• Severity determined by actual position of the gingiva, not apparent position
Gingival Enlargement Gingival Recession

40. Management of gingivitis
BDS/10/18
Undisa Euro

41. Work up and diagnosis
• Review of your dental and medical history and conditions that may
contribute to your symptoms.
• Examination of your teeth, gums, mouth and tongue for signs of
plaque and inflammation.
• Measuring the pocket depth. In a healthy mouth, the pocket depth is
usually between 1 and 3 millimeters (mm). Pockets deeper than 4
mm may indicate gum disease.
• Dental X-rays to check for bone loss in areas where your dentist sees
deeper pockets.
• Other tests as needed to check for underlying health conditions

42. Gingivitis treatment options
Treatment aim;
• Reduce inflammation
• Removing plaque
• Adoption of good oral care habits
• Antibiotics and antiseptics to control bacteria growth under gums and
teeth.

43. Outline of gingivitis treatment
Good oral hygiene is the main treatment approach to managing tooth and gum
diseases. This involves:
• Brushing the teeth with a manual or electric toothbrush at least twice a day for at
least 2 to 3 minutes at a time.
• Using toothpaste containing recommended fluoride levels.
• Flossing the teeth at least once daily
• Stopping smoking and tobacco chewing
• Using antiseptic mouthwash that contains chlorhexidine may help prevent the
build up of plaque. After using the mouthwash, the mouth should not be rinsed
to allow the antiseptic components to be retained in the mouth.

44. • Regularly attending dental check ups can be helpful in detecting and treating early
gum disease.
• Most adults with healthy gums require at least one visit every two years while those
under 18 years require an annual check up.
• Antibiotics are useful when there is severe gum involvement due to conditions such
as ANUG, trench mouth or periodontitis.
• Some of the most effective antibiotics for ANUG include metronidazole and
amoxicillin.
• Patients with ANUG should be seen within 24-48 hours for re evaluation because of
risk of local or systemic spread of infection
• Gingivitis may cause toothache and painful gums. Anti-inflammatory pain relievers
such as paracetamol and ibuprofen may help ease the pain, swelling and discomfort.

45. • Dental treatments include scaling and polish and root planning. Root
planning is usually only needed in cases of severe gingivitis,
periodontitis or ANUG
• Dental work repair: The dentist may fix or remove crowns, fillings or
bridges that stick out or don’t fit right. Smoother surfaces are easier
to keep clean

46. References
• Carranza FA 12th edition
• Periodontics revisited by Jaypee brothers
• Journal of Periodontology- 2017 Classification of Periodontal an Peri-
Implant Diseases.
• https://my.clevelandclinic.org/health/diseases/10950-gingivitis-and-
periodontal-disease-gum-disease
• https://www.mayoclinic.org/diseases-conditions/gingivitis/diagnosis-
treatment/drc-20354459
• https://emedicine.medscape.com/article/763801-
treatment?form=fpf