Periodontitis- inflammation of the tissues located in the periodontal gap (periodontitis) - can be infectious, traumatic and medicinal.

Infectious periodontitis occurs when an autoinfection occurs in the oral cavity. More often the root membrane at the apex of the tooth is affected, less often - the marginal part of the periodontium.

Traumatic periodontitis develops as a result of both single (blow, bruise) and chronic trauma (occlusion disturbance when the height of a tooth is increased with an artificial crown or filling; in the presence of bad habits - holding nails in teeth, biting threads, peeling seeds, cracking nuts, etc. ). Drug-induced periodontitis can occur during the treatment of pulpitis, when potent medicinal substances are used in the treatment of the canal, as well as due to an allergic reaction of the periodontium to drugs. In clinical practice, infectious apical periodontitis is the most common.

According to the clinical picture and pathoanatomical changes, inflammatory periodontal lesions can be divided into the following groups (according to I.G. Lukomsky):

I. Acute periodontitis

1. Serous (limited and diffuse)

2. Purulent (limited and diffuse)

II. Chronic periodontitis

1. Granulating

2. Granulomatous

3. Fibrous

III. Chronic periodontitis in the acute stage.

WHO classification of periodontitis (ICD-10)

K04 Diseases of periapical tissues

K04.4 Acute apical periodontitis of pulpal origin

• Acute apical periodontitis NOS

K04.5 Chronic apical periodontitis T

• Apical granuloma

K04.6 Periapical abscess with fistula

• dental
• dentoalveolar
• periodontal abscess of pulpal origin.

K04.60 Having communication [fistula] with the maxillary sinus

K04.61 Having communication [fistula] with the nasal cavity

K04.62 Having communication [fistula] with the oral cavity

K04.63 Having communication [fistula] with the skin

K04.69 Periapical abscess with fistula, unspecified

K04.7 Periapical abscess without fistula

• Dental abscess
• Dentoalveolar abscess
• Periodontal abscess of pulpal origin
• Periapical abscess without fistula

K04.8 Root cyst

Periodontitis is a common inflammatory disease in the periapical tissues. According to statistics, more than 40% of diseases of the dental system are periodontal inflammations, ahead of them only caries and pulpitis.

Periodontal diseases affect literally all age groups - from young to old. Percentages based on 100 cases of visiting a dentist for dental pain:

• Ages from 8 to 12 years – 35% of cases.
• Age 12-14 years – 35-40% (loss of 3-4 teeth).
• From 14 to 18 years – 45% (with the loss of 1-2 teeth).
• 25-35 years old – 42%.
• Persons over 65 years old – 75% (loss of 2 to 5 teeth).

If periodontitis is not treated, chronic foci of infection in the oral cavity lead to pathologies of internal organs, among which endocarditis is the leader. All periodontal diseases in general, one way or another, affect a person’s health and significantly reduce their quality of life.

ICD 10 code

In dental practice, it is customary to classify diseases of periapical tissues according to ICD-10. In addition, there is an internal classification, which was compiled by specialists from the Moscow Medical Dental Institute (MMDI), which is accepted in many medical institutions in the post-Soviet space.

However, ICD-10 still remains officially recognized and used in documentation; periodontitis is described in it as follows:

	Name
	Diseases of periapical tissues
	Acute apical periodontitis of pulpal origin
	Acute apical periodontitis NOS
	Chronic apical periodontitis
	Apical granuloma
	Periapical abscess with fistula: Dental Dentoalveolar
	Fistula communicating with the maxillary sinus
	Fistula communicating with the nasal cavity
	Fistula communicating with the oral cavity
	Fistula communicating with the skin
	Periapical abscess, unspecified, with fistula
	Periapical abscess without fistula: Dental abscess Dentoalveolar abscess Periodontal abscess of pulpal etiology Periapical abscess without fistula
	Root cyst (root cyst): Apical (periodontal) Periapical
	Apical, lateral cyst
	Residual cyst
	Paradental inflammatory cyst
	Root cyst, unspecified
	Other unspecified diseases of periapical tissues

It should be recognized that there is still some confusion in the classification of periodontal diseases, this is due to the fact that in addition to the internal systematization of MMIS adopted by dental practitioners in the countries of the former CIS, in addition to ICD-10, there are also WHO classification recommendations. These documents, which deserve respect and attention, do not have major differences; however, the section “chronic periodontitis” can be interpreted variably. In Russia and Ukraine there is a clinically substantiated definition of “fibrous, granulating, granulomatous periodontitis”, while in ICD-10 it is described as apical granuloma, in addition, in the international classification of diseases of the 10th revision there is no nosological form “chronic periodontitis in the acute stage ", which is used by almost all domestic doctors. This definition, adopted in our educational and medical institutions, in ICD-10 replaces the code K04.7 “periapical abscess without fistula formation,” which completely coincides in clinical picture and pathomorphological justification. However, in terms of documenting diseases of periapical tissues, ICD-10 is generally accepted.

Causes of periodontitis

Etiology, causes of periodontitis are divided into three categories:

1. Infectious periodontitis.
2. Periodontitis caused by trauma.
3. Periodontitis provoked by taking medications.

Pathogenetic therapy depends on etiological factors; its effectiveness is directly determined by the presence or absence of infection, the degree of change in the trophism of periodontal tissue, the severity of injury or exposure to aggressive chemical agents.

1. Periodontitis caused by infection. Most often, periodontal tissue is affected by microbes, among which the leading ones are hemolytic streptococci (62-65%), as well as saprophytic streptococci and staphylococci, non-hemolytic (12-15%) and other microorganisms. Epidermal streptococci are normally present in the oral cavity, without causing inflammatory processes, but there is a subspecies - the so-called “green” streptococcus, which contains a surface protein element. This protein is able to bind salivary glycoproteins, combine with other pathogenic microorganisms (yeast-like fungi, veyonella, fusobacteria) and form specific plaques on teeth. Bacterial compounds destroy tooth enamel, simultaneously releasing toxins directly into the periodontium through the gum pockets and root canals. Caries and pulpitis are among the main causes of infectious periodontitis. Other factors may be viral and bacterial infections that penetrate the periodontium through the blood or lymph, such as influenza, sinusitis, osteomyelitis. In this regard, infectious inflammatory processes in the periodontium are divided into the following groups:

• Intradental periodontitis.
• Extradental periodontitis.

1. Periodontitis caused by traumatic injury. Such an injury can be a blow, bruise, or being caught when chewing a hard element (pebble, bone). In addition to one-time injuries, there is also chronic trauma caused by incorrect dental treatment (incorrectly applied filling), as well as malocclusion, pressure on a number of teeth in the process of professional activity (the mouthpiece of a wind instrument), bad habits (biting hard objects with teeth - nuts, the habit of chewing pens , pencils). With chronic tissue damage, at first there is a forced adaptation to overload; repeated trauma gradually transforms the compensation process into inflammation.
2. Periodontitis caused by a drug factor is usually the result of incorrect therapy in the management of pulpitis or the periodontium itself. Potent chemicals penetrate into tissues, causing inflammation. This could be tricresolfor, arsenic, formalin, phenol, resorcinol, phosphate cement, paracin, filling materials, and so on. In addition, all allergic reactions that develop in response to the use of antibiotics in dentistry also fall into the category of drug-induced periodontitis.

The most common causes of periodontitis can be associated with pathologies such as chronic gingivitis, periodontitis, pulpitis, when periodontal inflammation can be considered secondary. In children, periodontitis often develops against the background of caries. Factors that provoke periodontal inflammation can also be caused by non-compliance with the rules of oral hygiene, vitamin deficiency, and lack of microelements. It should be noted that there are also somatic diseases that contribute to the development of periodontitis:

• Diabetes.
• Chronic pathologies of the endocrine system.
• Cardiovascular diseases, which can also be provoked by a chronic source of infection in the oral cavity.
• Chronic pathologies of the bronchopulmonary system.
• Diseases of the digestive tract.

To summarize, we can identify the 10 most common factors that provoke periodontitis:

• Inflammatory process in the pulp, acute or chronic.
• Gangrenous lesion of the pulp.
• Overdose of medications in the treatment of pulpitis (treatment period or amount of drug).
• Traumatic damage to the periodontium during pulp treatment or canal treatment. Chemical trauma during sterilization and canal sanitation.
• Traumatic damage to the periodontium during filling (pushing through the filling material).
• Residual pulpitis (root).
• Penetration of infection located in the canal beyond the apex.
• An allergic reaction of periodontal tissue to medications or decay products of microorganisms that cause inflammation.
• Periodontal infection through blood, lymph, and less often by contact.
• Mechanical trauma to the tooth – functional, therapeutic (orthodontic manipulation), malocclusion.

Pathogenesis of periodontitis

The pathogenetic mechanism for the development of inflammation of periodontal tissue is due to the spread of infection and toxins. Inflammation can be localized only within the boundaries of the affected tooth, but it can also affect neighboring teeth, the soft gum tissue surrounding them, and sometimes even the tissue of the opposite jaw. The pathogenesis of periodontitis is also characterized by the development of phlegmon, periostitis during an advanced chronic process and its subsequent exacerbation. Acute periodontitis develops very quickly, inflammation occurs in an anaphylactic, hyperergic type with a sharp reactive response of the body, increased sensitivity to the slightest irritant. If the immune system is weakened or the irritant is not too active (low-virulent bacteria), periodontitis becomes chronic, often asymptomatic. A constantly active periapical focus of inflammation affects the body in a sensitizing manner, which leads to chronic inflammatory processes in the digestive organs, heart (endocarditis), and kidneys.

The route of infection into the periodontium:

• Complicated pulpitis provokes the entry of toxic contents into the periodontium through the apical foramen. This process is activated by food intake and chewing function, especially with malocclusion. If the cavity of the affected tooth is sealed, and necrotic decay products have already appeared in the pulp, any chewing movement pushes the infection upward.
• Trauma to a tooth (impact) provokes destruction of the dental bed and periodontium; infection can penetrate into the tissue by contact if oral hygiene is not observed.
• Hematogenous or lymphogenous infection of periodontal tissue is possible in case of viral diseases - influenza, tuberculosis, hepatitis, while periodontitis occurs in a chronic, often asymptomatic form.

Statistics say that the most common is the descending route of infection with streptococci. The data for the last 10 years is as follows:

• Strains of non-hemolytic streptococci – 62-65%.
• Strains of alpha-hemolytic viridans streptococci (Streptococcus mutans, Streptococcus sanguis) – 23-26%.
• Hemolytic streptococci – 12%.

Periodontitis of the tooth

Periodontium is a complex connective tissue that is part of the periodontal tissue complex. Periodontal tissue fills the space between the teeth, the so-called periodontal gaps (between the plate, the alveolar wall and the cementum of the tooth root). Inflammatory processes in this area are called periodontitis, from the Greek words: about - peri, tooth - odontos and inflammation - itis, the disease can also be called pericementitis, since it directly concerns the dental cement of the root. Inflammation is localized at the top - in the apical part, that is, at the apex of the root (apex in translation top) or along the edge of the gums, less often the inflammation is diffuse, spread throughout the periodontium. Dental periodontitis is considered a focal inflammatory disease, which relates to diseases of periapical tissues in the same way as pulpitis. According to practical observations of dentists, periodontal inflammation is most often a consequence of chronic caries and pulpitis, when decay products of a bacterial infection, toxins, and microparticles of dead pulp fall from the root hole into the socket, causing infection of the dental ligaments and gums. The magnitude of focal damage to bone tissue depends on the period, duration of inflammation and the type of microorganism - the causative agent. The inflamed root membrane of the tooth and the tissues adjacent to it interfere with the normal process of eating; the constant presence of an infectious focus provokes a painful symptom, which is often intolerable when the process worsens. In addition, toxins enter the internal organs through the bloodstream and can cause many pathological processes in the body.

Periodontitis and pulpitis

Periodontitis is a consequence of pulpitis, therefore, pathogenetically, these two diseases of the dental system are related, but are considered different nosological forms. How to distinguish periodontitis and pulpitis? Most often, it is difficult to differentiate the acute course of periodontitis or pulpitis, so we offer the following criteria for distinction, presented in this version:

Serous periodontitis, acute form	Acute pulpitis (localized)
Increasing pain symptom Pain does not depend on irritants Probing does not cause pain The mucous membrane is changed	The pain is paroxysmal and spontaneous Probing causes pain Mucous membrane without changes
Acute purulent process in the periodontium	Acute diffuse pulpitis
Constant pain, spontaneous pain The pain is clearly localized in the causative tooth Probing – no pain The mucous membrane is changed Deterioration of general condition X-ray shows changes in periodontal structure	Paroxysmal pain Pain radiates to the trigeminal nerve canal Mucous membrane without changes
Chronic periodontitis, fibrous form	Caries, beginning of pulpitis
Changing the color of the tooth crown Probing – no pain No reaction to temperature influence	The color of the tooth crown is preserved Probing is painful Pronounced temperature tests
Chronic granulating periodontitis	Gangrenous pulpitis (partial)
Transient spontaneous pain Probing – no pain The mucous membrane is changed General condition suffers	Pain worsens from hot, warm food or drink Probing causes pain Mucous membrane without changes General condition is within normal limits
Chronic granulomatous periodontitis	Simple pulpitis in chronic form
The pain is minor and tolerable Tooth discoloration Probing without pain No reaction to temperature stimuli	Pain due to temperature stimulation The color of the tooth crown remains unchanged Probing is painful Elevated temperature tests

It is imperative to differentiate periodontitis and pulpitis, since this helps to build the right therapeutic strategy and reduces the risk of exacerbations and complications.

Periodontitis in children

Unfortunately, periodontitis is increasingly being diagnosed in children. As a rule, inflammation of periodontal tissue provokes caries - a disease of civilization. In addition, children rarely complain about dental problems, and parents neglect preventive examinations of the pediatric dentist. Therefore, according to statistics, childhood periodontitis accounts for about 50% of all cases of visits to dental institutions.

The inflammatory process of periodontium can be divided into 2 categories:

1. Periodontitis of baby teeth.
2. Periodontitis of permanent teeth.

Otherwise, the classification of inflammation of periapical tissues in children is systematized in the same way as periodontal disease in adult patients.

Complications of periodontitis

Complications that are provoked by inflammation of the periapical tissues are conventionally divided into local and general.

General complications of periodontitis:

• Persistent headache.
• General intoxication of the body (most often with acute purulent periodontitis).
• Hyperthermia sometimes reaches critical levels of 39-40 degrees.
• The chronic course of periodontitis provokes many autoimmune diseases, among which rheumatism and endocarditis are leading; kidney pathologies are less common.

Complications of local periodontitis:

• Cysts, fistulas.
• Purulent formations in the form of abscesses.
• The development of a purulent process can lead to phlegmon of the neck.
• Osteomyelitis.
• Odontogenic sinusitis when contents rupture into the maxillary sinus.

The most dangerous complications are caused by a purulent process, when pus spreads in the direction of the bone tissue of the jaw and exits into the periosteum (under the periosteum). Necrotization and melting of tissue provoke the development of extensive phlegmon in the neck area. With purulent periodontitis of the upper jaw (premolars, molars), the most common complication is submucosal abscess and odontogenic sinusitis.

The outcome of complications is very difficult to predict, since the migration of bacteria occurs quickly, they are localized in the jaw bone, spreading through nearby tissues. The reactivity of the process depends on the type and form of periodontitis, the state of the body and its protective properties. Timely diagnosis and therapy help reduce the risk of complications, but often this depends not on the doctor, but on the patient himself, that is, on the timing of seeking dental care.

Diagnosis of periodontitis

Diagnostic measures are not only important, they are, perhaps, the main criterion that determines the effective treatment of periodontal inflammation.

Diagnosis of periodontitis involves the collection of anamnestic data, examination of the oral cavity, additional methods and methods of examination to assess the condition of the apex and all periapical zones. In addition, the diagnosis must identify the root cause of inflammation, which is sometimes very difficult to do due to the patient’s delay in seeking help. It is easier to assess acute conditions than to diagnose an advanced, chronic process.

In addition to the etiological reasons and assessment of the clinical manifestations of periodontitis, the following points are important in diagnosis:

• Resistance or intolerance to medications or dental materials to avoid drug reactions.
• General condition of the patient, presence of concomitant pathological factors.
• Acute inflammation of the oral mucosa and assessment of the red border of the lips.
• The presence of chronic or acute inflammatory diseases of internal organs and systems.
• Threatening conditions - heart attack, cerebrovascular accident.

The main diagnostic burden falls on x-ray examination, which helps to accurately differentiate the diagnosis of diseases of the periapical system.

Diagnosis of periodontitis involves determining and recording the following information according to the recommended examination protocol:

• Process stage.
• Process phase.
• The presence or absence of complications.
• Classification according to ICD-10.
• Criteria that help determine the condition of the dentition - permanent or temporary teeth.
• Patency of channels.
• Localization of pain.
• Condition of the lymph nodes.
• Tooth mobility.
• The degree of pain during percussion and palpation.
• Changes in the structure of periapical tissue on an x-ray.

It is also considered important to correctly assess the characteristics of a pain symptom, its duration, frequency, localization zone, presence or absence of irradiation, dependence on food intake and temperature stimuli.

What measures are taken to examine inflammation of periodontal tissue?

• Visual inspection and examination.
• Palpation.
• Percussion.
• External examination of the facial area.
• Instrumental examination of the oral cavity.
• Channel sounding.
• Thermodiagnostic test.
• Bite assessment.
• Radiation imaging.
• Electroodontometric examination.
• Local radiograph.
• Orthopantomogram.
• Radiovision method.
• Oral hygiene index assessment.
• Determination of periodontal index.

Differential diagnosis of periodontitis

Since periodontitis is pathogenetically related to previous inflammatory destructive conditions, it is often similar in clinical manifestations to its predecessors. Differential diagnosis helps to separate similar nosological forms and choose the right tactics and treatment strategy, this is especially important for the management of chronic processes.

1. Acute apical periodontitis is differentiated from diffuse pulpitis, gangrenous pulpitis, exacerbation of chronic periodontitis, acute osteomyelitis, periostitis.
2. The purulent form of periodontitis should be separated from perihilar cysts with similar symptoms. Perihilar cysts are characterized by signs of bone resorption, which does not occur with periodontal inflammation. In addition, the perihilar cyst bulges greatly in the area of ​​the alveolar bone, causing tooth displacement, which is not typical for periodontitis.

Treatment of periodontitis

Treatment of periodontitis is aimed at solving the following problems:

• Relief of inflammation.
• Maximum preservation of the anatomical structure of the tooth and its functions.
• Improving the patient's general condition and quality of life in general.

What does periodontitis treatment include?

• Local anesthesia, anesthesia.
• Providing access to the inflamed canal by opening.
• Expansion of the tooth cavity.
• Providing access to the root.
• Probing, passage of the canal, often unsealing it.
• Measuring the length of the channel.
• Mechanical and medicinal treatment of the canal.
• If necessary, remove necrotic pulp.
• Placement of temporary filling material.
• After a certain period of time, installation of a permanent filling.
• Dental restoration, including damaged teeth, endodontic therapy.

The entire treatment process is accompanied by regular monitoring using X-rays; in cases where standard conservative methods do not lead to success, treatment is carried out surgically, including root amputation and tooth extraction.

What criteria does a doctor use when choosing a treatment method for periodontitis?

• Anatomical specificity of the tooth, structure of the roots.
• Severe pathological conditions are tooth trauma, root fracture, and so on.
• Results of previous treatment (several years ago).
• The degree of accessibility or isolation of the tooth, its root, canal.
• The value of a tooth is functional as well as aesthetic.
• Possibility or lack thereof in terms of tooth restoration (tooth crown).
• Condition of periodontal and periapical tissues.

As a rule, treatment measures are painless, carried out under local anesthesia, and timely contact with the dentist makes treatment effective and quick.

1. Medicinal periodontitis is a conservative treatment; surgery is rarely used.
2. Traumatic periodontitis is treated conservatively, possibly with surgical intervention to remove bone particles from the gums.
3. Infectious purulent periodontitis. If the patient presents on time, treatment is carried out conservatively; an advanced purulent process often requires surgical manipulation, including tooth extraction.
4. Fibrous periodontitis is treated with local medications and physiotherapy; standard conservative treatment is ineffective and there are no indications for it. Surgery to remove coarse fibrous formations on the gums is rarely used.

Periodontitis is an inflammation of the periodontium, characterized by a violation of the integrity of the ligaments that hold the tooth in the alveolus, the cortical plate of the bone surrounding the tooth and the resorption of bone tissue from small sizes to the formation of large cysts.

Classification

Classification according to clinical course

Acute periodontitis . Depending on the nature of the exudate, acute serous and acute purulent are distinguished. But this distinction is not always possible, moreover, the transition from the serous form to the purulent form occurs quite quickly and depends on certain conditions.

Chronic periodontitis. Divided based on the nature and degree of damage to periodontal tissue and bone. Highlight chronic fibrous periodontitis , chronic granulating And chronic granulomatous periodontitis .

Chronic periodontitis in the acute stage. The clinical course is similar to acute forms, but has its own characteristics, for example, the presence of destructive changes in bone tissue.

By origin

Infectious periodontitis . It develops due to the penetration of bacteria and their toxins into periodontal tissues with the subsequent development of inflammation in them.

Traumatic periodontitis . Caused as a result of exposure to a traumatic factor on the periodontium. This can be a strong one-time injury, for example, a blow or a bruised tooth. Or there may be a long-term, low-intensity microtrauma, for example, an over-inflated filling, a “straight” bite, overloading of the teeth or bad habits.

Medicinal periodontitis . Occurs due to the penetration of potent chemicals such as arsenic paste, formaldehyde, phenol, etc.

Classification of periodontitis ICD-10

Acute apical periodontitis NOS

K04.5 Chronic apical periodontitis

Apical granuloma

dental

dentoalveolar

Dental abscess

Dentoalveolar abscess

K04.8 Root cyst

apical (periodontal)

periapical

K04.80 Apical and lateral

K04.81 Residual

Classification of periodontitis

Periodontitis - inflammation of the tissues located in the periodontal gap (periodontitis) - can be infectious, traumatic and medicinal.

Infectious periodontitis occurs when an autoinfection occurs in the oral cavity. More often the root membrane at the apex of the tooth is affected, less often - the marginal part of the periodontium.

Traumatic periodontitis develops as a result of both single (blow, bruise) and chronic trauma (occlusion disturbance when the height of the tooth is increased with an artificial crown or filling; in the presence of bad habits - holding nails in the teeth, biting threads, peeling seeds, cracking nuts, etc.). Drug-induced periodontitis can occur during the treatment of pulpitis, when potent medicinal substances are used in the treatment of the canal, as well as due to an allergic reaction of the periodontium to drugs. In clinical practice, infectious apical periodontitis is the most common.

According to the clinical picture and pathoanatomical changes, inflammatory periodontal lesions can be divided into the following groups (according to I.G. Lukomsky): I. Acute periodontitis 1. Serous (limited and diffuse) 2. Purulent (limited and diffuse)

II. Chronic periodontitis 1. Granulating 2. Granulomatous 3. Fibrous

III. Chronic periodontitis in the acute stage.

WHO classification of periodontitis (ICD-10)

K04 Diseases of periapical tissues

K04.4 Acute apical periodontitis of pulpal origin

Acute apical periodontitis NOS

K04.5 Chronic apical periodontitis T

Apical granuloma

K04.6 Periapical abscess with fistula

dental

dentoalveolar

periodontal abscess of pulpal origin.

K04.60 Having communication [fistula] with the maxillary sinus

K04.61 Having communication [fistula] with the nasal cavity

K04.62 Having communication [fistula] with the oral cavity

K04.63 Having communication [fistula] with the skin

K04.69 Periapical abscess with fistula, unspecified

K04.7 Periapical abscess without fistula

Dental abscess

Dentoalveolar abscess

Periodontal abscess of pulpal origin

Periapical abscess without fistula

K04.8 Root cyst

apical (periodontal)

periapical

K04.80 Apical and lateral

K04.81 Residual

K04.82 Inflammatory paradental

K04.89 Root cyst, unspecified

K04.9 Other and unspecified diseases of periapical tissues

Acute periodontitis

Acute periodontitis - acute periodontal inflammation.

Etiology. Acute purulent periodontitis develops under the influence of mixed flora, where streptococci(mainly non-hemolytic, but also greening and hemolytic), sometimes staphylococci and pneumococci. Possible rod-shaped forms (gram-positive and gram-negative), anaerobic infection, which is represented by obligate anaerobic infection, non-fermenting gram-negative bacteria, veillonella, lactobacilli, yeast-like fungi. In untreated forms of apical periodontitis, microbial associations number 3-7 types. Pure cultures are extremely rarely isolated. With marginal periodontitis, in addition to the listed microbes, there is a large number of spirochetes, actinomycetes, including pigment-forming ones. Pathogenesis. An acute inflammatory process in the periodontium primarily occurs as a result of the penetration of infection through an opening in the apex of the tooth, or less often through a pathological periodontal pocket. Damage to the apical part of the periodontium is possible due to inflammatory changes in the pulp, its necrosis, when the abundant microflora of the tooth canal spreads into the periodontium through the apical opening of the root. Sometimes the putrefactive contents of the root canal are pushed into the periodontium during chewing, under the pressure of food.

Marginal, or marginal, periodontitis develops as a result of the penetration of infection through the gum pocket due to injury or the contact of medicinal substances, including arsenic paste, on the gum. Microbes that have penetrated into the periodontal gap multiply, form endotoxins and cause inflammation in periodontal tissues.

Some local features are of great importance in the development of the primary acute process in the periodontium: lack of outflow from the pulp chamber and canal (presence of an unopened pulp chamber, filling), microtrauma during active chewing load on a tooth with an affected pulp.

General reasons also play a role: hypothermia, past infections, etc., but most often the primary impact of microbes and their toxins is compensated by various nonspecific and specific reactions of periodontal tissues and the body as a whole. Then an acute infectious-inflammatory process does not occur. Repeated, sometimes prolonged exposure to microbes and their toxins leads to sensitization, and antibody-dependent and cellular reactions develop. A Antibody-dependent reactions develop as a result of immunocomplex and IgE-mediated processes. Cellular reactions reflect a delayed-type allergic hypersensitivity reaction.

The mechanism of immune reactions, on the one hand, is due to a violation of phagocytosis, the complement system and an increase in polymorphonuclear leukocytes; on the other hand, by the proliferation of lymphocytes and the release of lymphokines from them, causing destruction of periodontal tissue and resorption of nearby bone.

Various cellular reactions develop in the periodontium: chronic fibrous, granulating or granulomatous periodontitis. Violation of protective reactions and repeated exposure to microbes can cause the development of an acute inflammatory process in the periodontium, which in essence is an exacerbation of chronic periodontitis. Clinically, they are often the first symptoms of inflammation. The development of pronounced vascular reactions in a fairly closed periodontal space, an adequate protective response of the body, as a rule, contributes to inflammation with a normergic inflammatory reaction.

The compensatory nature of the response of periodontal tissues during a primary acute process and exacerbation of a chronic one is limited by the development of an abscess in the periodontium. It can be emptied through the root canal, gum pocket when opening a periapical lesion or removing a tooth. In some cases, under certain general and local pathogenetic conditions, a purulent focus is the cause of complications of odontogenic infection, when purulent diseases develop in the periosteum, bone, and perimaxillary soft tissues.

Pathological anatomy. During an acute process, the main phenomena of inflammation appear in the periodontium - alteration, exudation and proliferation.

Acute periodontitis is characterized by the development of two phases - intoxication and a pronounced exudative process.

In the intoxication phase, migration of various cells occurs - macrophages, mononuclear cells, granulocytes, etc. - into the zone of microbial accumulation. In the phase of the exudative process, inflammatory phenomena increase, microabscesses form, periodontal tissue melts and a limited abscess is formed. On microscopic examination, in the initial stage of acute periodontitis, one can see hyperemia, swelling and a small leukocyte infiltration of the periodontal area around the root apex. During this period, perivascular lymphohistiocytic infiltrates containing single polynuclear cells are detected. As the inflammatory phenomena further increase, leukocyte infiltration intensifies, capturing larger areas of the periodontium. Separate purulent lesions form - microabscesses, and periodontal tissue melts. Microabscesses connect with each other, forming an abscess. When a tooth is removed, only individual remaining areas of sharply hyperemic periodontium are revealed, and throughout the rest of the root the root is exposed and covered with pus.

An acute purulent process in the periodontium causes changes in the tissues surrounding it (bone tissue of the alveolar walls, periosteum of the alveolar process, peri-maxillary soft tissues, tissues of regional lymph nodes). First of all, the bone tissue of the alveoli changes. In the bone marrow spaces adjacent to the periodontium and located over a considerable extent, bone marrow edema and varying degrees of pronounced, sometimes diffuse, infiltration of neutrophilic leukocytes are noted. In the area of ​​the cortical plate of the alveoli, lacunae filled with osteoclasts appear, with a predominance of resorption (Fig. 7.1, a). Restructuring of bone tissue is observed in the walls of the socket and mainly in the area of ​​its bottom. The predominant resorption of bone leads to the expansion of the holes in the walls of the socket and the opening of the bone marrow cavities towards the periodontium. There is no necrosis of the bone beams (Fig. 7.1, b). Thus, the restriction of the periodontium from the alveolar bone is broken. In the periosteum covering the alveolar process, and sometimes the body of the jaw, in the adjacent soft tissues - gums, peri-maxillary tissues - signs of reactive inflammation are recorded in the form of hyperemia, edema, and inflammatory changes are also observed in the lymph node or 2-3 nodes, respectively, of the affected periodontium of the tooth . Inflammatory infiltration is observed in them. In acute periodontitis, the focus of inflammation in the form of abscess formation is mainly localized in the periodontal fissure. Inflammatory changes in the alveolar bone and other tissues are reactive, perifocal in nature. And it is impossible to interpret reactive inflammatory changes, especially in the bone adjacent to the affected periodontium, as its true inflammation.

Clinical picture . In acute periodontitis, the patient indicates pain in the causative tooth, which intensifies when pressing on it, chewing, and also when tapping (percussion) on the chewing or cutting surface. The feeling of “growing” or lengthening of the tooth is characteristic. With prolonged pressure on the tooth, the pain subsides somewhat. Subsequently, the pain intensifies, becoming continuous or with short light intervals. They are often pulsating.

Thermal effects, the patient taking a horizontal position, touching the tooth, and biting increase the pain. The pain spreads along the branches of the trigeminal nerve. The general condition of the patient is satisfactory. On external examination, as a rule, there are no changes. Enlargement and tenderness of the lymph node or nodes associated with the affected tooth are observed. Some patients may have mildly expressed collateral edema of the perimaxillary soft tissues adjacent to this tooth. Percussion is painful in both vertical and horizontal directions.

The mucous membrane of the gums, alveolar process, and sometimes the transitional fold in the projection of the tooth root is hyperemic and swollen. Palpation of the alveolar process along the root, especially corresponding to the opening of the apex of the tooth, is painful. Sometimes, when pressing with an instrument on the soft tissues of the vestibule of the mouth along the root and transitional fold, an impression remains, indicating their swelling.

Diagnostics Temperature stimuli and electrical odontometry data indicate a lack of pulp response due to its necrosis. On an x-ray during an acute process of pathological changes in the periodontium, it is possible not to detect or to detect an expansion of the periodontal fissure, blurred cortical plasticity of the alveoli. With an exacerbation of the chronic process, changes characteristic of granulating, granulomatous, and rarely fibrous periodontitis occur. As a rule, there are no changes in the blood, but in some patients leukocytosis (up to 9-10 9 /l), moderate neutrophilia due to band and segmented leukocytes are possible; ESR is often within normal limits.

Differential diagnosis . Acute periodontitis is differentiated from acute pulpitis, periostitis, osteomyelitis of the jaw, suppuration of the root cyst, acute odontogenic sinusitis.

Unlike pulpitis, in acute periodontitis the pain is constant, and in diffuse inflammation of the pulp it is paroxysmal. In acute periodontitis, in contrast to acute pulpitis, inflammatory changes are observed in the gum adjacent to the tooth; percussion is more painful. In addition, electrical odontometry data helps in diagnosis.

Differential diagnosis of acute periodontitis and acute purulent periostitis of the jaw is based on more pronounced complaints, feverish reaction, the presence of collateral inflammatory edema of the peri-maxillary soft tissues and diffuse infiltration along the transitional fold of the jaw with the formation of a subperiosteal abscess.

Percussion of the tooth during periostitis of the jaw is less painful, unlike acute periodontitis. Based on the same, more pronounced general and local symptoms, differential diagnosis of acute periodontitis and acute osteomyelitis of the jaw is carried out. Acute osteomyelitis of the jaw is characterized by inflammatory changes in the adjacent soft tissues on both sides of the alveolar process and the body of the jaw. In acute periodontitis, percussion is sharply painful in the area of ​​one tooth, in osteomyelitis - in several teeth. Moreover, the tooth that was the source of the disease reacts to percussion less than neighboring intact teeth. Laboratory data - leukocytosis, ESR, etc. - allow us to distinguish between these diseases.

Purulent periodontitis should be differentiated from suppuration of a perihilar cyst. The presence of limited bulging of the alveolar process, sometimes the absence of bone tissue in the center, and displacement of teeth, in contrast to acute periodontitis, characterize a suppurating perihilar cyst. An x-ray of a cyst reveals a round or oval area of ​​bone resorption.

Acute purulent periodontitis must be differentiated from acute odontogenic inflammation of the maxillary sinus, in which pain can develop in one or more adjacent teeth. However, congestion of the corresponding half of the nose, purulent discharge from the nasal passage, headache, and general malaise are characteristic of acute inflammation of the maxillary sinus. Violation of the transparency of the maxillary sinus, revealed on an x-ray, allows you to clarify the diagnosis.

Treatment. Therapy for acute apical periodontitis or exacerbation of chronic periodontitis is aimed at stopping the inflammatory process in the periodontium and preventing the spread of purulent exudate into the surrounding tissues - the periosteum, perimaxillary soft tissues, bone. Treatment is predominantly conservative. Conservative treatment is more effective with infiltration or conduction anesthesia with 1-2% solutions of lidocaine, trimecaine, ultracaine.

A more rapid subsidence of inflammatory phenomena is facilitated by a blockade - the introduction of an infiltration anesthesia type of 5-10 ml of a 0.25-0.5% solution of an anesthetic (lidocaine, trimecaine, ultracaine) with lincomycin into the area of ​​the vestibule of the mouth along the alveolar process, respectively, to the affected one and 2-3 neighboring teeth. The anti-edematous effect is provided by the introduction of the homeopathic remedy “Traumel” in the amount of 2 ml along the transitional fold or external dressings with ointment of this drug.

It must be borne in mind that without the outflow of exudate from the periodontium (through the tooth canal), blockades are ineffective and often ineffective. The latter can be combined with an incision along the transitional fold to the bone, with perforation of the anterior wall of the bone using a bur, corresponding to the peri-apical part of the root. This is also indicated in case of unsuccessful conservative therapy and an increase in inflammatory phenomena, when it is not possible to remove the tooth due to some circumstances. If treatment measures are ineffective and inflammation increases, the tooth should be removed. Tooth extraction is indicated when there is significant destruction, obstruction of the canal or canals, or the presence of foreign bodies in the canal. As a rule, tooth extraction leads to rapid subsidence and subsequent disappearance of inflammatory phenomena. This can be combined with an incision along the transitional fold to the bone in the area of ​​the root of the tooth affected by acute periodontitis. After tooth extraction during a primary acute process, curettage of the hole is not recommended, but should only be washed with a solution of dioxidine, chlorhexedine and its derivatives, gramicidin. After tooth extraction, pain may intensify and body temperature may rise, which is often due to the traumatic nature of the intervention. However, after 1-2 days, these phenomena, especially with appropriate anti-inflammatory drug therapy, disappear.

To prevent complications after tooth extraction, you can inject anti-staphylococcal plasma into the dental alveolus, wash it with streptococcal or staphylococcal bacteriophage, enzymes, chlorhexidine, gramicidin, leave an iodoform swab and a sponge with gentamicin in the mouth. General treatment of acute or exacerbation of chronic periodontitis consists of oral administration of pyrazolone drugs - analgin, amidopyrine (0.25-0.5 g each), phenacetin (0.25-0.5 g each), acetylsalicylic acid (0.25-0.5 g each). 0.5 g). These drugs have analgesic, anti-inflammatory and desensitizing properties. Some patients are prescribed sulfonamide drugs according to indications (streptocide, sulfadimezin - 0.5-1 g every 4 hours or sulfadimethoxine, sulfapyridazine - 1-2 g per day). However, the microflora, as a rule, is resistant to sulfonamide drugs. In this regard, it is more advisable to prescribe 2-3 pyrosolone drugs (acetylsalicylic acid, analgin, amidopyrine) 4 tablets of each, 3 times a day. This combination of drugs gives an anti-inflammatory, desensitizing and analgesic effect. Weakened patients burdened with other diseases, especially the cardiovascular system, connective tissue, and kidney diseases are treated with antibiotics - erythromycin, kanamycin, oletethrin (250,000 units 4-6 times a day), lincomycin, indomethacin, voltaren (0. 25 g) 3-4 times a day. Foreign specialists, after tooth extraction due to an acute process, necessarily recommend treatment with antibiotics, considering such therapy also as a prevention of endocarditis and myocarditis. After tooth extraction in acute periodontitis, in order to stop the development of inflammatory phenomena, it is advisable to use cold (an ice pack on the soft tissue area corresponding to the tooth for 1-2-3 hours). Next, warm rinses, Sollux are prescribed, and when the inflammatory phenomena subside, other physical methods of treatment are prescribed: UHF, fluctuarization, electrophoresis of diphenhydramine, calcium chloride, proteolytic enzymes, exposure to helium-neon and infrared lasers.

Exodus. With proper and timely conservative treatment, in most cases of acute and exacerbation of chronic periodontitis, recovery occurs. (Insufficient treatment of acute periodontitis leads to the development of a chronic process in the periodontium.) It is possible for the inflammatory process to spread from the periodontium to the periosteum, bone tissue, peri-maxillary soft tissues, i.e. Acute periostitis, osteomyelitis of the jaw, abscess, phlegmon, lymphadenitis, inflammation of the maxillary sinus may develop.

Prevention is based on the sanitation of the oral cavity, timely and correct treatment of pathological odontogenic foci, functional unloading of teeth using orthopedic treatment methods, as well as on the implementation of hygienic and health measures.

One of the most insidious dental diseases is periodontitis. Its symptoms are not always pronounced, so patients often seek medical help at the wrong time. This complicates treatment, leads to complications and even tooth loss. The article clearly addresses the questions of what periodontitis is, its symptoms, treatment and preventive measures.

In medicine, this disease is defined as follows: periodontitis is an inflammation of the periodontium, that is, the connective tissue between the cortical plate of the tooth socket (alveoli) and the cementum of the tooth root. The thickness of the periodontium is different for everyone, on average it is 0.19-0.26 mm.

Simply put, with the development of periodontitis, the area of ​​tissue that surrounds the root of the tooth and is responsible for its stability becomes inflamed. The periodontium is closely connected with the surrounding tissues: along its entire length - with the jaw bone, through the apical foramen - with the pulp, at the edges of the tooth socket - with the periosteum and gum.

The disease is characterized mainly by damage to the ligaments that hold the tooth in the alveolus, degradation of bone tissue of varying severity, resorption (destruction) of the walls of the tooth socket and even root cement.

According to statistics, this is a common disease, diagnosed in 45-50% of cases dental problems. Periodontitis never occurs out of nowhere. As a rule, it is a consequence. The disease is quite serious, it is not so easy to cope with, it has a negative effect on the entire human body and can cause such serious complications as an abscess, acute sinusitis, osteomyelitis, or sepsis.

Types and classification

Periodontitis can occur for a number of reasons, its course can be different, which requires different treatment methods. That is why classification of this disease is necessary.

In medical practice, there are three types of classification of periodontitis:

• by origin,
• from WHO according to ICD-10,
• according to the Lukomsky system.

Based on their origin, the following types of periodontitis are distinguished:

• infectious – this form of the disease occurs most often, in 70-75% of cases of periodontitis. The development of pathology is provoked by harmful bacteria,
• traumatic - develops due to injuries, bruises, unnatural loads on the teeth (for example, opening bottles with teeth or opening nut shells),
• medicinal – occurs when there is a violation of the treatment technology or as a reaction to certain medications.

WHO (World Health Organization, works under the UN) in the late 90s of the twentieth century proposed taking into account its most common consequences when classifying periodontitis. According to experts, this approach makes it possible to comprehensively cover the problem, influence not only the disease itself, but also minimize the risks of complications, and also combine the efforts of specialized specialists (for example, a dentist and a therapist or surgeon, or an ENT doctor).

Taking this into account, a new system was developed, which was included in the International Classification of Diseases, Tenth Revision ( ICD-10). Periodontitis is presented here in the section “Diseases of the oral cavity, salivary glands and jaws” under the code K04, which combines diseases of the pulp and periapical tissues. This is due to the close connection between periodontitis and pulpitis.

Classification of periodontitis according to ICD-10:

• acute apical (apical) periodontitis of pulpal origin (code K04.4). According to dentists, this is a classic version of this disease. There are no problems with determining the cause of the pathology and making a diagnosis. The doctor must first eliminate the source of infection and relieve the severity of the process,
• chronic apical (apical) (code K04.5). In this case, a pathological formation of a round shape develops at the apex of the tooth root - an apical granuloma. It has sizes from 2 to 7 mm in diameter. Over time, without proper treatment, it can degenerate into a cyst,
• periapical abscess with or without fistula (code K04.6 and K04.7, respectively). Depending on the location, dental, dentoalveolar and periodontal suppuration are distinguished. Fistulas can communicate with the maxillary sinus, with the skin, or extend into the nasal cavity (very dangerous if the fistula canal extends into the maxillary sinus) or into the oral cavity,
• radicular cyst (code K04.8). It can be lateral, near-apical, residual, or root.

All other unspecified pathological processes in pariapical tissues are collected under the code K04.9.

In practice it is very often used classification of periodontitis according to Lukomsky. The system is very simple, but at the same time it covers all possible forms of periodontitis:

• spicy;
• serous - in this case, blood capillaries locally expand, blood cells accumulate, and the volume of intercellular fluid increases at the site of inflammation. Serous filling provokes periodontal edema;
• purulent - pus accumulates at the site of inflammation, swelling of nearby tissues and slight swelling of the lymph nodes are possible. Purulent contents can find their way out of the periodontium through a fistula;
• chronic;
• granulating - destruction of bone structures occurs with simultaneous rapid growth of connective tissue;
• granulomatous - the inflammatory focus is limited to the walls of the connective tissue capsule, which can transform into a cyst;
• fibrous – periodontal tissues expand, thicken, and scar;
• chronic in the acute stage - chronic inflammation is activated under the influence of various factors - decreased immunity, injury, allergic reactions.

Causes

The main reason for the development of periodontitis is neglected or improperly treated caries. In this case, an infection penetrates through the carious cavity, the dental pulp is first affected, and necrotization and destruction occurs. Further, the inflammation spreads to the ligamentous apparatus, periosteum and bone, forming serous and purulent sacs, fibrous capsules and cysts.

If, during filling, the dental canal was poorly cleaned, depulped or filled with filling material not up to the root apex, then after a while the patient will develop periodontitis as a consequence of poor treatment of pulpitis. The same consequences arise if a dental instrument breaks and remains in the root of the tooth, or during treatment due to the negligence of the dentist, perforation of the tooth root occurs (that is, the doctor breaks through the root wall).

If a crown is placed on a “living” tooth, during grinding of which a thermal burn of the pulp occurred, then such a medical error will first lead to the death of the pulp, and after a while to the development of periodontitis.

The cause of the development of periodontitis can be a periodontal (gingival) pocket. Infection from such a pocket penetrates to the tips of the roots and provokes the occurrence of so-called marginal periodontitis.

A common cause of pathology is injury: dislocation or fracture of a tooth, rupture of the neurovascular bundle from a strong blow (the crown of the tooth turns pink), fracture of the tooth root.

In case of illiterate prosthetics or overestimation of the height of the filling, or congenital malocclusion, the tooth experiences loads that exceed the physiological norm. This leads to the development of chronic traumatic periodontitis.

In dentistry, strong antiseptics and medicated pastes are used during dental treatment. In rare cases, they can cause an allergic reaction in the patient and provoke periodontitis.

Diseases of the body, such as diabetes, gastritis, ulcers, frequent bronchitis and pneumonia, sinusitis, chronic tonsillitis and others can cause various diseases of the oral cavity, including periodontitis.

Symptoms - what to look for

With the development of acute periodontitis, a general clinical picture is observed: a feeling of “pushing out” of the tooth appears; when biting, pressing or tapping, a sharp pain is felt, and local redness of the gums is possible. In complicated cases, there is an accumulation of pus, the appearance of fistulas, and a very unpleasant putrid odor is felt from the mouth.

A distinctive feature of periodontitis is the fact that the patient clearly indicates which tooth hurts, whereas with other inflammations, for example, pulpitis, the pain often radiates far beyond the diseased tooth.

In case of advanced disease, general intoxication may begin, the temperature may rise, the patient complains of weakness, nausea and poor sleep.

Chronic periodontitis is most often asymptomatic. Especially if a person has good immunity, which inhibits the spread of infection beyond the damaged tissues. Only when you lightly tap on the aching tooth and press on it, discomfort or slight pain is felt.

Diagnosis of the disease

A doctor can diagnose the presence of periodontitis by visually examining the oral cavity and facial area, taking into account the clinical picture and patient complaints. An instrumental examination, percussion (tapping) of the tooth, probing of the dental canal, and an assessment of the bite are also carried out.

But the surest way is. It will show a clear darkening at the site of inflammation, and in addition, the x-ray will help identify the cause of the development of the pathology, which is very important for successful therapy. For example, an x-ray will clearly show a piece of instrument stuck in a dental canal or an unfilled tooth root.

When making a diagnosis, it is important to differentiate periodontitis from the following diseases:

• diffuse or gangrenous pulpitis,
• acute osteomyelitis,
• perihilar cyst,
• odontogenic sinusitis,
• purulent sinusitis.

Treatment methods

Periodontitis must be treated! Moreover, both in acute and chronic forms, the disease requires close attention. If you do not deal with this problem, then you cannot avoid serious complications - periostitis of the jaw (), osteomyelitis (purulent-necrotic process) of bone tissue, abscess, acute sinusitis and even the development of sepsis in response to a local infectious process.

We must not forget that in the immediate vicinity of the oral cavity there are the eyes and the human brain, where infection and pus can spread through the bloodstream. Therefore, you should immediately contact your dentist if symptoms of periodontitis appear.

There are traditional methods for treating this pathology, but given the nature of the lesion, they can only act as an effective adjuvant to the main therapy.

First, the doctor will necessarily open the tooth to provide good access to the inflamed periapical tissues that are located behind the root of the tooth. Under anesthesia, she will perform mechanical cleaning of the canals., if necessary, change their length, treat them with an antiseptic, introduce the necessary antibacterial medications (for example), which will stop inflammation, stop further tissue destruction and promote their speedy recovery. It is not a fact that a one-time administration of the medicine will help. Periodontitis usually requires several treatment sessions. All this time the tooth remains open or under a temporary filling.

After the pain subsides and the inflammation subsides, the doctor will place a permanent filling and take a control x-ray. Tissue regeneration processes will be completed in approximately 6-10 months. Then we can assume that periodontitis has been defeated.

In difficult cases, for example, with the development of a cyst or fistula formation, a more radical method of treatment is required - surgery. Conservative treatment of a cyst - drainage of the cystic cavity, elimination of pathogenic microflora, destruction of the internal lining of the cyst - is a long process that does not always end in success.

Physiotherapeutic procedures and warm soda 15-minute baths up to 7-10 times a day are effective.

Modern dentistry is one of the most progressive areas of medicine, therefore in 85% of cases there is a complete cure of periodontitis while maintaining the anatomical integrity and functions of the tooth.

Prevention

Since in most cases periodontitis develops against the background of caries or periodontal disease, the prevention of these diseases simultaneously prevents complications. Basic ways to keep your teeth healthy:

• observe ,
• use toothpastes containing fluoride,
• eat nutritiously, follow a daily routine, maintain immunity at the proper level,
• in the presence of diseases of the gastrointestinal tract, endocrine, bronchopulmonary and cardiovascular systems, pay increased attention to dental health
• visit the dentist at least once every six months,
• remove it periodically (it forms differently for everyone, so the dentist will determine how often this procedure needs to be done for a particular person),
• do not chew hard objects with your teeth, do not open bottles,
• visit a dentist with a good reputation. Do not trust your health to non-professionals.

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