Definition and classification of periodontitis
Periodontitis is an inflammation of the periodontal tissues. Despite the brevity of the definition, it fully captures the essence of the pathological process developing in the tooth ligamentous apparatus.
In clinical practice, several classifications are used:
- By localization: apical, marginal, diffuse.
- By etiology: infectious, traumatic, drug-induced (the latter may acquire an allergic form in case of sensitization to a medication extruded beyond the apex).
- According to Lukomsky (the most commonly used): acute, chronic, and acute exacerbation of chronic. Acute is divided into serous and purulent (each being localized or diffuse). Chronic is represented by three forms: fibrous, granulomatous, granulating.
- According to ICD-10 — for medical documentation; codes correspond to the formulations of Lukomsky's classification.
Etiology
The microbial landscape of the periodontitis focus is diverse and represented by associations of microorganisms. Among them, the prevalent ones are:
- streptococci (predominantly non-hemolytic, less frequently viridans and hemolytic);
- staphylococci, pneumococci;
- rod-shaped forms, obligate anaerobes;
- non-fermenting Gram-negative bacteria, veillonellae, lactobacilli;
- yeast-like fungi, neisseriae, actinomycetes, corynebacteria.
In chronic forms, associations number from 3 to 7 species; pure cultures are isolated extremely rarely. Changes in quantitative ratio, virulence, and interaction of microorganisms activate the most aggressive forms and provoke exacerbation.
Pathogenesis of acute periodontitis
Acute inflammation develops when infection penetrates the periodontium via three pathways: through the root canal from a necrotic and infected pulp (via the apical foramen), through the periodontal pocket (in marginal periodontitis), and hematogenously (retrograde pathway).
Multiplying microorganisms release endotoxins, triggering an inflammatory response with all classical components: alteration, exudation, proliferation.
The course is influenced by local factors: lack of exudate outflow from the pulp chamber and root canal (massive orthopedic restoration, extensive filling), increased masticatory load on a tooth with affected pulp. General factors — past infections, hypothermia, overheating — also contribute to the development of the process.
Pathogenesis of chronic periodontitis and radicular cysts
Chronic periodontitis proceeds as an immune process — a response to continuous antigenic irritation of the delayed-type hypersensitivity reaction type. The marker of transition to the chronic stage is the formation of granulation tissue.
Bone tissue resorption in the periapical region is caused by bacterial toxins and breakdown products. The osteoclast-activating factor — a lymphokine of T-effectors — increases osteoclast activity millions of times. Inflammation persists until the antigen is eliminated, i.e., until high-quality endodontic or surgical debridement is performed.
In immunodeficiencies (HIV, intoxication, trauma, immunosuppressive therapy, radiation therapy), the process is resistant to conservative treatment.
Radicular cysts have a specific pathogenesis. Their capsule is formed from Malassez epithelial rests — remnants of odontogenic epithelium. In the focus of inflammation, upon a decrease in pH and carbon dioxide partial pressure, the rests are activated, begin to divide, and form a cystic lesion. In 85% of cases, the cyst communicates with the root canal — bay cyst. In other cases, it is separated by a thin epithelial layer — true cyst, which does not respond to endodontic treatment.
Clinical presentation of acute apical periodontitis
Acute apical periodontitis proceeds in two phases.
- Intoxication phase. Symptoms are scarce: aching pain in the causative tooth.
- Serous exudation phase. Prolonged moderate aching pain, aggravation upon biting, increased sensitivity to vertical percussion. The mucosa of the mucobuccal fold shows no visible changes. The patient often cannot precisely point to the causative tooth; there is no response to thermal stimuli.
- Purulent exudation phase (3rd–4th day). Pain is throbbing and constant. The «increased tooth» symptom is characteristic — the sensation of tooth elongation, inability to bite. Pathological mobility is possible due to the separation of periodontal fibers. Edema and hyperemia of the mucobuccal fold appear in the projection of the root, regional lymph nodes are slightly enlarged and mildly tender. There is no response to EPT.
The general condition depends on immunoreactivity: low-grade fever, weakness, elevated ESR, and leukocytosis are possible. With prolonged exposure to a chemical factor, inflammation acquires a persistent course; in severe cases, necrosis of the adjacent bone tissue area with subsequent sequestration is possible.
Diagnostics
Diagnosis is based on two principles.
- Anamnesis: the tooth was previously treated or pulpitis-like pain was noted.
- X-ray examination — periapical radiograph, orthopantomogram (OPG), CBCT. Since periapical radiography and OPG provide a two-dimensional image, they do not always fully reflect the extent of the process; CBCT is preferable.
In the exudative form, widening of the periodontal ligament space in the apical part is determined, sometimes extending to marginal areas. Visually and radiographically, a carious cavity communicating with the dental cavity is detected; the root canal is usually unfilled or improperly filled.
Key points
- Periodontitis is an inflammation of periodontal tissues; the main clinical classification is according to Lukomsky.
- The microbial landscape is represented by associations of 3–7 species with a predominance of streptococci and anaerobes.
- Acute inflammation develops upon infection penetration via the root canal, periodontal pocket, or hematogenously.
- The chronic process is a delayed-type hypersensitivity reaction with the formation of granulation tissue.
- Bone resorption is driven by the osteoclast-activating factor of T-effectors.
- Radicular cysts are formed from Malassez epithelial rests; true cysts do not respond to conservative therapy.
- Acute apical periodontitis goes through phases of intoxication, serous, and purulent exudation; the «increased tooth» symptom is characteristic.
- The main method of instrumental diagnostics is X-ray examination, optimally CBCT.