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Stages of Gingivitis

Stages of Gingivitis

Gingival Diseases

Gingivitis refers to the inflammation of gingiva. The main causative factor is dental plaque (plaque microorganisms are responsible for the pathological changes in gingivitis).

Stages of Gingival Inflammation

  • Initial
  • Early
  • Established
  • Advanced

Image Source: https://www.colgateprofessional.com/students-faculty/trending-topics/can-you-take-a-vacation-from-oral-care

Stage I: The Initial Lesion


The initial response of gingiva is clinically not apparent. Hence, it is called subclinical gingivitis. Vascular changes are the first manifestation of gingival inflammation.

Clinical Manifestations

  • Vascular changes: Dilated capillaries and increased blood flow.
  • The vascular changes are due to microbial activation of leukocytes and subsequent stimulation of endothelial cells.
  • Perivascular connective tissue matrix becomes altered.
  • Exudation and deposition of fibrin in the affected area.
  • Increase in GCF flow.

Microscopic Features

(Seen in connective tissue beneath junctional epithelium)

  • Blood vessel morphology: Widening of small capillaries.
  • Margination: Adherence of neutrophils to the vessel wall (occur in 1 week).
  • Diapedesis (Emigration): PMNs leave the capillaries by migrating through the walls.
  • PMNs can be seen in increased quantities in the connective tissue, the junctional epithelium and the gingival sulcus.
  • Exudation of fluid from the gingival sulcus.

Stage II: The Early Lesion


It is called early gingivitis because of the presence of clinical signs of inflammation, and, occurs 1 week after the beginning of plaque accumulation.

Clinical Manifestations

  • Erythema, due to proliferation of capillaries and increased formation of capillary loops between rete pegs and ridges.
  • Bleeding on probing.
  • Increase in GCF flow.

Microscopic Features

  • Leukocyte infiltration: Seen in the connective tissue beneath the junctional epithelium, consisting mainly of lymphocytes (T cells) and neutrophils, as well as macrophages, plasma cells and mast cells.
  • Increased transmigration of leukocytes in 6-12 days.
  • Phagocytosis: PMNs are attracted to bacteria and engulf them in the process of phagocytosis.
  • PMNs leave the blood vessel -> Follow the chemotactic stimuli from plaque bacteria -> Travel to epithelium -> Cross the basement membrane -> Reach the gingival sulcus.
  • The amount of collagen destruction increases (70%).
  • The main fibers affected are circular and dentogingival fiber groups.
  • Fibroblasts show cytotoxic alteration with increased capacity to collagen production.

Stage III: The Established Lesion


Some established lesion remain stable, do not progress for months or years, while, others are more active and convert to progressively destructive lesions.

Clinical Manifestations

  • Blood vessels become engorged and congested, venous return is impaired, and the blood flow becomes sluggish.
  • The result is localized gingival anoxemia which superimposes a somewhat bluish hue on the reddened gingiva.
  • Deepening of the color of gingiva is due to the extravasation of erythrocytes into connective tissue and the breakdown of hemoglobin.

Microscopic Features

  • An intense, chronic inflammatory reaction is seen.
  • Increased number of plasma cells (key feature). Plasma cells invade deep into the connective tissue, around blood vessels and between bundles of collagen fibers.
  • Predominance of B lymphocytes (immunoglobulin G1 and G3).
  • Junctional epithelium presents widened intercellular spaces filled with lysosomes. The lysosomes contain acid hydrolases that can destroy tissue components.
  • Rete pegs or ridges protrude into the connective tissue, and the basal lamina is destroyed in some areas.

Other Findings

  • Increased collagenolytic activity (due to collagenase enzyme).
  • Increased levels of acid and alkaline phosphatase, beta-glucuronidase, beta-glucosidase, beta-galactosidase, esterase, aminopeptidase and cytochrome oxidase.

Stage IV: The Advanced Lesion


The lesion extends into the alveolar bone and is characterised by periodontal breakdown

Microscopic Features

  • Fibrosis of gingiva.
  • Widespread inflammatory and immunopathologic tissue damage.
  • Plasma cells continue to dominate the connective tissue, and neutrophils continue to dominate the junctional epithelium and gingival crevice.

Important Points


  • Sluggish: A marked slow movement or flow.
  • Anoxemia: Abnormally low oxygen content in arterial blood.
  • Collagenase: An enzyme normally present in gingival tissue and is produced by some oral bacteria and by PMNs in inflammatory conditions. It destroys the collagen by breaking the peptide bonds in it.
  • With good periodontal therapy, stage III gingivitis appears to be reversible.
  • Stage IV is irreversible because it involves the breakdown of alveolar bone.

References


  1. Newman and Carranza's Clinical Periodontology (11th edition), Elsevier, https://amzn.to/49PAzIx
  2. The image used in the cover photo is available on Adobe Stock, https://stock.adobe.com/search?k=gingivitis&asset_id=270061168.

*This article is an excerpt from the above mentioned book and Medical Sutras does not make any ownership or affiliation claims.