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The periodontium is a part of the periodontal tissue complex, which heads the morphofunctional unity of the tissues surrounding the tooth; it is represented by highly differentiated connective tissue, which is located in a closed space between the compact plate of the alveoli and the cement of the tooth root.

Periodontitis is an inflammation of the periodontal tissues.


Cause (etiology) of periodontitis

By its origin, apical periodontitis is divided into:

  1. infectious periodontitis
  2. traumatic periodontitis
  3. medication periodontitis

Infectious apical periodontitis often occurs when microorganisms enter the periodontium (Staphylococcus aureus and white, non-hemolytic streptococcus and hemolytic streptococcus, fusobacteria, spirochetes, fungi), their toxins, decay products of the pulp and dentin into the periodontium from the root canal or periodontal pocket.

According to the method of bacteria penetration, infectious periodontitis is divided into intradental and extradental, intradental and extradental. The latter may include infectious periodontitis, which develops as a result of the transition of the inflammatory process from the surrounding tissues with osteomyelitis, osteitis, periostitis, sinusitis, rhinitis, periodontitis. There are also possible hematogenous and lymphogenous pathways of periodontal disease with tuberculosis, hepatitis, typhoid, and influenza. The intradental pathway of penetration of microorganisms into the periodontium is associated with their entry from the carious cavity or root canal independently or forcibly during endodontic manipulations.

Traumatic apical periodontitis occurs when the peri-apical tissues are injured by endocanal instruments or in the process of pushing a root filling or a pin through the apical opening. The traumatic causes of apical periodontitis also include a blow to the tooth, bruise, fall, push, accidental biting on hard objects. Acute trauma often causes relatively quickly passing irritation of the periodontium and its recovery. But sometimes these injuries are accompanied by hemorrhage, impaired blood circulation in the pulp, followed by its necrosis. This condition does not manifest itself for a long time and is accompanied only by a change in tooth color and a lack of sensitivity to various stimuli. A high filling and an artificial crown, overestimating the bite, are often the cause of the development of traumatic periodontitis due to chronic periodontal microtrauma.

Drug-induced apical periodontitis can occur as a result of the ingress of potent chemical and medicinal substances into the periodontium: arsenous acid, phenol, formalin. The cause of apical periodontitis can be the excretion of phosphate cement, resorcinol-formalin and zinc-eugenol pastes, a pin, and other filling materials behind the apex. This also includes periodontitis, which developed as a result of a local immunological reaction in response to the ingestion of antibiotics, eugenol, chloramine, chlorhexidine, dimexide, iodine for the root apex.


Development (pathogenesis) of periodontitis

The development of periodontal inflammation is associated with the entry of the infectious-toxic contents of the root canal into the periodontal fissure; an irritating agent-coccus, its metabolic products, and drugs are required. In the course of the inflammatory process in the periodontium, an important role is played by endotoxins, which are formed when the membrane of gram-positive bacteria growing in the root canals of teeth devoid of pulp is damaged, in particular, bacterial endotoxin, which has a toxic and pyrogenic effect.

With periodontitis, there is multiple damages to connective tissue cells and a massive release of lysosomal enzymes. Endotoxin trapped in the supra-apical tissues leads to degranulation of mast cells, which are the source of heparin and histamine.

Biologically active components cause a sharp increase in vascular permeability, edema, and infiltration increase. Microcirculation is disturbed, thrombosis, hyperfibrinolysis, and secondary hypoxia are observed, which leads to depolymerization of the basic substance. Hypoxia increases, tropism is disturbed, signs of inflammation are manifested: local temperature rise, pain, edema, hyperemia, dysfunction. The tissue becomes permeable due to the formation of voids in the base substance, its main function is fulfilled - protective. The trophic function is sharply disrupted: the cell is not able to receive oxygen and LHC from the basic substance and, conversely, to give it waste products. Slagging of both cells and intercellular substance is noted, the latter is associated with dysfunction of the vascular wall.

Bacterial endotoxins activate complement components, biologically active substances are formed that enhance vascular permeability, and the result is the accumulation of mononuclear lymphocytes and macrophages. These cells secrete enzymes that increase the activity of osteoclasts, which lead to the destruction of bone tissue.


Periodontitis classification

In the practice of therapeutic dentistry, the Periodontitis classification is adopted as a basis, which makes it possible to characterize the degree of damage to periodontal tissues.

Classification of apical periodontitis:

  1. Acute apical periodontitis:
    • phase of intoxication
    • phase of exudation: serous, purulent
  2. Chronic apical periodontitis:
    • chronic apical fibrous periodontitis
    • chronic apical granulating periodontitis
    • chronic apical granulomatous periodontitis
  3. Chronic apical periodontitis in the acute stage:
    • chronic apical fibrous periodontitis in the acute stage
    • chronic apical granulating periodontitis in the acute stage
    • chronic apical granulomatous periodontitis in the acute stage


Clinical symptoms of periodontitis

Diagnosis of periodontitis

Acute apical periodontitis

The main symptom of acute apical periodontitis is persistent localized pain. The nature of pain, its severity, as well as other signs of the course of acute apical periodontitis, have local and general manifestations, depend on the accumulation of serous or purulent exudate in the root apex.

Clinical manifestations of acute apical periodontitis are due to the phase of the course of acute periodontal inflammation. There are two main phases:

  1. Intoxication phase - this stage is characterized by the patient's complaints of constant localized pain of varying intensity, aggravated by biting and touching the tooth. The patient always accurately identifies the affected tooth.
    Objectively: the face is symmetrical, mouth opening is free. The mucous membrane in the projection of the affected tooth is pale pink. The tooth crown is not discolored, there is a cavity or permanent filling. Percussion is slightly painful, signs of the increased sensitivity of the periodontium appear.
  2. Exudation phase - at this stage, the severity of the symptoms of inflammation depends on the nature of the exudate. The patient's complaints of continuous pain, which can be kept at the same level or intensify. The patient accurately points to the affected tooth, the feeling of a "grown" tooth, pain when biting or even lightly touching the tooth.
    Objectively: percussion is painful in the vertical direction, and then in the horizontal direction. The tooth is mobile, not changed in color. Often the crown is intact, and in the presence of a carious cavity, probing of the walls and bottom of the carious cavity is painless. The cavity of the tooth is usually not opened, and when it is opened (in the cavity of the tooth and root canals), necrotic decay of the pulp is observed. The mucous membrane in the projection of the diseased tooth is hyperemic and edematous, palpation is painful.

The exudation phase is characterized by all five signs of inflammation: local fever, pain, edema, hyperemia, and dysfunction. The progression of an acute inflammatory process at the stage of exudation can lead to significant collateral edema of the peri-maxillary tissues. Regional lymph nodes are unchanged or slightly enlarged on the side of the diseased tooth, painless on palpation, mobile. Body temperature is normal. The general condition is not disturbed.

The serous phase of acute periodontitis can turn into purulent, which lasts about 20 days. The clinical picture becomes brighter, the pain intensifies, becomes pulsating, most often becomes continuous, radiates along the branches of the trigeminal nerve. The pain is especially aggravated by touching the tooth, and therefore the patient keeps his mouth half-open.

The condition of the affected tooth is similar to that of serous acute apical periodontitis. The color of the tooth is not changed, the crown of the tooth may be intact or destroyed, with the presence of a deep carious cavity filled with necrotic dentin. The cavity of the tooth is often not opened, probing of the walls, the bottom of the carious cavity is painless. The affected tooth is pathologically mobile, percussion is sharply painful. The mucous membrane of the transitional fold, palate, sometimes the alveolar process of the lingual surface in the area of the affected and adjacent teeth is edematous, hyperemic. Lymph nodes submandibular, chin, less often buccal enlarged, painful on palpation, mobile.

All these phenomena increase with the accumulation of exudate in the periodontal gap. The excruciating pain can last for several days. As soon as the purulent exudate finds a way out, often through the periosteum, the pain syndrome weakens, patients may notice pain in the jaw, deterioration of the general condition, a complication of acute purulent apical periodontitis develops - periostitis, and in more advanced cases - phlegmon of the peri-maxillary region, acute odontogenic osteomyelitis.


Periodontitis treatment

The objects of intervention in the treatment of apical periodontitis are the root canal with its numerous branches, dentinal tubules with abundant microflora, as well as periodontal tissue in a state of acute or chronic inflammation.

Treatment of acute apical periodontitis

  1. treatment in the intoxication stage (performed in one visit):
    • anesthesia (modern highly effective anesthetics - 4% ultracaine, 4% alfacaine, 4% septonest solution, 2% lidocaine solution). To enhance the analgesic effect and prolong the action of the anesthetic, you can add a 0.1% solution of epinephrine hydrochloride (1 drop per 10-15 ml of anesthetic). But it must be remembered that vasoconstrictors are contraindicated in patients with diseases of the cardiovascular system, diabetes mellitus in the stage of decompensation, as well as in the elderly.
    • removal of a dressing or old filling, preparation of a carious cavity;
    • opening of the tooth cavity (creating wide and convenient access of the instrument to the tooth cavities and the mouth of the root canal);
    • expansion of the root canal orifice;
    • evacuation of the disintegration of the pulp from the root canal (work with all endodontic instruments should be carried out in stages, parietal and half-turned).
    • drug treatment of the root canal (with appropriate antidotes, non-irritating antiseptics heated to 40 °, 0.1% potassium permanganate solution, 3% sodium hypochloride solution, 0.02% furacilin solution, 0.1% dimexide solution, 0.06% chlorhexidine solution bigluconate. After drug treatment, the root canal is defatted and dried with dry sterile tampons on a root needle or paper pins of an appropriate size.
    • root canal filling (completion of the procedure - X-ray control);
    • the imposition of a permanent seal.
  2. treatment in the phase of exudation (carried out in two visits)

On the first visit, preparation of the carious cavity or trepanation of the crown of the tooth with a turbine tip, opening the cavity of the tooth, widening the mouth of the root canal, removing the disintegration of the pulp from the root canal, and opening the apical opening is performed with anesthesia. The criterion for controlling the opening of the apical foramen is the appearance of exudate in the lumen of the root canal. From the first visit, we leave the tooth open, warn the patient that it is necessary to insert a small cotton swab into the tooth before eating, and after eating, remove the cotton swab from the carious cavity and rinse the mouth with water. If apical periodontitis is complicated by periostitis, there is hyperemia and edema of the mucous membrane, painful palpation and smoothness of the transitional fold in the area of the diseased tooth, an increase in body temperature, a change in the blood formula, then a course of broad-spectrum antibiotics, desensitizing drugs is prescribed. At the same time, an incision is made along the transitional fold, with a dissection of the periosteum, the wound is drained.

On the second visit, anamnesis is collected (whether the tooth hurt, whether there was a pain when chewing food), after which the objective status is assessed: the state of the mucous membrane surrounding the diseased tooth, lymph nodes, percussion data, the presence or absence of exudate in the root canal.

In the absence of complaints and a satisfactory general and local condition of the patient, they begin instrumental treatment of the root canal. Further - drug treatment of the root canal: solutions of proteolytic enzymes, antiseptics are used.

Then degrease, dry, seal, make a control X-ray examination of the filled root canal, put a permanent seal.

Treatment of chronic forms of apical periodontitis.

The goal of treatment of chronic apical periodontitis is to exclude the root canal as a source of periodontal inflammation and to actively influence the destructive processes in the periapical tissues.reatment of any form of chronic apical periodontitis is indicated in one visit:

  1. preparation of a carious cavity in compliance with all the rules and stages;
  2. opening of the tooth cavity;
  3. widening the mouth of the root canal and creating good access to it;
  4. removal of putrid masses and necrotic dentin under an antiseptic bath using the entire range of endodontic instruments.
  5. Degreasing and dehydrating the walls of the root canal: for this purpose, modern dentistry recommends the use of drugs: Netispad, Styptic, Largal ultra, Canal plus.
  6. Root canal filling up to the physiological apex followed by X-ray, confirming the quality of the root canal obturation. Filling of the root canal with hardening pastes and gutta-percha is shown. The first portion of the filling material is introduced into the root canal at the tip of the Miller's needle and brought under pressure to the apex of the tooth root using a cotton swab, which makes it possible to effectively obturate the apex; the second portion - on the channel filler.
  7. Permanent filling.

Patients with destructive forms of apical periodontitis are registered in the dispensary. Repeated clinical and X-ray examination is carried out after 3, 6, 12 months. If upon examination after 12 months, the patient does not present any complaints, and no pathological changes are found on the roentgenogram in the root apex, then further observation is not required, the patient is removed from the dispensary. If, after 12 months, even in the absence of patient complaints, the destruction of the peri-apical tissues is radiologically determined, repeated treatment is required - removal of the root filling, drug treatment, and mechanical treatment of the root canals with their subsequent filling.