Gingival Inflammation :

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CLASSIFICATION
I. According to duration:
1. Acute gingivitis: It is sudden in onset and of short duration which is painful. 
2. Chronic gingivitis: It is slow in onset and of long duration, and is painless, unless complicated by acute or subacute exacerbations. It is the most common type of gingivitis.
II. According to distribution:
1. Localized gingivitis: Gingivitis confined to the
gingiva of a single tooth or group of teeth (Fig. 1).
2. Generalized gingivitis: Involves the entire mouth.
3. Marginal gingivitis: Involves the gingival margin and may include a portion of the contiguous attached gingiva (Fig. 2).

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Fig. 1: Localized gingivitis in left maxillary anterior region


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Fig.2: Marginal gingivitis

4. Papillary gingivitis: Involves the interdental papillae and often extends into the adjacent portion of the gingival margin (Fig. 3


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Fig3: Papillary gingivitis

5. Diffuse gingivitis: Affects the gingival margin, the attached gingiva and the interdental papillae.



STAGES OF GINGIVITIS
Page and Schroeder developed a system to categorize the clinical and histopathological stages of periodontaldiseases and defined four histopathological stages of periodontal inflammatory changes: The initial, early and established gingival lesions and an advanced periodontal lesion (Fig. 4). It is important to note that the evidence available at that time largely consisted of animal and human adolescent biopsies. Their description, based on these material, is now considered to be not fully applicable to the normal adult situation. Kinane and Lindhe recently classified healthy gingiva into two types:
• Super healthy or ‘pristine’ state, which histologically has little or no inflammatory infiltrate.
• ‘Clinically healthy’ gingiva, which looks similar clinically, but histologically, has features of an inflammatory infiltrate. In everyday, clinical situations one would normally see the healthy gingiva type and only in exceptional circumstances, such as in a clinical trial with supervised daily cleaning and professional assistance, one would see pristine gingiva


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Fig. 4: Stages of gingivitis

The initial and early lesion descriptions were thought to reflect the histopathology of clinically early stages of gingivitis, while the established lesion reflected the histopathology of more chronic gingivitis. The description of the histopathology of the advanced lesion was considered to reflect the progression of gingivitis to periodontitis.
Stage I: The Initial Lesion
Initial changes in the development of gingivitis occur after 2 to 4 days of plaque accumulation. The first manifestations of gingival inflammation are vascular changes which include dilation of arterioles, capillaries and venules of the dentogingival plexus and increased blood flow. There is increase in the permeability of the microvascular bed resulting in exudation of fluids and proteins into the tissues. As the lesion enlarges, and gingival crevicular fluid flow increases, noxious substances from microbes will be diluted both in the tissue and the crevice. The quantities of leukocytes, mainly polymorphonuclear neutrophils (PMNs) are increased in the connective tissue, the junctional epithelium and the gingival sulcus. The recruitment of leukocytes (predominantly PMNs) from the tissues to the crevice is due to the chemoattractant actions of the host systems (interleukin-8, C5a) and products derived from the biofilm (lipopolysaccharide ). Thus, the increase in the migration of leukocytes and their accumulation within the gingival sulcus is correlated with an increase in the flow of gingival fluid into the sulcus. There is little or no proliferation of junctional epithelium laterally (rete pegs). Collagen depletion within the infiltrated area is noted along with an increase in vascular structures. Exudative and transudative fluid and plasma proteins arrive in the gingival crevice region.
Stage II: The Early Lesion
Initial lesion may be transitory and may be quickly repaired after the removal of plaque. But after 4 to 7 days of plaque accumulation, the clinical signs of erythema appear. There is proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges and thus, bleeding on probing is evident. Lymphocytes (mainly T lymphocytes) and PMNs are predominant at this stage and very few plasma cells are noted within the lesion. 70% of the collagen is destroyed around the cellular infiltrate. The main fiber groups affected appear to be the circular and dentogingival fiber assemblies. The junctional epithelium develops widened intracellular spaces that are infiltrated mainly by neutrophils and small numbers of mononuclear cells, especially monocytes.
Stage III: The Established Lesion
The gingiva gives bluish hue due to engorged and congested blood vessels. Venous return is impaired, and the blood flow becomes sluggish. Extravasation of red blood cells (RBCs) into the connective tissue and breakdown of hemoglobin into its component pigments can also deepen the color of the chronically inflamed gingiva. There is increased fluid exudation and leukocyte migration into the tissues and the gingival crevice. The established lesion as defined by Page and Schroeder is dominated by plasma cells. Collagen loss continues in both lateral and apical directions as the inflammatory cell infiltrate expands, resulting in collagen depleted spaces extending deeper into the tissues which are then available for leukocytic infiltration. The dentogingival epithelium continues to proliferate and the rete pegs extend deeper into the connective tissue in an attempt to maintain epithelial integrity and a barrier to microbial entry. The junctional epithelium is no longer closely attached to the tooth surface. There is no evidence of alveolar bone loss at this stage, or of apical migration of junctional epithelium. Within 2 to 4 weeks after the beginning of plaque accumulation, the gingivitis become established. Migrating leukocytes are found in the junctional epithelium, within widened intercellular spaces.
Stage IV: Advanced Lesion
This is the final stage called as the advanced lesion. The inflammatory cell infiltrate extends laterally and further apically into the connective tissue. The advanced lesion has all the characteristics of the established lesion but differs importantly in that alveolar bone loss occurs, fiber damage is extensive and the junctional epithelium migrates apically from the cementoenamel junction (CEJ). It is generally accepted that plasma cells are the dominant cell type in the advanced lesion.
CLINICAL FEATURES OF GINGIVITIS
Gingival Bleeding
Gingival bleeding is one of the earliest symptoms of gingival inflammation. Gingival bleeding varies in severity, duration, and the ease with which it is provoked. Gingival bleeding is mainly due to the dilation and engorgement of capillaries. Permeability of the sulcular epithelium is increased by degradation of intercellular cementing substances and widening o intercellular spaces. As the inflammation becomes chronic, ulceration of sulcular epithelium takes place. Because the capillaries are engorged and closer to the surface and epithelium being ulcerated and less protective, stimuli that are ordinally innocuous causes rupture of capillaries and gingival bleeding. Etiological factors responsible for gingival bleeding are:
A. Local factors:
a. Acute bleeding: Aggressive toothbrushing, sharp pieces of hard food, gingival burns from hot food or chemicals and necrotizing ulcerative gingivitis.
b. Chronic bleeding: Chronic gingival inflammation.
B. Systemic factors:
a. Vascular abnormality: Vitamin C deficiency and allergy such as Henoch Schönlein purpura
b. Vitamin K deficiency.
c. Platelet disorder: Idiopathic thrombocytopenic purpura.
d. Deficient platelet thromboplastic factors: Uremia, multiple myeloma and postrubella purpura.
e. Coagulation defects: Hemophilia, Christmas disease.
f. Malignancy: Leukemia.
g. Drugs: Salicylates and anticoagulants (dicoumarol, heparin).
Significance of gingival bleeding: Bleeding on probingis easily detectable clinically and therefore, is of value
for the early diagnosis and prevention of more advanced gingivitis. It is a more objective sign and therefore requires less subjective estimation by the examiner. It appears earlier than other visual signs of inflammation. Thus, several gingival indices have been developed based on this earliest sign. Gingival bleeding on probing helps to determine whether the lesion is an active or inactive.
Changes in Gingival Color
The normal gingival color is coral pink which is produced mainly by the vascular supply and modified by overlying keratinized layer. The gingiva become red when there is an increase in vascularization and reduction of keratinization. Color changes vary with the intensity of the inflammation. Initially, there is an increasingly red erythema.
Factors responsible for change in gingival color are:
A. Color changes associated with local factors:
a. Acute gingivitis:
• NUG- marginal bright red erythema. In severe
acute inflammation, the red color gradually becomes a dull, whitish gray (Fig. 5). The gray discoloration produced by tissue necrosis is demarcated from the adjacent gingiva by a thin, sharply defined erythematous zone.
• Herpetic gingivostomatitis: Diffuse
 • Chemical irritations: Patch like/diffuse




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Fig. 5: NUG


b. Chronic gingivitis: Chronic inflammation intensifies the red or bluish red color because of vascular proliferation and reduction of keratinization due to epithelial compression by the inflamed tissue.
c. Metallic pigmentation: Gingival pigmentation from systemically absorbed metals results from perivascular precipitation of metallic sulfides in the subepithelial 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.
• Bismuth pigmentation – Black line
• Arsenic pigmentation – Black
• Mercury pigmentation – Black line
• Lead pigmentation – Bluish red, deep blue o gray (Burtonian line)
• Silver pigmentation – Voilet marginal line
B. Color changes associated with systemic factors:
a. Endogenous factors:
• Addison’s disease – Increased Melanin pigmentation
• Peutz-Jeghers syndrome – Increased Melanin pigmentation
• Albright’s syndrome – Increased Melanin pigmentation
• Jaundice – Yellowish color due to deposti of bilirubin
• Hemochromatosis – Bluish gray due to depostion of Iron
• Diabetes
• Pregnancy
• Blood dyscrasias
• Hyperthyroidism
• Drugs—Chloroquine (slate gray), Minocycline (brown), Chlorpromazine, Zidovudine, Ketoconazole, Methyldopa and Busulphan.
b. Exogenous factors:
• Tobacco/smoking—Grayish color due toincreased melanin pigmentation
• Amalgam – Localized bluish black areas (Fig. 6)
• Coloring agents in food, lozenges and betel.



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Fig. 6: Amalgam tattoo


Changes in Gingival Contour
Normally the contour of marginal gingiva is scalloped and knife-edged. Interdental papilla is pointed and pyramidal in anterior region whereas in posterior region it is tent - shaped, filling the area. The various diseased conditions related to gingival
contour are:
a. Acute and chronic gingivitis: Marginal gingiva may be rounded or rolled.
b. Gingival enlargement: Papilla may be bulbous.
c. Stillman’s clefts: These are apostrophe – shaped identations which extend from and into gingival margin along the root surface, most frequently on the labial or buccal surfaces (Fig. 7). The marginsof the cleft are rolled underneath the linear gap in the gingiva and remainder of gingival margin is blunt instead of knife – edge (Fig. 8). It was originally described by Stillman, as a result of occlusal trauma. It may be simple – cleavage in a single direction or compound – cleavage in more than one direction.
d. McCall’s festoons: McCall’s festoons are the enlargement of the marginal gingiva with the formation of “life-saver” like gingival prominence in relation to canine and premolar facial surfaces mostly (Figs 9 and 10). These are semilunar enlargements named after John Opple McCall who along with Paul R Stillman, believed occlusal traumatism to be an etiologic factor.
e. NUG: Papillae may be cratered.


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Fig. 7: Gingival clefts


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Fig. 8: Stillman's clefts

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Fig. 9: McCall’s festoons in relation to canine and premolars


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Fig. 10: McCall’s festoons

Changes in Gingival Consistency
In acute gingivitis, there is puffiness and softening of the gingiva. In chronic gingivitis, there is soggy puffiness that pits on pressure or firm, leathery consistency. Both destructive (edematous) and reparative (fibrotic) changes coexist in chronic gingivitis and the consistency of the gingival is determined by their relative predominance. Gingival lump is seen in the following conditions: erupting third molars, pregnancy gingivitis, fibroepithelial polyp and malignant conditions (Carcinoma, Kaposi’s sarcoma, Lymphoma).
Changes in the Surface Texture of Gingiva
Conditions in which there is change in the surface texture of gingiva are:
A. Loss of stippling (smooth, shiny surface) is seen in chronic gingivitis (Fig. 11), atrophic gingivitis and chronic desquamative gingivitis.
B. Leathery texture is seen in hyperkeratosis.
C. Nodular surface is seen in drug induced gingival overgrowth (Fig. 12).

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Fig. 11: Loss of stippling producing smooth, shiny surface in mandibular anterior region

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Fig. 12: Nodular surface seen in drug induced gingival enlargement
Changes in the Position of the Gingiva

In fully erupted tooth, position of gingival margin is 1 - 2 mm above CEJ, at or slightly below the enamel contour. The junctional epithelium is at the CEJ. 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 which is seen by direct observation. Actual position is not directly visible but can be determined by probing.
A. Enlargement: When the gingiva enlarges, the gingival margin may be high on the enamel, partly or nearly covering the anatomic crown (Fig. 13).
B. Recession: It is exposure of the root surface by an apical shift in the position of the gingiva. The severity of recession is determined by the actual position of the gingiva, not its apparent position (Fig. 14).

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Fig. 13: Idiopathic hyperplastic gingival enlargement



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Fig. 14: Localized recession around malposed incisor and canine
The characteristics of plaque-induced gingivitis (Mariotti, 1999) are:
• Plaque present in relation to gingival margin
• Disease begins at the gingival margin
• Change in gingival color
• Change in gingival contour
• Sulcular temperature change
• Increased gingival exudates
• Bleeding upon provocation
• Absence of attachment and bone loss
• Histological changes including an inflammatory lesion
• Reversible with plaque removal
POINTS TO PONDER
Gingival conditions/diseases that mainly involve interdental papilla and gingival margin are gingival abscess, necrotizing ulcerative gingivitis, linear gingival erythema and drug induced gingival
enlargement.
Gingival ulcers are usually seen in NUG, herpes simplex virus stomatitis, aphthae, self-injury, malignant neoplasms, drugs, dermatoses, systemic diseases (hematological disorders, tuberculosis, syphilis, herpes virus, HIV).
Gingival changes seen in mouth-breathers are erythema, edema, enlargement, diffuse smooth and shiny surface in the exposed gingival area affecting mainly maxillary anterior region.
Gingival red lesions are usually seen in desquamative gingivitis, erythroplasia, hemangiomas, orofacial granulomatosis, Crohn’s disease, sarcoidosis, Wegener’s granulomatosis,
BIBLIOGRAPHY
1. Carranza FA, Rapley JW, Haake SK. Gingival inflammation. In, Newman, Takei, Carranza. Clinical Periodontology 9th ed WB Saunders 2003;263-68.
2. Carranza FA, Rapley JW. Clinical features of gingivitis. In, Newman, Takei, Carranza. Clinical Periodontology 9th ed WB Saunders 2003;269-78.
3. Carranza FA, Hogan EL. Gingival enlargement. In, Newman, Takei, Carranza. Clinical Periodontology 9th ed WB Saunders 2003;279-96.
4. Claffey N. Plaque Induced Gingival Disease. In, Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant dentistry. 4th ed Blackwell Munksgaard 2003;198-08.
5. Garant PR, Mulvihill JE. The fine structure of gingivitis in the beagle III Plasma cell infiltration of the subepithelial connectivetissue. J Periodontol Res 1972;7:161-72.
6. Gingivitis. In, Grant DA, Stern IB, Listgarten MA. Periodontics. 6th ed CV Mosby Company 1988;315-47.
MCQs
1. The radiographic findings of gingivitis will demonstrate:
A. Vertical bone loss
B. Horizontal bone loss
C. Change in bone trabeculation
D. Normal bone pattern
2. Gingivitis is initiated MOST often by:
A. Malocclusion
B. A hormonal imbalance
C. Vitamin deficiency
D. Microorganisms and their products
E. Psychosocial factors
3. Gingival bleeding on probing appears:
A. Before the color changes
B. After the color changes
C. At the same time as the color changes
D. Not related with the color changes
4. Junctional epithelium shows formation of rete pegs in:
A. Stage I gingivitis (Initial)
B. Stage II gingivitis (Early)
C. Stage III gingivitis (Established)
D. Stage IV gingivitis (Advanced)
5. The predominant inflammatory cell in early lesion:
A. Neutrophil B. T lymphocytes
C. Plasma cell D. Macrophages
6. McCall’s festoon is common in:
A. Incisor area
B. Canine and premolar area
C. Molar area
D. Same in all of the above
7. Crater-like deformities are seen in:
A. NUG
B. Aggressive periodontitis
C. Chronic gingivitis
D. Chronic periodontitis
8. Which of the following is not a clinical feature of necrotizing ulcerative gingivitis:
A. Pocket formation
B. Spontaneous bleeding
C. Pain
D. All of the above
9. All of the exogenous factors can cause gingival colour changes except:
A. Coal dust
B. Alcohol
C. Tobacco
D. Amalgam
10. Endogenous gingival pigmentation can be caused by all of the following except:
A. Iron
B. Melanin
C. Bilirubin
D. Metronidazole
11. Burtonian line is a linear pigmentation of gingival margin due to over exposure to:
A. Bismuth
B. Silver
C. Lead
D. Arsenic
Answers
. 1D           2. D               3. A                       4. B                     5. B
 6B           7. A                8. A                       9. B                   10. D
 11C

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