Apical periodontitis: etiology, pathogenesis, classification. Acute apical periodontitis: etiology, pathogenesis, clinic, diagnostics, differential diagnostics.
Chronic apical periodontitis: etiology, pathogenesis, clinic, diagnostics, differential diagnostics. X-ray diagnostics of apical periodontitis.
Periodontium is a connective tissue formation, which fills the space between a root and an inner side of alveoli, and connects teeth with jaw bones. The width of this space (periodontal gap) varies from 0.15 mm to 0.4 mm with a significant narrowing in the middle of a root. Periodontal gap is filled with a dense, soft connective tissue, which provides retention of a tooth in a socket of an alveolar bone of a jaw.
The main structure of periodontium is presented by bundles of a dense fibrous tissue consisting of tightly interwoven collagen fibers.
They are stretched between the alveolar bone and the tooth root cement, and are S-shaped. In various parts of the periodontal gap these bundles have different positions. They are stretched almost horizontally, forming a circular ligament of a tooth (ligamentum circullare) around the edge of the dental alveoli. Fibers of the ligament differ both in size and in orientation. They include dentogingival (cement gingival), alveolar gingival, circular, tooth periodontal (cement periodontal) and transseptal fiber groups.
1 – collagen fibers, 2 – elastic fibers, 3-cell, 4-core.
Circular ligament provides attachment of the coronal edge of connective tissue to the tooth, increases resistance of the free gingival edge and protects periodontium from the external irritants.
Major periodontium fibers start from the root cement of a tooth crossing the periodontal gap in different directions and rooting themselves into the alveolar bone in the form of Sharpey fibers. According to their directions the following groups of fibers bundles are distinguished: alveolar crest fibers, horizontal fibers, oblique fibers, apical fibers and interroot fibers. The major part of periodontium consists of oblique fibers. They are rooted in the alveolar bone close to the tooth crown than to the place of their attachment to the cement. A tooth seems to be suspended on the fibers of this group.
1 – enamel, 2-dentin 3 – pulp 4 – bone alveoli, 5 – periodontal gap; 6 – gums 7 – cement, 8 – connection between teeth, 9 – extragingival fibers; 10 – teethperiosteal fiber, 11 – teethcrest fibers; 12 – Spit teethalveolar fiber, 13 – apical fibers;
2-dentin3pulp;4-bonealveoli,5-periodontalgap;7-cement,14-tangentiafibers;15 radial fibers
In small amounts in the walls of blood vessels of periodont is elastic fibers. Between the walls of blood vessels and the main fibers in an oblique direction are periosteum fibers, which are also immature collagen fibers. They provide attachment of blood vessels and They provide attachment of blood vessels and prevents ¬ tion of deformation during operation periodontium. Between the fibers are the main ingredient loose connective tissues, cells, blood, lymph vessels and nerves periodontium.
The main substance Periodontal contains 70% water which allows to distribute the pressure of chewing on the walls of alveolus The most common cells it contains fibroblasts, which located along the main direction of bundles of fibers as involved in their formation. These cells produce elastin, glycoproteins.
In addition, there periodontal epithelial cells, which are the remnants of the epithelial root sheath Hertviha. They form bands, stripes, follicles that are closer to the cement, and are called islands Malyasse. Sometimes anastomosing epithelial strands together, permeating the entire periodontium. These epithelial cells in the case of specific pathological conditions may participate in the formation of granulomas, cystogranulomas and around root cysts. An important component of cellular Periodontal mesenchymal cells are poorly differentiated. They are located around blood vessels and, if necessary, differentiate into fibroblasts, osteoblasts and cementoblasty Throughout Periodontal especially in periapical part located reticuloendothelial cells and blood cells who migrated from the vessels: erythrocytes, leukocytes, lymphocytes, monocytes, at least – macrophages and plasmocytes.
The most important function is Periodontal fixing teeth in the jaw bone. It provides bundles of collagen fibers – their tortuous course provides physiological mobility of the teeth.
1. Barrier function. Periodontal especially circular ligament tooth protects the body from the penetration of microorganisms, toxins and other harmful agents.
2. dumper function. The presence of up to 70% of fluid in periodontal disease and a significant amount of fibrous structures provide periodontal to not only withstand considerable chewing pressure, and evenly distribute it on all the walls of fissure periodontitis.
3. Trophic function. A dense network of blood vessels provides periodontal trophic function of the hard tissues. This even teeth without pulp for a long time successfully operate.
4. Plastic function. Periodontal cells, forming secondary cement and bone, giving it plastic features, which is especially important when you move your teeth.
5. Sensory function due to the rich innervation Periodontal, so it is as if the body senses tooth. It is a most important function is Periodontal fixing teeth in the jaw bone. It provides bundles of collagen fibers – their tortuous course provides physiological mobility of the teeth.
6. Barrier function. Periodontal especially circular ligament tooth protects the body from the penetration of microorganisms, toxins and other harmful agents.
7. Dumper function. The presence of up to 70% of fluid in periodontal disease and a significant amount of fibrous structures provide periodontal to not only withstand considerable chewing pressure, and evenly distribute it on all the walls of fissure periodontitis.
8. Trophic function. A dense network of blood vessels provides periodontal trophic function of the hard tissues. This even teeth without pulp for a long time successfully operate.
9. Plastic function. Periodontal cells, forming secondary cement and bone, giving it plastic features.
Pathogenesis of periodontitis
The major changes in the case of periodontal disease include various forms of inflammatory manifestations of alteration, exudation and proliferation No matter how etiological factor caused by a inflammatory response – the action of infectious and toxic agents, as a result of traumatic or chemical injury, inflammation begins of alteration cells or tissues periodontium.
In the area of damage accumulate inflamed mediators (histamine, serotonin, acetylcholine, etc.) as well as tissue proteolytic enzymes along with other alternative change begins we automatically trigger inflammatory reactions. As a result, there are changes in the vascular wall, circulation disorders, is the output of plasma proteins and fluid forms. Along with the changes that come with alteration and exudation, early inflammatory response showing proliferative processes inherent in the acute, subacute and chronic inflammation begins Lenny. The process ends with the formation of proliferation granulator tissue, which further transformed into fibrous, scaring tissue.
The nature of inflammation in periodontal depends on the intensity and duration of the etiological factor, reflect the characteristics destruction area and the state of the defenses. Inflammatory processes in the degree and nature of the pathological manifestations of the clinical course can be divided into two main groups: 1) acute inflammation – characterized advantage of alternative-exudative changes, less prolonged and intensive course, a more severe clinical picture, 2) chronic inflammation – characterized advantage liferatively-regenerative processes, longer course and less severe clinical symptoms.
Pathogenesis of acute periodontitis
If high levels of defenses and low intensity pathogenic etiological factor arises acure serous periodontitis. This form can be developed by root canal treatment of necrotic pulp tissue when the canal through apical hole gets infectious with severe virulence or when the effect of trauma or chemical agent is negligible. Аcute serous inflammation Periodontal early characterized hyperemia. There have been filling vessels and slow down of blood flow. Leukocytes are shifted to the vascular wall and reached stasis. Because vascular wall begin to penetrate the liquid part of blood proteins that are able colloid, and small of neutrophilic leukocytes, lymphocytes and monocytes. Fluid loosens the connective tissue elements and collagen fibrils periodontium. At this stage of the inflammatory process extends to the bone, which is very responsive thanks to its close association with periodontal. In the adjacent periodontal bone marrow-filled intervals spongy substance possible extension blood vessels and stagnation.
Depending on the reactive capacity of the organism and timely therapeutic intervention process may cease or intensify and move in purulent inflammation.
Acute suppurative periodontitis develops if the infection that got into Periodontal has high virulence, damaged factor very aggressive and protective reactions of the organism at a low level. Due to the high penetration of blood vessels due to activation such enzymes as leykotoksyn, trypsin, penetrate through the vascular wall in a large number of white blood cells, lymphocytes and monocytes. Neutrophilic leukocytes phage bacteria and then die. their destruction accompanied by the release of enzymes – protease, cathepsin, chymotrypsin, alkaline phosphatase and others., and also spe There is a breakdown of tissue with the formation of pus. In hyperacidosis tissue in the area of inflammation are active lymphocytes monocytes blood, and settled macrophagocytes. Macrophages clean the area of inflammation from dead cells and large unorganizedcific antigens that are needed for the next formation Rennie antibodies.
A – periodontitis B – endosteal B – subperiosteal abscess, G – submucous abscess
CLASSIFICATION OF PERIODONTITIS
Acute and chronic periodontitis is one of the main causes of premature loss of teeth. Among those seeking dental care, patients with various forms of periodontitis ranged from 15 to 30%. This high percentage of this type of pathology, from our point of view, because in 20% of teeth treated about diseases of the pulp by her previous devitalization drugs arsenic during the first year after treatment clinically developing some form of years periodontitis. During the X-ray examination of the teeth changes in periodontal found in 2 times more likely (40 – 45%) than in patients treated by other methods
Often periodontitis seen in villagers, as well as persons who for various reasons is not timely dental care.
The relatively high incidence of periodontitis and serious difficulties of its diagnosis and treatment is especially necessary to develop a common classification.
Even in the XIX century. proposed classification of periodontitis, based mainly on clinical signs. In 1891 O.K. Limberg systematized clinical signs of inflammation periodont and proposed a classification.
Later appeared classification, which take into account not only clinical symptoms but also data cards pathoanatomical us. These include classification of BI Mohylnytskoho and AI Evdokimov. In 1924, JM Hofunh proposed clinical and anatomical classification, which was reflected as localization and pathological changes in periodontal inflammation. The author has divided the processes that occur in periodontal into acute and chronic.
I.Acute periodontitis.
1.acute marginal periodontitis.
2.Acute apical periodontitis.
3.Acute diffuse periodontitis.
II.Chronic periodontitis.
1.Chronic fibrotic periodontitis.
2. Chronic granulomatous periodontitis.
However, proposed in the early XX century. classification of incompletely revealed clinical features that are not always allowed to use them. IG Lukomski (1955) investigated the pathophysiological and pathomorphological changes in the state of periodontal inflammation and its proposed classification that now common in clinical practice. It allows more directed diagnose wool periodontitis and implement differential therapeutic measures. According to this classification, periodontitis is divided into 3 main groups
I. Acute periodontitis (periodontitis acuta).
1. Acute serous periodontitis (periodontitis acuta serosa).
2. Acute suppurative periodontitis (periodontitis acuta purulenta).
I. Chronic periodontitis (periodontitis chronica).
1. Chronic fibrotic periodontitis (periodontitis chronica fibrosa).
2. Chronic granulomatous periodontitis (periodontitis chronica granulomatosa).
3. Chronic granulating periodontitis (periodontitis chronica granulans).
III. Exacerbations of chronic periodontitis.
WHO Classification (ICD-X)
K04.4 Acute apical periodontitis pulp origin
K04.5 Chronic apical periodontitis apical granuloma
K04.6 periapical abscess with fistula
K04.60 What is communication (fistula) with maxillary bosom
K04.61 What is communication (fistula) with nasal cavity
K04.62 What is communication (fistula) with oral
K04.63 What is communication (fistula) with skin
K04.69 periapical abscess with fistula unspecified
K04.7 periapical abscess without fistula
K04.8 root cyst
K04.80 apical and lateral
K04.81 residual
K04.82 Inflammatory paradentalna
K04.89 root cyst unspecified
K04.9 Other and unspecified diseases of pulp and tissue periapical
DIFFERENTIAL DIAGNOSIS of ACUTE PERIODONTITIS
Acute serous periodontitis (periodontitis acuta serosa).
In clinical practice is most common periodontitis, which occurs under the influence of infection and usually develops as a complication of inflammation of the pulp or because of mistakes that were made during endodontic therapy.
Symptoms. Complaints patient so characteristic that often their is sufficient to establish a virtually error-free diagnosis. Initially, the patient feels heaviness and tension in the tooth, which was like the big, longer than others. Gradually there is quite a lot of pain spontaneous nature. The pain is constant, localized, not radiating, worse at night and barely suppressed conventional analgesics. Since the process is constantly evolving, pain intensity grows.
Also, can occur characteristic provoked pain. All that can increase blood flow in the area of the tooth and change its mobility, provokes attacks of pain. Yes, there is pain during eating. In the initial stage, however, passive, slow, long-term pressing reduces the pain that is associated with the outflow of fluid from periodontal reducing congestion and compression of nerve endings. Therefore, clutching a tooth in the alveoli, patients temporarily improve their condition. Pain when touching the tooth can occur under the influence of heat, if periodontitis is a complication of gangrene of the pulp with a closed cavity of a tooth. The temperature difference can cause pain if the change is sudden. In the case of a gradual increase in temperature and prolonged exposure to heat achieved calming effect due to sustained vasodilation, which promotes blood flow areas of inflammation.
OBJECTIVE. Sick tooth may be intact, that does not exclude injury (such as when you use orthodontic appliances). Often, however, it is caries, devital, with an open cavity of a tooth filled or a great seal. Enamel loses its characteristic luster, is gray. It is clear in the area of apex often hiperemic and swollen, sometimes existing congestion and adjacent areas gums. Vertical percussion painful. The reason for such a reaction is to increase the sensitivity of nerve receptors in the area of periapical inflammation.
Palpation of the gums in the area of the top teeth (especially front) painful, because of the proximity of the root to the periosteum.
Regional lymph nodes are enlarged, become painful during palpation. Depending on the top “that limphatic nodes swollen in diagnostically difficult cases can be differentiated tooth. Yes, periodontitis lower front teeth accompanied by inflammation limphatic Submental nodes periodontitis upper incisors and upper and lower canines and premolars – Front submandybulyar lymph node corresponding side and periodontitis molars of both jaws – middle and rear submandybulyar lymph nodes.
electrical conductivity – higher than 100 mi-A, except traumatic injury period when kept alive pulp and response to constant current associated with its response.
X-ray changes usually are not found only in the later stages of a possible slight expansion pieriodontal slit.
Depending on the etiology of the clinical picture of acute serous periodontitis can have its own specifics that should be considered during the differential diagnosis.
In patients with traumatic periodontitis clinical picture depends largely on the state of the pulp is exposed to ‘severe injury. If the pulp is alive, the course of the process becomes lighter forms, weather favorable treatment. In the case of septic necrosis of the pulp always joins periodontal infection and there is clinical picture of infectious periodontitis.
Often inflammation may be caused by medications, or used in the treatment of pulpitis (eg arsenious paste trykrezol (formalin) or filling materials that have a necrotizing effect on periodontal tissue. Periodontitis For this group, the typical steady nature of the flow and resistance to therapy .
In practice often become allergic meet periodontitis, which is associated with sensitization of patients to drugs used. Serous overall process in this form of periodontitis allergy accompany such as skin rash, swelling of the face and mucous membranes of the mouth, throat irritation with characteristic cough etc. that contribute clarifying the nature of the disease. Revealing a history of exposure to allergic reactions, as well as positive results allergy tests help clarify the diagnosis and identify therapies.
The differential diagnosis of acute serous periodontitis should be conducted with acute diffuse pulpitis. Characteristic for irradiation pulpitis pain, acute onset, remission and intermission in progress sharply distinguish it from periodontitis. Pain in patients with periodontitis is dumber, is not as sharp as with pulpitis. Lymph nodes in patients with pulpitis not affected.
Differential diagnosis between serous and purulent periodontitis based on the severity of the patient and the nature of pain and overall clinical picture. In patients with serous periodontitis pain less pronounced, not as intense, strictly localized. Changes in the mucosa in the area of the root apex small, often in the form of mild hyperemia. Tooth barely moving only in the transverse direction. The general condition of the patient does not suffer.
Acute suppurative periodontitis (periodontitis acuta purulenta) usually develops after serous. But often it can begin spontaneously in the case of massive penetration of virulent infections in periodontal and reduced reactivity of the patient. The clinical picture of this fairly typical periodontitis. In comparison with serous form of his more rapid progress, expressed common manifestations. Founded in periodontal space purulent exudate, which looks out, often breaks out, destroying the periodontal tissue.
Patients complain of spontaneous acute continuous pain pulsating character. At the beginning of the pain is localized. However, he soon becomes diffuse, radiating from the teeth of the mandible in the ear, and the top – in the temporal area. Patient always indicates tooth that he feels like “higher” very painful when pressed, contact with antagonists or even if you touch your tongue while talking. Pain aggravated by heat, whereas cold, on the contrary, has a sedative effect. Any physical effort leading to increased pain.
OBJECTIVE. Sick tooth may be intact, although its color is changed, sometimes significantly carious defect or seal. Pulp cavity in most cases closed, but may be open. elektrosensitivity – 120-150 mA, which determines necrosis of the pulp. In canals during sensing there gangrenous decay, often under pressure turns manure. Horizontal and vertical percussion tooth is very painful. Tooth movement in moesia distal direction and in the direction of the longitudinal axis. Mobility is particularly significant, if manure reaches the circular connections and looking out in the area of gingival pockets. In this case, the tooth as if floating in the accumulation of manure
Tooth allegedly grew not only a subjective feeling sick, but determined during the review, because it really is somewhat supplanted with alveoli accumulated Indepth inflammatory exudate. Mucosa in the area of the top bloodshots and edematous. Transitional fold smoothed due to the accumulation of inflammatory infiltrate, very painful during palpation. Depending upon the stage of suppurative periodontitis can be detected by palpation extremely painful hardening of the periosteum in the case of formation of subperiosteal abscess.
In the case of case of protruding abscess during palpation reveal not only the pain but also the phenomenon of fluctuations arise collateral changes, such as edema of the soft tissues of the face, the size of which does not always correspond to the severity of injury. Swelling can lead to significant asymmetry and deformation face, especially in pasty tissues. If collateral edema should always perform a differential diagnosis of cellulitis, phlegmon but for the expressed pain and tension and elegance skin. shine Promotion purulent exudate and abscess localization depend on the location of the root, which is the source of infection, and anatomic and histologic features section of the jaw.
In some cases, pus, which met in Periodontal could spill across the canal tooth (Fig. 2). This is the most favorable option evacuation of pus, but it is possible only when the canal is open and passable. Often in the case of lesions of the lower molars manure flows through the marginal gingival pocket that after melting circular links periodontium. This path is unfavorable because the cortical plate subsequently melted and formed bone pocket.
Fig.2. Ways evacuation of purulent exudate in acute exacerbations or chronic periodontitis:
1-root canal;
2-gingival pocket;
3 sponge bone (underperiosteum)
CLINICAL PICTURE, DIAGNOSIS OF PERIODONTITIS, DIFFERENTIAL DIAGNOSIS OF CHRONIC PERIODONTITIS
Chronic periodontitis is a disease that has a variety of clinical and radiological picture and the most common among people with periodontal pathology.
If a patient with acute periodontitis causes pain without hesitation to seek dental care, then chronic periodontitis usually does not cause subjective sensations. Often he found by chance on radiographs when the patient is not even aware that he has the disease. Accurate diagnosis can be established only after a thorough clinical and radiological examination.
Chronic fibrotic periodontitis (periodontitis chronica fibrosa). Symptoms. Chronic fibrotic periodontitis is asymptomatic, only occasionally patients experience minor pain during chewing coarse meal. The same may be determined by gangrene of the pulp if cavities filled remnants of food. Diseases found ba x-ray. From history establish that before (1-2 years ago), the patient was unwarranted causal or pain and were treated tooth root.
OBJECTIVE. They exhibit a carious tooth or sealed devitalization. The pain from the effects of thermal stimuli and percussion available. Palpation in the area of apex painless. If fibrotic periodontitis developed after treatment of acute suppurative or chronic granulating periodontitis, it may be outdated scar. Sometimes fibrotic periodontitis may be a patient with intact teeth. In such cases, fibrotic periodontitis arose as a result of chronic injury or traumatic occlusion.
Radiologically often exhibit periodontitis expansion slot in the top section in the form of genital cap.
Fig.3. Chronic fibrotic periodontitis (X-ray)
Chronic granulating periodontitis (periodontitis chronica granulans) is 65 70% of all cases of chronic periodontitis.
Symptoms. Patients complaiumb tooth, some pain while eating and pressing. In the top section of patient feels heaviness and slight fullness. If there is a carious defect, then filling it with food remnants can cause deterioration process and pain. From history clarifies the process repeated exacerbation of severe pain, swelling, formation of abscesses and fistulas appearance and oozing pus.
OBJECTIVE. They exhibit a gangrenous or sealed devitalization tooth with changed color. The tooth may also be externally intact or have broken the crown (in the case of traumatic etiology lesions). Vertical percussion tooth quite palpable or gives light pain reaction. During horizontal percussion if bone perforated wall or thinned after the introduction of the index finger in the mouth vestibule area Apex felt tapping, which is transmitted directly from the crown of the tooth to its root. Such a percussion entitled phenomenon allotted effort and most apparent in the area of one root of the teeth. Tooth mobility may vary depending on the degree of destruction of the alveolar bone. During the inspection of the mucous membrane in the region of the apex is congestion with a bluish tinge.
But congestion is not too severe, so its detection mouth should begin to examine with porch. IG Lukomski (1955) described the typical granulating periodontitis vazopareus symptom that occurs when pressing the swollen gums – they seem swollen pillow. This is due to the growth of granulation infiltration foci, which applies not only to the bone, but also the soft tissue surrounding the alveoli. When you click on such a clear fine instrument (head plugger or blunt side of the excavator) remain hollow and grinding mucosa, which is rapidly changing bright red stripe, stored long time, sometimes a few minutes (due to paresis vessels ash).
In case of frequent exacerbations in the mucosa may occur permanent gingival or cutaneous fistula (fistula), which while pressing pours a drop of pus. Fistula course connects the source of infection of the mouth, where it opens fistula hole, which is often plugging granulation tissue that acts with him, giving the hole look navel. Occasionally plot fistula may see one or more scars.
Palpation in the area depending on the top step of the process is accompanied by more or less severe pain. During palpation can be defined cortical layer of bone resorption, regional lymph nodes are usually enlarged and painful when pressed.
Chronic granulating periodontitis
On radiographs in the area of apex turns focus enlightenment different sizes, shapes which resemble flames. There has gradual transition from areas of bone destruction to healthy bones in a light shade. This shows the inflamed bone demineralization. In the case of a long course of the process in some areas there is resorption of cement and dentin of the tooth root that a picture can be obliquely truncated cone shape more than 1/3 the length of the root. You can also determine the direction fistulnoho speed (Fig. 4).
Fig.4 chronic granulating periodontitis
In case of successful treatment of periodontitis in 4 – 8 months defect begins to decrease, and on its peripherals, a new bone. It is also possible the formation of bone trabeculae, which is defined in the picture as a characteristic gray shadow. A year later section enlightenment completely replaced by bone, sometimes more dense thaormal bone.
Differential diagnosis. Chronic granulating periodontitis can be easily differentiated from fibrous periodontitis in character traits that are percussion and palpation, the presence of hyperemia and edema of the mucous membrane in the region of the apex, and fistulas or scar in place of the latter. Diffuse illumination irregular in some areas of the alveoli in the apical radiographs helps to clarify the diagnosis.
Chronic granulomatous periodontitis (periodontitis chronica granulomatosa) appears limited periodontal inflammation around the apical hole tooth usually has no symptom-course. Dentist finds it as fibrous accidentally during radiological examination. Medical history can establish that sometimes during colds or active chewing solid foods patients feel heaviness, tension, even pain in the root apex of the tooth.
OBJECTIVE. Identify tooth color changed, it may be intact or sealed. Vertical percussion often painless. However, compared to neighboring teeth causal tooth may be sensitive. Horizontal percussion in cases of considerable size granulomas determine symptom of the reflected shock. Mucosa in the area of Apex is not changed, only in the acute stage it is hyperemic and edematous.
Fig.5 Chronic granulomatous periodontitis
Radiography is an important part of dental diagnostic.
