Canis ISSN: 2398-2942

Periodontitis

Contributor(s): MarkThompson, Matthew Oxford

Introduction

  • Periodontitis is where mucosal inflammation which has progressed past the level of gingival tissues Periodontal disease severe 01.
  • Signs: halitosis, inflamed gingiva, ulceration, gingival recession, tooth mobility.
  • Diagnosis: conscious examination followed by examination under anesthetic to include periodontal probing and dental radiography.
  • Treatment: periodontal therapy or tooth extraxtion under anesthetic followed by meticulous home care.
Follow the diagnostic tree for Halitosis Halitosis.

Pathogenesis

Etiology

  • Active plaque is the cause of periodontal disease.
  • Plaque is a biofilm of salivary proteins and oral bacteria which adheres to the exposed tooth surface. Plaque is a very stable environment, which can be affected only very minimally by chemicals such as disinfectants and antibiotics. Plaque elimination requires mechanical removal.
  • If plaque persists for a prolonged period it can become calcified to form calculus Teeth: calculus. Calculus is a largely inert material, however it has two factors that promote the progression of periodontal disease. It increases surface area, which is rough and aids plaque deposition.
  • As calculus forms, the oxygen tension within the gingival sulcus changes, promoting the proliferation of anaerobic organisms. It is this switch that leads to the progression of periodontal disease. Inflammatory mediators released in response to the anaerobes promote osteolysis which will cause alveolar bone loss. This may lead to gingival recession or periodontal pocket formation or a combination of both. As the epithelial attachment recedes apically, alveolar bone loss exposes the root surface and the cementum layer. Cementum is rough which promotes in turn greater plaque and calculus deposition as subgingival accumulations. This then further promotes alveolar bone loss in spiralling progression. This is periodontitis, and it is irreversible. It can however be managed and its progession prevented with good professional therapy followed by good home care.
  • If the full thickness of alveolar bone is destroyed bone loss proceeds horizontally from the alveolar crest. In this case, the epithelial attachment usually remains coronal to remaining alveolar bone, forming a suprabony pocket. With horizontal bone loss the gingival margin often recedes with the epithelial attachment which gives periodontitis without pocket formation, known as gingival recession.
  • If a partial thickness of alveolar bone destroyed, especially along the root surface, this is called vertical bone loss. In this case, the epithelial attachment often recedes apically beyond the crest alveolar bone, forming an infrabony pocket. This is a periodontal pocket and owing to the reduced oxygen tension in the pocket, will rapidly progress to deep pocket formation, often exuding pus. Periodontal pockets are harder to manage than gingival recession.
  • The tooth will become mobile when >50% periodontium destroyed. This will weaken the remaining periodontal ligament even more, and most significantly, the periodontal disease will now become significantly more painful for the patient. As the tooth moves within the alveolus, there is stimulation of nerves within the periodontal ligament and at the apex of the tooth supplying the pulp.
  • Eventually the tooth will be exfoliated, taking the majority of bacteria with it.
  • The alveolus will then heal slowly with sclerotic bone (3-6 months).

Predisposing factors

General

Diagnosis

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed papers


ADDED