Specifics of the surgical intervention
Although the topic directly concerns indications for extraction, understanding the consequences of the procedure itself is of fundamental importance. Tooth extraction involves the application of significant mechanical forces.
During extraction, complex trauma to the tooth-supporting apparatus occurs:
- The mucous membrane and periodontal ligaments are ruptured.
- The periosteum and bone tissue of the dental alveolus are traumatized.
- Local blood vessels and nerve endings are damaged.
The result of this mechanical impact is the triggering of a cascade of reactions that form the clinical picture of acute or chronic odontogenic inflammation (Lat. inflammatio).
Pathogenesis of the acute inflammatory response
Inflammation has an evolutionary, protective, and adaptive character. Its global task is the elimination of the damaging factor and the restoration of tissue structure. The process strictly proceeds in stages:
- Stage of alteration. Initiating factor. Primary alteration is caused by the agent itself (e.g., bacterial toxins or trauma during extraction), while secondary alteration is caused by lysosomal enzymes and tissue acidosis ("self-damage").
- Stage of vascular changes (exudation). Includes a complex vascular reaction. First, a short-term arteriolar spasm occurs, leading to ischemia and pain. Then, arterial hyperemia develops (redness caused by the action of mediators), which is replaced by venous hyperemia. The latter is characterized by slowed blood flow up to stasis, edema, and cyanosis. At the same time, the fluid part of the blood and leukocytes migrate outside the vessels.
- Stage of proliferation. The final stage, ensuring repair through local cell division (fibroblasts) and connective tissue formation.
Cellular mechanisms and phagocytosis
Obligate phagocytes—neutrophils and macrophages—play a key role in pathogen destruction. Leukocyte emigration from the bloodstream into tissues is directed by chemotaxis—directional movement toward the focus along a chemical concentration gradient (chemoattractants such as the C3a and C5a complement fractions).
The process of destroying a foreign agent (phagocytosis) is divided into three stages:
- Recognition of the agent using opsonins (e.g., IgG antibodies).
- Ingestion with the formation of an intracellular phagosome and its subsequent fusion with a lysosome.
- Destruction (killing) through the generation of active bio-oxidants (hydrogen peroxide, superoxide anion radical).
Chronification of the process and microbiota
Periapical inflammation most commonly arises from the introduction of polymicrobial associations from the affected pulp into the periodontium (due to caries, poor-quality endodontic treatment, or dental trauma). It is important to understand that periapical infection cannot resolve spontaneously.
Unlike acute inflammation, where neutrophils play the main role, chronic inflammation is characterized by the formation of persistent infiltrates of macrophages and lymphocytes. Macrophages are capable of releasing fibronectins, anchoring in the focus and forming granulomas.
A huge role in maintaining the infection is played by the unique oral microbiota organized into biofilms on the enamel and mucosa. Among the bacteria, Actinobacteria, Bacteroidetes, Fusobacteria, and spirochetes dominate, supporting inflammation in periodontal tissues.
Briefly: answers to topical questions
What are the absolute indications for tooth extraction?
- Purulent inflammatory process in periapical tissues — unresponsive to conservative therapy and posing a direct threat of purulent-inflammatory complications: acute jaw osteomyelitis, abscess or phlegmon, maxillary sinusitis, lymphadenitis, and other complications.
What are the relative indications for tooth extraction?
- Impossibility of conservative therapy — due to total destruction of the coronal part of the tooth or anatomical/iatrogenic root canal obstruction.
- Perforation of the tooth root wall — caused by an endodontic instrument.
- Inefficacy of conservative treatment — of periodontitis (typical for multi-rooted teeth).
- Location of the tooth — directly within a jaw fracture line.
- Involvement of the tooth in the inflammation zone — in specific infectious diseases (syphilis, actinomycosis, tuberculosis).
- Causative (odontogenic) teeth — which caused inflammation in the maxillary sinus.
- Grade III–IV tooth mobility — in severe periodontitis.
- Supernumerary teeth — when they cause eruption difficulties.
- Chronic trauma to the mucous membrane — of the oral cavity by a tooth.
- Impacted and dystopic teeth — associated with local pathological processes.
What are the local contraindications for tooth extraction?
- Acute herpetic lesion — of the oral mucosa (OM), vermilion border of the lips, and skin.
- Ulcerative gingivitis and stomatitis — inflammatory diseases of the gums and mucosa.
- Location of the tooth — within a malignant or vascular tumor.
What are the general (somatic) contraindications for tooth extraction?
- Infectious diseases — in the acute stage of development (influenza, ARVI, tonsillitis, diphtheria, hepatitis A).
- Systemic blood disorders — leukemia, leukopenia, agranulocytosis, hemophilia, reduced blood clotting, Werlhof's disease.
- Physiological states in women — pregnancy before the 3rd and after the 7th month, menstruation.
- Endocrine pathology — in the stage of decompensation, diabetic coma, hypothyroidism and hyperthyroidism in the acute stage.
- Cardiovascular diseases — in the acute or decompensated stage (acute myocardial infarction, angina pectoris at rest, hypertensive crisis, arrhythmias).
- Nervous system disorders — acute cerebrovascular accident, meningitis, encephalitis, epilepsy, psychoses, traumatic brain injury.
- Mental illnesses — in the acute stage (schizophrenia, manic-depressive psychosis).
- Acute diseases of parenchymal organs — liver, kidneys, pancreas.
Class and exam questions
Why does throbbing pain occur during inflammation?
The throbbing nature of the pain is associated with the phenomenon of prestasis, when a pendulum-like movement of blood occurs in the microvessels: during systole, it moves toward the veins, and during diastole, it flows back.
What triggers arterial hyperemia?
It develops due to the accumulation of vasoactive inflammatory mediators in the focus, which relax the smooth muscle walls of microvessels, increasing blood flow.
Which cells predominate in a chronic inflammatory infiltrate?
The basis of persistent infiltrates in chronic inflammation (e.g., in granulomas) is mononuclear phagocytes—macrophages and lymphocytes.
What else to study on this topic
- Classification of inflammatory mediators (cellular and humoral)
- Pathogenesis of pain: the role of prostaglandins and algogenic substances
- Hormonal regulation of proliferation and regeneration processes
- Mechanisms of increased vascular permeability in exudation
- Kinetics of cellular migration in the first 48 hours of inflammation
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