Odontogenic diseases of the maxillofacial. Classification of odontogenic inflammatory diseases of the maxillofacial region
Inflammatory diseases of the maxillofacial region are among the most common lesions of the jaw.
The main causes of inflammatory diseases of the maxillofacial area are streptococci and staphylococci. In addition to these reasons, inflammation of the jaws develops in a small percentage of meningococci, diphtheria bacilli, spirochetes and others. Inflammatory diseases can occur with metastatic infection, with acute infectious diseases such as scarlet fever, influenza, typhoid, measles, diphtheria, etc.
Odontogenic inflammatory diseases of the maxillofacial region
Frequency - 90%
Etiology and pathogenesis
- The most common causes of the development of odontogenic inflammatory diseases of the maxillary sinus are: periodontitis, periodontitis, cysts, complications during the eruption of the wisdom tooth
- anaerobic infection
Classification
- Lymphadenitis
- Maxillary sinusitis
Abscesses and phlegmon
Kinds:
- superficial and deep
- localization - face, collarbone, neck, floor of the mouth, tongue, etc.
Clinical picture
Anamnesis
- swelling
- dysphagia
- labored breathing
Objectively
- redness of the skin / mucosa
- palpable pain
- fluctuation
- general weakness
- accelerated heartbeat
Laboratory research methods
- accelerated ESR
- leukocytosis with degeneration
Treatment
- incision and drainage
Lymphadenitis
Kinds
- Acute - serous, purulent (abscessing) and phlegmonous
- Chronic - fibrinous, granulomatous, fistulating
Clinical picture
Palpable painful infiltrate.
Differential Diagnosis
- Infectious mononucleosis
- piggy
- rubella
Treatment
Surgical removal of the focus of infection.
Periostitis
Kinds
- Acute - serous and purulent
- Chronic - fibrinous and ossifying
Clinic
- more likely to develop mandible
- thickening of the bone in a limited area
Osteomyelitis (acute - limited and disseminated)
local symptoms
- acute spontaneous pain in the area of one or more teeth
- coated tongue
- regional lymphadenitis
- fistulas form on the skin/oral mucosa
- decay around the teeth
- possible pathological
General state
- fever syndrome
- general intoxication
Neonatal osteomyelitis differs significantly from osteomyelitis in older children, adolescents, and adults. It is more common in premature babies but is rare in infants. Premature infants are more susceptible to infection due to immature immunity due to frequent blood collections, invasive control procedures, etc. Neonatal osteomyelitis occurs due to hematogenous proliferation of microorganisms, which is the most common mode of infection. In preterm infants, neonatal osteomyelitis is often the result of direct inoculation of venipuncture bacteria, umbilical catheterization, etc. The most common bacterial pathogens causing osteomyelitis in children are Staphylococcus aureus in all age groups, group B Streptococcus agalactiae, and Gram-negative organisms (E. coli and pneumoniae Klebsiella) are also important bacteria in the neonatal period. Society-acquired strains of methicillin-resistant Staphylococcus aureus in recent years have great importance and cause serious infections in newborns.
Treatment of inflammatory diseases of the maxillofacial region should be prescribed accordingly. The use of broad-spectrum antibiotics, calcium, salicylates and vitamins, together with early incision and extraction of the tooth, which is the cause of this process, gives excellent results.
This treatment can be supplemented with various. The treatment of chronic osteomyelitis is mainly to help the body in its protective, isolating reaction and removal of the sequester. During the entire period of time, first of all, it is necessary to monitor the possibility of drainage of pus, since any preservation of the latter leads to an aggravation of the process and prevents the healing process.
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Diseases of the nerves of the maxillofacial region include lesions of the systems of the trigeminal, facial, glossopharyngeal, and also the hypoglossal nerves of various etiologies.
Classification
There are various classifications depending on the location of the lesion and the nature pathological changes.According to the localization of the lesion, they distinguish:
- damage to the trigeminal nerve;
- damage to the facial nerve;
- defeat glossopharyngeal nerve;
- lesion of the hypoglossal nerve.
- neuralgia;
- neuropathy (neuritis).
Etiology and pathogenesis
In the etiology of nerve lesions of predominantly central origin, the following matters:- acute traumatic brain injury;
- development of benign and malignant neoplasms in the cranial cavity;
- trophic changes due to disturbances cerebral circulation;
- development of inflammatory processes (meningitis, meningoencephalitis, etc.).
- trauma (fractures of the jaw and facial bones; changes due to traumatic extraction of teeth and other surgical interventions; trauma with instruments and filling materials when filling the canals of the teeth; chronic trauma due to the use of irrationally made prostheses and orthodontic appliances, etc.);
- acute and chronic inflammatory processes ( chronic periodontitis; osteomyelitis; odontogenic maxillary sinusitis; rarely - acute inflammatory processes);
- neoplasms of the maxillofacial region (malignant neoplasms of the maxillofacial region, neurinoma);
- infectious and catarrhal diseases (specific and nonspecific).
Clinical signs and symptoms
The clinical picture depends on the location and nature of the lesion. For trigeminal neuralgia predominantly of central origin are characterized by:- short-term excruciating, paroxysmal pains that suddenly appear and quickly stop;
- pain attacks are accompanied by vegetative manifestations on the face (skin hyperemia, lacrimation, salivation, reflex contractions of mimic and chewing muscles);
- pain attacks are often preceded by prolonged pain in the zone of innervation of the corresponding trunk.
Neuralgia of the nasociliary nerve (unilateral and bilateral Charpin's syndrome) is characterized by:
- attacks of excruciating pain in the eyeball, eyebrows and the corresponding half of the nose;
- pain occurs at night and is accompanied by lacrimation, swelling of the nasal mucosa;
- there may be changes in the anterior part of the eye in the form of keratoconjunctivitis and pain on palpation of the inner corner of the eye.
- pain in the temple, inner ear, anterior wall of the outer ear canal, temporomandibular joint;
- sweating and reddening of the skin in the region of innervation of the ear-temporal nerve during meals is pathognomonic.
Trigeminal neuritis is characterized by pain, parasthesia, and sensory disturbances in the areas of innervation of the affected branches. Neuritis of the facial nerve is characterized by acutely developed prosopoparesis, sensory and autonomic disorders. Neuritis of the glossopharyngeal nerve is characterized by paroxysmal short-term pain in the region of the root of the tongue or tonsil, spreading to the palatine curtain, throat, ear. Pain radiates to the angle of the jaw, eyes, neck.
Hypoglossal neuritis is characterized by:
- with isolated neuritis, motor disorders of the muscles of the tongue occur, sometimes pain in the root of the tongue and headache;
- in the initial stages of the disease, upon careful examination, it is possible to note that the seam of the tongue has the shape of an arc, curved towards the healthy side, the root part of the tongue on the affected side is slightly higher due to paralysis;
- when protruding, the tongue deviates towards the lesion.
Complications
The nature of the complications is due to the weakening or shutdown of individual functions due to damage to one or another nerve branch. The diagnosis is made on the basis of the results of a physical examination (you should pay attention to the history, complaints of the patient and the presence of sensory and functional disorders). X-ray examination is carried out in order to identify areas of damage to the jaw and facial bones, which may be the cause of neuropathology. In order to clarify the localization of the affected nerve branch, diagnostic blockades are carried out with a 1-2% solution of lidocaine.To identify central (intracranial) pathological changes, it is shown to perform computed tomography skulls. To clarify the diagnosis, electroodontodiagnostics is performed, ultrasound procedure, color dopplerography, magnetic resonance imaging (MRI), encephalography, etc.
Differential Diagnosis
Diseases of the nerves of the maxillofacial region are differentiated from each other. Neuralgia and neuropathy of the II and III branches of the trigeminal nerve are differentiated from pulpitis and periodontitis. Neuralgia and neuropathy of the II branch of the trigeminal nerve are also differentiated from maxillary sinusitis. It should be remembered that the symptoms of neuritis of the trigeminal, facial and other nerves can occur with malignant extra- and intracranial neoplasms. On the early stages conservative treatment is carried out, in the later stages and in case of mechanical (due to trauma) rupture of the nerve trunk, surgical treatment is possible.Neuralgia
Treatment of neuralgia should be combined and prescribed with the participation of a stomato-neurologist and a neuropathologist. If these specialists are not available, the treatment is carried out by a dentist. The choice and tactics of treatment depend on the etiology of the disease, its duration, the intensity of the pain syndrome and the age of the patient.Usually, treatment begins with the appointment of carbamazepine (at first, minimal doses are used, gradually increasing them until an analgesic effect is obtained):
Oral carbamazepine 100 mg bid until clinical improvement.
You can use other drugs:
Thiamine / pyridoxine / cyanocobalamin IM 2 ml (100 mg / 100 mg / 1 mg) 1 r / day or every other day, 10 injections
±
Glycine inside 100 mg 3 r / day, 30 days, then a break for 30 days, then a second course or
Piracetam inside 800 mg 2 r / day, 6-8 weeks.
With strong pain syndromes NSAIDs may be included in the treatment regimen:
Diclofenac 50 mg orally 2-3 r / day, until clinical improvement or
Indomethacin orally 25 mg 3 times a day, until clinical improvement.
Neuritis
For the treatment of neuritis, NSAIDs are used:Diclofenac inside 50 mg 2-3 r / day, 10 days or
Indomethacin orally 25 mg 3 r / day, 10 days or
Ketoprofen 50 mg 3-4 times a day (1 capsule in the morning and afternoon and 2 capsules in the evening) or
Ketorolac 10 mg orally every 4-6 hours for 10 days or
Nimesulide inside 100 mg 2 r / day, 10 days.
NSAIDs can be combined with the appointment of vitamins:
Thiamine / pyridoxine / cyanocobalamin IM 2 ml (100 mg / 100 mg / 1 mg) 1 r / day, 10 days or inside 1 tablet (100 mg / 200 mg / 200 mcg) 3 r / day, 20 days or
Pyridoxine IM 100 mg 1 r / day, 10 days
+
(alternate every other day) Thiamine IM 100 mg 1 r / day, 10 days
+
Cyanocobalamin i / m 1 mg 1 r / day, 10 days.
In the treatment of neuritis, in addition to pharmacotherapy, the following are additionally prescribed:
- physiotherapy;
- acupuncture;
- hirudotherapy;
- transcutaneous electrical nerve stimulation.
Evaluation of the effectiveness of treatment
Treatment is effective in the absence of seizures (long-term remission).Mistakes and unreasonable appointments
Unreasonable appointments are the result of an erroneous diagnosis. It is necessary to take into account concomitant diseases to exclude polypharmacy (simultaneous intake of a large number of drugs of various groups).Forecast
With proper diagnosis and adequate treatment, the prognosis is relatively favorable.G.M. Barer, E.V. Zoryan
In case of odontogenic inflammatory diseases, due to the close anatomical connection of the tooth with the jaw, there is always, to one degree or another, the spread of the infectious-inflammatory process to bone tissue. If the zone of distribution of this process is limited to the periodontal tissues of one tooth, it is considered as periodontitis. The spread of the infectious-inflammatory process in the jaw beyond the periodontium of one tooth with the involvement of adjacent bone structures leads to the emergence of a qualitatively new state of osteomyelitis. Although the term "osteomyelitis" literally translates as inflammation of the bone marrow, in the clinic it is used to refer to an inflammatory process that spreads to all elements of the bone as an organ: the bone marrow, the main substance of the bone with the contents of the nutrient channels and channels of the osteon system, the periosteum (periosteum).
The infectious-inflammatory process in the maxillary tissues can proceed as a diffuse purulent inflammation (phlegmon) or in the form of a delimited purulent process (abscesses). Phlegmons and abscesses, the development of which is associated with an infectious and inflammatory process in the periodontium of the tooth, are treated as odontogenic.
Thus, depending on the volume of bone tissue damage and the prevalence of the infectious and inflammatory process in the maxillary soft tissues There are the following main forms of odontogenic inflammatory diseases:
1) periodontitis;
2) odontogenic osteomyelitis;
3) odontogenic periostitis;
4) odontogenic abscesses and phlegmons;
5) odontogenic lymphadenitis.
Pathogenesis
The term "odontogenic inflammatory diseases" is a collective term. It includes a number of clinically well-defined forms of diseases (periodontitis, periostitis, osteomyelitis, abscess and phlegmon, lymphadenitis, odontogenic sinusitis), which at the same time can be considered as a variety of manifestations of a dynamic odontogenic infectious process.
Attempts to understand the causes and patterns of development of this process, to study the relationship of these clinical manifestations have been made for a long time. Much is being done in this direction today.
However, in order to build a sufficiently complete and universal theory of the pathogenesis of odontogenic inflammatory diseases, it is necessary to first answer a number of particular questions, the main of which can be formulated as follows:
1. In what way are weakly pathogenic and non-pathogenic microorganisms, penetrating from the oral cavity into the periodontium, bone tissue, causing the development of a rapid infectious and inflammatory process there?
2. What are the mechanisms of exacerbation of chronic odontogenic infection?
3. what are the mechanisms of spread of odontogenic infectious process?
4. What factors determine the volume of bone tissue damage in odontogenic osteomyelitis?
Mechanisms of allergy in the pathogenesis of odontogenic inflammatory diseases.
In essence, the answer to the question of how weakly pathogenic and non-pathogenic microorganisms, penetrating from the oral cavity into the periodontium and bone tissue, cause a violent infectious and inflammatory process there, was given at the beginning of the 20th century by M. Artyus and G. P. Sakharov. They found that after a 4-5-fold subcutaneous injection of horse serum to rabbits, a violent inflammatory reaction with severe alteration occurs at the site of the permissive intradermal injection of serum. Since throughout the experiment the animals were injected with identical serum, it was concluded that the mechanism of the observed phenomenon is associated with a change in the ability of the rabbit's body to respond to repeated administration of a foreign protein. Later, this phenomenon was used to reproduce osteomyelitis of long bones in the experiment (Derizhanov S. M.) and osteomyelitis of the lower jaw (Snezhko Ya. M., Vasiliev G. A.).
At present, the mechanism of the Artyus-Sakharov phenomenon has been studied quite well. According to the classification, it belongs to the III type of immunopathological reactions. Its essence is as follows. Under the influence of whey protein entering the body, which has antigenic properties, antibodies are produced, and this underlies the sensitization of the body. Against this background, the local administration of a permissive dose of the antigen is accompanied by the penetration of the latter into the vascular bed, where the antigen-antibody complex is formed. This complex is fixed on the membranes of vascular endothelial cells, thus turning them into target cells. Neutrophilic leukocytes, phagocytizing immune complexes, simultaneously damage the cell membrane, which leads to the release of lysosomal enzymes, inflammatory mediators. This is accompanied by activation of platelet factor 3 and may be the cause of intravascular coagulation, leading to impaired microcirculation and tissue necrosis.
There is reason to believe that the described immunopathological reaction also takes place in the pathogenesis of odontogenic infection. True, in odontogenic inflammatory diseases, antigens of a different nature act than in the experiments of Artyus-Sakharov, S. M. Derizhanov, and others. The role of the antigen in them is the waste products of microbes, the structural elements of the microbial cell, released after its death. Such an interpretation of one of the links in the pathogenesis of odontogenic infection allows us to understand the reason why in many patients non-pathogenic microbes turn out to be the causative agent of the disease. Apparently, in a sensitized organism, their damaging effect is mediated through the mechanisms of the just described immunopathological reaction (Fig. 1).
As for the sensitization of the macroorganism to staphylococci and streptococci as the most likely causative agents of odontogenic inflammatory diseases, it may precede the onset of an odontogenic infectious process, i.e., sensitization occurs under the influence of the same type of microflora of the infectious focus of any other localization.
Rice. 1. Some mechanisms of tissue damage during the development of an odontogenic infectious-inflammatory process.
With the penetration of microbes through the defect of the hard tissues of the tooth into the pulp and especially periodontal tissue, the sensitization of the organism increases.
However, it would be wrong to consider the fact of the development of infectious-allergic inflammation at the site of the introduction of microbes into the periodontium as a phenomenon that is absolutely harmful to the macroorganism. The biological meaning of this reaction is to quickly turn on the immune mechanisms to localize the infectious focus, prevent the generalization of the infection and thereby maintain the constancy of the internal environment of the macroorganism.
A peculiar feature of odontogenic infection is that the patient's body cannot independently, without appropriate therapeutic measures, stop the entry of microorganisms into the periodontium through the root canal. And this means that it is not necessary to count on self-healing and complete elimination of the infectious-inflammatory focus in the periodontium. At best, the process stabilizes, resulting in the formation of a chronic focus of odontogenic infection, which is in a state of dynamic equilibrium with the patient's body.
Periostitis of the jaw
One of the fairly common complications of inflammatory processes in periodontal tissues is periostitis of the jaw. Periostitis can occur as a result of further spread of the process in acute apical, as well as exacerbation of chronic apical periodontitis. In some cases, it may be the result of marginal periodontitis or infection of the wound after tooth extraction.
Purulent exudate from the periodontium falls under the periosteum of the jaw. Most often, the exudate accumulated in the periodontal fissure passes through small holes in the bone tissue (the system of the so-called Haversian and Volkmann tubules) and the cortical plate and reaches the periosteum. There is a detachment of it in a certain area. Inflammatory exudate also affects the outer layer of bone tissue, but bone necrosis, as well as other changes characteristic of the osteomyelitic process, does not occur (Fig. 37).
The disease is accompanied by severe (sometimes throbbing) pain, which is the result of exfoliation and stretching of the inflammatory exudate of the periosteum. The pain is severe, can radiate to the temple, eye, ear. As a rule, cold softens pain, and heat, on the contrary, intensifies them.
Periostitis is accompanied by changes in the surrounding soft tissues. There is swelling of the soft tissues of the cheek, chin, submandibular region, depending on the localization of the process. As G. A. Vasiliev notes, with the spread of periostitis "from the upper canine and upper premolars, collateral edema, located somewhat to the side, captures a large area of the face. Not only tissues in the buccal and zygomatic region swell strongly, but there is a transition of swelling to the lower one, and often and upper eyelid. For the process that arose from the upper large molars, a swelling is characteristic, reaching backwards almost to the auricle.
Exudate with periostitis can penetrate not only into the vestibular side, but also towards the oral cavity - cause the formation of an abscess (abscess) in the sky or in the bottom of the mouth, and also with an inflammatory process in the upper jaw, it can get into the maxillary cavity and cause sinusitis.
The mucous membrane in the area of the causative tooth is always hyperemic and edematous. The transitional fold is smoothed out. Palpation of the affected area is painful. Percussion of the tooth causes less pain than with the phenomena of acute periodontitis. With further progression of the process in the area of edema, fluctuation is noted, then the formation of a fistulous tract in the vestibule or the oral cavity proper. In the worst case, the penetration of pus into the soft tissues surrounding the jaw.
The general condition of patients with periostitis worsens. The reaction to inflammation depends on the prevalence and severity of the process, as well as on the reactivity of the patient's body. The temperature rises to an average of 37.7-38.2°C. There is a general weakness, insomnia, no appetite.
Experience shows that the treatment of acute periostitis should be radical, surgical. It is necessary to make a wide opening of the inflammatory focus and create enough good conditions for free outflow of exudate. To do this, soft tissues and periosteum are dissected from the side of the oral cavity in the area where the greatest accumulation of pus is observed. As a rule, the intervention is performed under local anesthesia. In order for the edges of the wound not to stick together and not interfere with the outflow of pus, a rubber strip or a strip of iodoform gauze is inserted into the wound.
Patients are prescribed mouthwash weak solution potassium permanganate or soda solution, sulfa drugs 1.0 g 4-6 times a day, analgesics for pain, calcium chloride 10%, 1 tablespoon 3 times a day. In some cases, it is necessary to resort to intramuscular injections of antibiotics.
V initial stage periostitis of the jaw in a satisfactory condition of the patient and the absence of fluctuations, resorption of the infiltrate can occur without surgical intervention. In these cases, you can resort to the help of physiotherapeutic methods of treatment (UHF, Solux, blue light lamp), recommend patients to rinse the mouth with warm disinfectant solutions and prescribe sulfanilamide preparations. Some note a good effect when applying a warming ointment bandage according to Dubrovin (4% yellow mercury ointment). If within a few days there is no improvement, it is necessary to move on to radical treatment.
During treatment, it is necessary to immediately assess the feasibility of preserving the causative tooth. If the tooth is of no value for the chewing function (the crown is destroyed, the root is exposed, the mobility of the tooth is pronounced, etc.), it must be removed. In some cases, the timely removal of the causative tooth gives a good outflow of exudate and allows you to eliminate the inflammatory process without additional surgical interventions.
Properly conducted treatment makes it possible to restore the patient's ability to work within 2-4 days. With improper treatment, the process can move to the jawbone, resulting in odontogenic (tooth origin) osteomyelitis.
Osteomyelitis of the jaw
This is a disease of the jaw bones that occurs as a result of the penetration of infection from the periodontal focus into the thickness of the jaw bones. Odontogenic osteomyelitis is a fairly common disease. Approximately 35-55% of all osteomyelitis are osteomyelitis of the jaws, among them odontogenic osteomyelitis occupy the main place. With this form of the inflammatory process, the penetration of infection into the bone tissue is associated with dental diseases. Topographically, there is a very close relationship between the periodontium and the bone marrow of the jaw. Very often, an infection from the apical and, less often, from the marginal periodontium penetrates into the bone tissue. Odontogenic osteomyelitis can also occur when the wound becomes infected after tooth extraction. The most common localization of the inflammatory process is the lower jaw, according to M. G. Lukomsky - in 89.6% of cases, and the region of the lower molars is affected in 70%, while the upper jaw accounts for only 10.4% of monogenic osteomyelitis.
As already mentioned, the cause of the development of odontogenic osteomyelitis of the jaw is most often apical periodontitis of the tooth. At the same time, patients note that at first one specific tooth hurt, and then the pains become diffuse, capture a group of teeth of this jaw. There is swelling of the soft tissues of the face, and pus, breaking through the bone tubules, can cause inflammation of the soft tissues - an abscess or phlegmon.
When examining the oral cavity, there is hyperemia and swelling of the mucous membrane on both sides of the alveolar process in the affected area, which captures the area of several teeth. The teeth are mobile, their percussion is painful. Palpation of the affected area also causes pain, there is some thickening of the body of the jaw. Regional The lymph nodes enlarged, painful.
With the localization of inflammation in the area of the molars, especially the lower ones, the opening of the mouth is limited due to the involvement of the masticatory muscles in the process. The general condition of the patients is severe. The temperature rises to 39-39.5°C. Patients complain of headache, insomnia, loss of appetite, general weakness. The phenomena of the general intoxication of an organism are noted. The skin and mucous membranes are pale, the pulse is quickened. Eating is difficult due to poor mouth opening and the presence of an inflammatory process. Saliva is viscous. Putrid odor from the mouth. The work of the gastrointestinal tract is disturbed.
Erythrocytes fall, and the number of leukocytes reaches 2x10³ with a decrease in the number of lymphocytes. ESR reaches high numbers. The specific gravity of urine is high, protein appears in it. The general condition of patients requires their hospitalization and treatment by a dentist, and in his absence - by a surgeon.
A reptgenogram can help in making a diagnosis no earlier than 2 weeks after the disease.
During this period, violations of the bone structure of the jaw and thickening of the periosteum can be noted.
2-3 weeks after the onset of the disease, acute phenomena subside and the process can become chronic. At the same time, the general condition of patients improves. Pain gradually decreases or disappears completely. The teeth in the affected area continue to be somewhat mobile, but there may not be pain on percussion. Hyperemia of the mucous membrane disappears, swelling of the soft tissues of the oral cavity decreases. Through the fistulous passage or incision line, pus continues to be released for a long time. The temperature in patients drops to subfebrile. The phenomena of intoxication of the body decrease, sleep, appetite, work are restored. gastrointestinal tract. Data laboratory research approaching the norm.
The most characteristic for the stage of chronic osteomyelitis is the separation of dead areas of bone tissue - sequestration. Depending on the volume and degree of the inflammatory process, both small areas of bone tissue and very large areas of bone can be sequestered.
In some cases, osteomyelitis may be rejected on the upper jaw of the alveolar process, zygomatic bone, and on the lower jaw - even a part of the jaw body. The sequestration process is well expressed on the x-ray (Fig. 38).
Treatment acute osteomyelitis should be complex and include surgical, medical and physiotherapeutic methods.
In the initial stage, the removal of the causative tooth is shown. This ensures a good outflow of purulent exudate and in most cases eliminates the process. With diffuse osteomyelitis, it is impossible to confine oneself only to tooth extraction. It is necessary to eliminate the main purulent focus in soft tissues (abscess or phlegmon). Depending on its location, an intraoral or extraoral incision is made. The incision should be wide enough to allow good drainage of the pus. To do this, the wound is drained with a rubber strip or a strip of iodoform gauze. The use of iodoform gauze in such cases is not always effective, since it swells, saturated with exudate, and closes the wound lumen; while the outflow of pus stops.
Good results are obtained by applying a wet dressing to the wound with a hypertonic solution of magnesium sulfate or an antiseptic solution. Inside, patients are prescribed sulfa drugs up to 1 g every 4 hours, intramuscularly - injections of antibiotics 4 times a day, autohemotherapy, desensitizing agents, vitamins. To reduce severe pain, amidopyrine, phenacetin and other painkillers are prescribed orally with the addition of aspirin, caffeine or luminal.
Rp.: Phenacetini
Ac. acetylsalicylici aa.......... 0.25
M.f. pulv. D.t. d. No. 12
S. One powder 3-4 times a day
Rp. Phenobarbitali.............. 0.05
Amydopirini.............. 0.3
Phenacetini............... 0.25
Coffeini natrio-benzoici........ 0.05
M.f. pulv D. t. d. No. 12
S. 1 powder 1-2 times a day
Status needs to be monitored of cardio-vascular system.
Good nutrition is of great importance. But most patients cannot eat normally due to the inflammatory process in the maxillofacial region. Therefore, food should be high-calorie, fortified and chopped. If necessary (for example, when reducing the jaws), it can be introduced using a special drinker.
In the chronic course of the osteomyelitic process, the main point of treatment is the removal of the separated bone sequester. This operation is called a sequestrectomy. It is carried out when the sequester is completely separated from the surrounding bone tissue, which usually happens 4-5 weeks after the onset of the disease. After removing the sequester, the wound is sutured, leaving drainage, or tamponated with iodoform gauze, which is changed after 4-5 days. Patients are advised to give sulfa drugs. To speed up the restoration of the bone structure, calcium preparations are prescribed, as well as vitamins C and D. Physiotherapeutic procedures can be recommended: irradiation with a quartz lamp, UHF.
If the causative tooth (or teeth) was not removed in the acute period, then it is advisable to save it. In the chronic course of osteomyelitis, if there is no mobility of the teeth, one should refrain from removing them. If the pulp of such teeth has become dead, then it is necessary to trepan and seal them, which preserves the teeth for a long time.
pericoronitis
The inflammatory processes of the jaws also include cases of difficult eruption of the wisdom tooth, accompanied by damage to the surrounding tissues.
The eruption of both milk and permanent teeth normally proceeds without any complications. The exception is the eruption of wisdom teeth, which in some cases can be difficult. This is most often observed during the eruption of the wisdom teeth of the lower jaw and very rarely - the upper.
Difficult eruption of third molars is usually associated with a lack of space in the alveolar process, incorrect position of the tooth, or the presence of a dense mucous membrane that completely or partially covers the crown of the tooth. In these cases, most often one or two tubercles of the wisdom tooth erupt, after which the position of the tooth no longer changes (Fig. 39). Part of the chewing surface remains covered with a mucous membrane - the so-called hood. Mucus accumulates under the latter, food residues get in, oral microbes are introduced. In addition, the mucous membrane covering part of the chewing surface is subjected to trauma by antagonistic teeth during chewing. All these moments lead to the emergence of an inflammatory process, which gradually progresses. The edges of the mucosal hood may ulcerate. Chronic, sluggish inflammatory process gradually causes changes in the surrounding tissues. First of all, there are cicatricial changes in the hood, expansion of the periodontal gap, etc. This leads to the spread of the inflammatory process - pericoronitis, which is accompanied by pronounced clinical symptoms. Patients complain of pain in the area of the causative tooth, often radiating to the ear, pain when swallowing. Owing to the inflammatory hypostasis covering sites of an attachment of masticatory muscles, opening of a mouth is limited. Eating is difficult. Soft tissue edema appears in the area of the jaw angle of the corresponding side. The temperature rises to 37.3-38°C.
The mucous membrane in the area of the causative tooth is hyperemic, edematous. Abscesses may occur on the lingual or buccal side. Pus exudes from under the hood. The slightest pressure on it causes a sharp soreness and enhances the release of exudate. Regional lymph nodes are enlarged and painful on palpation.
With a further increase in the process, the opening of the mouth is even more limited up to the complete impossibility of taking solid food. Pain when swallowing intensifies. Lymphadenitis is on the rise. The process can be complicated by phlegmon or move to bone tissue - osteomyelitis occurs. With the phenomena of pericoronitis, treatment should be radical, although it does not always require surgical intervention.
Depending on the severity of the process and the general condition of the patient, various methods of treatment are recommended. With the reduction of the jaws and inflammatory edema, we now widely use the trigeminosympathetic blockade proposed by M.P. Zhakov, which turned out to be very effective.
After the removal of acute inflammatory phenomena, it is advisable to determine the position of the tooth using radiography. If the wisdom tooth is in a position that excludes its eruption, it should be removed (Fig. 40). In other cases, it is necessary to wash the pocket under the hood with a weak solution of chloramine, ethacridine lactate (rivanol) or potassium permanganate. Then, a strip of iodoform gauze is carefully inserted under the hood to squeeze it out a little and free the chewing surface of the crown. Iodoform gauze is changed every other day. At home, the patient is prescribed warm disinfectant rinses, sulfa drugs, 1 g 4-6 times a day.
If this treatment does not help, it is necessary to excise the hood covering the chewing surface of the wisdom tooth. It is performed under local infiltration anesthesia. The edges of the wound after excision of the hood can be coagulated. The removal of a wisdom tooth that cannot erupt or is the cause of relapses of pericoronitis is performed after the subsidence of acute inflammatory phenomena. It is carried out using an elevator, or you have to resort to a gouging operation with a chisel and a hammer, after which the wound is carefully treated. It is advisable to suture.
Abscesses and phlegmon
These inflammatory processes in the maxillofacial region most often accompany osteomyelitis of the jaws and other bones of the facial skeleton, and can also be a complication in purulent-dystrophic form of periodontal disease, gingivostomatitis, jaw fractures, and some other diseases. These are serious and extremely dangerous diseases.
Among microbial pathogens, various coccal groups (staphylococcus, streptococcus, pneumococcus, diplococcus), fusiform and Escherichia coli, as well as anaerobic forms were identified.
Abscesses and phlegmons are distinguished by a wide variety of clinical manifestations, which depends both on the general condition of the body, the virulence of the infection, and on the localization of the inflammatory process. The latter usually develops in the subcutaneous, intermuscular and interfascial loose tissue, and can also affect the lymph nodes.
Due to the resulting inflammatory infiltrate and concomitant collateral edema of the surrounding tissues, asymmetry of the face usually occurs. Natural facial wrinkles are smoothed out. The skin is tense. With superficially located phlegmon, hyperemia of the skin is expressed. The mucous membranes of the lips and oral cavity are dry, pale, the tongue is lined. Depending on the nature and clinical course of the inflammatory process, as well as the upcoming intoxication of the body, general disorders usually develop to one degree or another. They are expressed in malaise, insomnia, loss of appetite. Patients complain of headache, frequent chills. The temperature can range from subfebrile to 39-40°C. Pulse and respiration are quickened. Externally, the patient's face becomes pale, haggard.
Among local disorders, the most common are chewing disorders associated with inflammatory contracture, pain when swallowing, in some cases speech and breathing disorders, and copious secretion of viscous saliva.
The most severe phlegmons are caused by anaerobic forms of microbes. With a mild local tissue reaction and reduced body resistance, the prognosis may be doubtful.
The blood picture is characteristic of inflammatory processes: the number of erythrocytes and hemoglobin falls, a shift is noted leukocyte formula to the left, ESR is increased, in some cases it reaches 40 mm per hour.
As A. I. Evdokimov emphasizes, "at the height of the inflammatory process, protein is found in the urine (a sign of toxic nephritis), so a systematic study of urine is mandatory."
Treatment. Early opening of the focus of the inflammatory process (phlegmon or abscess) is the main therapeutic surgical measure. It is indicated in the presence of infiltration and elevated temperature. Even in cases where pus is not released, tissue tension decreases and conditions are created for the outflow of exudate. Surgical intervention should be performed by a dentist or general surgeon, based on the anatomical and topographic features of the affected area. The introduction of antibiotics, especially broad-spectrum antibiotics, as well as sulfonamides, has become widespread. In this case, it is necessary to take into account the resistance of bacteria and their sensitivity to a particular drug.
Painkillers should be prescribed to reduce pain. With a sluggish course of inflammation, as well as at the beginning of the disease, it is recommended to take UHF therapy, dry heat, as well as an ointment bandage according to Dubrovin.
It is necessary to pay great attention to the activity of the cardiovascular system. For this purpose, tinctures of valerian, cordiamine, camphor and some other means are recommended. Bed rest is mandatory in the acute period of the disease, and patients should be in a semi-sitting position in order to prevent aspiration pneumonia. A dairy-vegetarian diet, plenty of fluids, as well as vitamins, primarily ascorbic acid and vitamin B 1, are recommended.
Surgical intervention is most often performed under local anesthesia, although the use of anesthesia is not excluded. The incisions are made wide, up to 8-10 cm long, depending on the localization of the process, to the entire depth of the tissues. In this case, the location of large vessels and nerve branches must be taken into account so as not to damage them. To do this, it is necessary to adhere to the anatomical and topographic requirements for incisions in the maxillofacial region.
If pus is exuded upon opening, such a wound is usually drained with a rubber strip or rubber tube.
In case of putrefactive-necrotic decay of tissues, the wound is abundantly irrigated with a 3% solution of hydrogen peroxide, a weak solution of potassium permanganate, etc.
With dry tissues, to increase their vital activity and reduce the absorption of toxins, wet gauze dressings moistened with a hypertopic solution of sodium chloride or magnesium sulfate are applied to the wound surface.
In cases where the cause of the inflammatory process in the maxillofacial region is one or another tooth, with difficult access to it (due to edema, contracture, etc.), the removal can be postponed until the elimination of acute phenomena. In all other cases, the removal of the causative tooth should be performed simultaneously with the opening of the phlegmon.
Specific inflammatory processes require pathogenetic therapy.
Periostitis of the jaw is an inflammatory process that occurs as a complication of diseases of the teeth and periodontal tissues. More often it occurs in the form of limited inflammation of the periosteum of the alveolar process, less often inflammatory phenomena spread to the periosteum of the jaw body.
The initial period of the disease proceeds rapidly, inflammation increases every hour. However, it should be remembered that in some patients the pathological process develops slowly, within 1-2 days. During this period, the state of health worsens, weakness occurs, body temperature rises, headache appears, appetite disappears, sleep is disturbed. Pain in the area of the "causal" tooth becomes unbearable and spreads to the corresponding half of the jaw with irradiation along the branching of the trigeminal nerve: to the temple, ear, neck, eye. In the future, the pain decreases and becomes aching in nature.
In the oral cavity, hyperemia, swelling of the gums, the mucous membrane of the transitional fold and adjacent areas of the cheek develop over several teeth. In this case, the transitional fold is smoothed out, and a dense, sharply painful infiltrate is palpated in its thickness, with a purulent form, a roller-like protrusion is formed - a subperiosteal abscess. The focus of fluctuation is determined. Gradually, the pus melts the periosteum and pours out under the mucosa, forming a subgingival abscess. When examining the "causal" tooth, it is revealed that its cavity and root canals filled with putrefactive decay of the pulp. The tooth can be sealed, in some cases there is a deep pathological periodontal pocket. During this period, the pain reaction during percussion of the tooth is not pronounced, and sometimes absent. On the radiograph of the alveolar process and the body of the jaw in acute periostitis, no changes are detected.
The best results in the treatment of patients with acute purulent odontogenic periostitis are given by complex therapy, when timely surgical intervention is combined with drug and physiotherapy. For the successful implementation of surgical intervention, it is necessary to achieve good anesthesia of the tissues at the site of the future incision. Conduction and infiltration anesthesia is more often used. An incision for periostitis is made 1.5–2.5 cm long, dissecting the mucosa and periosteum along the transitional fold to the entire depth of the tissues to the bone. For a free outflow of purulent exudate and to prevent the edges of the wound from sticking together, a thin rubber drainage is introduced into it for 1-2 days, which can be made of surgical gloves or plastic film. Simultaneously with the opening of the subperiosteal focus, the "causal" tooth, which served as a source of infection, is removed if its further preservation is inappropriate.
After surgery, for the speedy resorption of the inflammatory infiltrate, rinse the mouth 4-6 times a day with a warm (40--42 ° C) solution of potassium permanganate (1: 3000) or 1-2% sodium bicarbonate solution. A good effect is given by UHF, microwave currents, fluctuorization, low-power helium-neon laser beams. It is advisable to prescribe sulfonamides (norsulfazol, sulfadimesin, sulfadimethoxine, biseptol), pyrazolone derivatives (analgin), antihistamines(diazolin, suprastin, tavegil, cetrin, fenkarol), calcium preparations, vitamins (especially vitamin C).
Osteomyelitis is an inflammation of the bone tissue and bone marrow. Inflammation usually develops due to the penetration of infection into the bone tissue. Osteomyelitis of the jaw in terms of prevalence occupies about a third of all osteomyelitis.
Depending on the source of infection, there are odontogenic(source - a bad tooth), hematogenous(infection with blood flow from any organ) and traumatic(including gunshot) osteomyelitis of the jaw.
Odontogenic osteomyelitis jaws are a rather formidable complication of neglected caries. This type of osteomyelitis occurs in approximately 75% of cases of all osteomyelitis of the jaw. Osteomyelitis in this case develops due to the penetration of infection from the carious cavity, first into the pulp, and then through the root of the tooth into the bone tissue. About 70% of osteomyelitis cases occur in the lower jaw and about 30% of osteomyelitis cases in the upper jaw. The etiology of odontogenic osteomyelitis is microorganisms of three groups: streptococci, staphylococci and some anaerobic bacteria. Microorganisms can penetrate into the bone tissue, both through the bone tubules and through the lymphatic vessels.
Acute osteomyelitis jaw is characterized by a pronounced reaction of the whole organism to infection. Patients complain of general malaise, headache, weakness, poor sleep. The temperature rises C, but sometimes a higher temperature rise is possible. The body temperature is up to 38 The absence of temperature in the presence of other signs of an acute process indicates a weakening of the body's defenses and requires special approach to the treatment of patients. The condition of patients can be both mild and severe. The first symptom in acute odontogenic osteomyelitis is pain in the area of the infected tooth. There is a sharp pain when tapping on the tooth, its moderate mobility is revealed. Moreover, the mobility of neighboring teeth is observed. The mucous membrane next to the tooth is edematous, loose and red, painful when touched. It is possible to develop a subperiosteal abscess, inflammatory contracture (decrease in mobility) of the lower jaw. On palpation of the neck region, enlarged and painful lymph nodes are noted. General form the patient usually indicates signs of intoxication: adynamia (lethargy), gray skin, pointed facial features, fever). Yellowness of the sclera of the eyes is possible (if intoxication affects the spleen and liver), protein and red blood cells in the urine (due to toxic injury kidneys). Sometimes there is a change blood pressure, both upward and downward. The blood picture is characteristic of inflammation: leukocytosis with a shift of the leukocyte formula to the left and increased ESR. On the first day of an acute reaction, the diagnosis of osteomyelitis of the jaw may be difficult due to the predominance of general symptoms over local ones.
Treatment implies the mandatory removal of the “causal” tooth (this is an example of an absolute indication for tooth extraction). An early wide periosteotomy (periosteal incisions) is indicated to ensure the outflow of exudate (inflammatory fluid). Prescribe antibiotics, detoxification therapy, symptomatic therapy, as well as local therapy (washing the bone cavity with antiseptics). Sometimes surgery is indicated (removal of sequesters), as well as bone grafting.
Pericoronitis is an inflammatory infection gum tissue, which occurs when the teeth are incompletely erupted (wisdom teeth, and more often the lower ones) or when the erupting teeth are in the wrong position. In the second case, an incorrectly located wisdom tooth tilts, which begins to put pressure on the adjacent tooth and can lead to its destruction, as well as injury to the gums and bone tissues.
The inflammatory process in pericoronitis accompanied by the following clinical symptoms: the patient in the area of the erupting tooth appears strong pain, which radiates to the ear or temple, while the patient hardly opens his mouth, swallows; his gums are hyperemic. Possible increase in body temperature; often occurs bad smell mouth or bad taste in the mouth.
A neglected disease can lead to the development of complications: subperiosteal abscess of the lower jaw. A purulent exudate may begin to be released from the focus of infection. Diagnosis of pericoronitis does not cause difficulties - it is based on clinical manifestations: eruption of wisdom teeth, tissue inflammation.
At treatment diseases to stop the spread of the inflammatory process, the gum pocket and tissues surrounding the tooth are treated, antiseptic preparations, if this is difficult, surgical excision of the gingival hood and its subsequent processing is necessary. Sometimes the patient is prescribed a physiotherapy treatment for pericoronitis (for example, UHF therapy). In severe cases, the extraction of the tooth that caused the development of the disease is required.
Lymphadenitis (lymphadenitis)- inflammation of the lymph nodes, often combined with lymphangitis.
Lymphadenitis resulting from the penetration of infection from the odontogenic focus of inflammation is called odontogenic lymphadenitis. It is caused by the usual pyogenic and putrefactive microflora (streptococci, staphylococci, diplococci or anaerobic gram-negative rods, etc.) and has the character of nonspecific inflammation.
Odontogenic lymphadenitis is observed in acute and chronic periodontitis, gingivitis, periodontitis, osteomyelitis, festering periradicular cyst, etc.; sometimes primary focus remains unrecognized or has time to stop and then it seems that lymphadenitis has arisen independently.
Clinic. Purulent melting of the lymph nodes allows you to establish a further increase in their soreness, an increase in swelling in their circumference, in most cases slowly - within a few days, and sometimes 1-2 weeks. At the same time, progressive infiltration of tissues adjacent to the lymph node can be observed, leading to a restriction of its mobility, soldering several nodes into one package, and then softening and fluctuation.
At acute lymphadenitis general phenomena - malaise, weakness - may be absent or are slightly expressed. Gradually, an abscess forms at the site of the inflamed lymph node. The general condition of patients depends on the volume of affected tissues and the severity of the process. Body temperature rises, but not in all patients, to approximately 37.6--37.8 ° C. Only in some patients, with a rapid increase in local phenomena, an increase in temperature is observed, mainly in the evening, by 1.5--2 ° C. In the blood, the same changes are observed as in odontogenic abscesses of the maxillofacial region.
Treatment: removal of the odontogenic source of infection (tooth extraction, treatment of periodontitis). Conservative treatment It is used only for acute serous lymphadenitis. Apply: dry heat, UHF therapy, short novocaine-antibiotic blockades, warming dressings-compresses. If the source of the infection is not established and suppuration of the node occurs, an abscess is opened and drained, and a drug effect on the focus of inflammation is performed. In all forms, treatment with antibiotics and sulfonamides is indicated.
Sialadenitis - inflammation of the salivary glands.
In etiology sialadenitis infection plays an important role. In the ducts of the salivary glands with sialadenitis, a mixed flora is found, consisting of staphylococci, pneumococci, streptococci. The cause of inflammation can be pathogens of actinomycosis, tuberculosis, syphilis, mumps viruses, cytomegaly, etc. Infectious agents enter the salivary gland through the mouth of the excretory duct, which is sometimes preceded by penetration into the duct foreign body(villi from a toothbrush, peel from apples, etc.), as well as by the lymphogenous or hematogenous route. S.'s emergence is promoted by infectious diseases, operative interventions, especially on abdominal organs, stagnation of a secret in channels salivary gland.
There are acute and chronic sialadenitis.
Acute sialadenitis characterized by edema, infiltration, purulent fusion and necrosis of the tissues of the gland, in place of which a scar is subsequently formed. However, acute inflammation does not always end with suppuration or necrosis, more often the process subsides at earlier stages. The main clinical signs of acute inflammation of the large salivary gland are pain in it and its increase; deterioration of state of health, increase in body temperature can be noted. The gland at the beginning of the disease is soft, painful; with the progression of the process, a dense infiltrate is formed, with purulent fusion over the affected area, fluctuation is determined. characteristic feature is a violation of the function of the gland in the form of hypo- or hypersalivation, as well as the appearance in saliva (flakes of mucus, pus, a large number of cells of a deflated epithelium. Acute sialadenitis can be complicated by an abscess and phlegmon of the surrounding soft tissues, stenosis of the salivary ducts, the formation of salivary fistulas, a persistent decrease in function glands.
In acute inflammation of the minor salivary glands (usually the mucous membrane of the lips), a limited painful induration appears in the area of the affected gland; on the surface of the mucous membrane, you can see the gaping mouth of the duct. The process may also end with abscess formation.
Treatment is carried out with antibacterial, antifungal, antiviral (depending on the type of pathogen) and hyposensitizing agents, as well as drugs that increase the body's resistance (vitamins, sodium nucleinate, etc.). In the presence of purulent discharge from the mouth of the duct, it is advisable to administer antibiotics directly into the duct of the gland. With the formed infiltrate good action have novocaine blockade, applications of a solution of dimexide. In the case of abscessing, an opening of the focus is shown. The prognosis for timely treatment is favorable. Prevention consists in observing the rules of oral hygiene, especially in case of infectious diseases and after surgical interventions.
Odontogenic sinusitis- an inflammatory disease of the mucous membrane lining the maxillary sinus.
Pathogenesis: source of inflammation- acute, aggravated chronic periodontitis of the teeth of the upper jaw, festering radicular cyst, osteomyelitis of the upper jaw, impacted teeth, traumatic extraction of teeth. Risk factors- proximity of the roots of the teeth to the bottom of the maxillary sinus, a decrease in the body's defense reactions.
Clinical picture of odontogenic sinusitis:
Acute pain in the area of the affected sinus, in the infraorbital, buccal regions or in the entire half of the face; feeling of heaviness, congestion of the corresponding half of the nose.
Irradiation of pain in the frontal, temporal, occipital region, teeth of the upper jaw.
Pain in the area of large and small molars, especially when biting.
Mucous, purulent discharge from the corresponding nasal passage.
General malaise, headaches, weakness, loss of appetite, impaired sense of smell up to complete loss.
Pain on palpation of the anterior wall of the maxillary sinus, percussion of the causative tooth, swelling in the buccal and infraorbital regions, regional lymph nodes on the side of the lesion are enlarged, painful.
The vestibule of the oral cavity is hyperemic, edematous.
In the nasal cavity on the corresponding side - swelling and hyperemia of the mucous membrane, an increase in the middle or lower shell, discharge from the nasal passage.
Treatment acute odontogenic sinusitis: elimination of the periapical inflammatory focus, which was the cause of the disease. A puncture is performed with washing and the introduction of antibiotics, enzymes into the sinus, washing it through the dental alveolus. In the nasal cavity - vasoconstrictors for anemizing the mucous membrane and creating an outflow from the sinus through the nasal passages. Physiotherapy procedures: UHF, fluctuorization, diathermy, helium-neon laser.
General treatment consists of prescriptions of analgin, acetylsalicylic acid; desensitizing agents: diphenhydramine, suprastin, diazolin. Assign a course of treatment with sulfonamides, antibiotics, restorative and stimulating therapy.
Periomandibular ascesses and phlegmon are observed relatively often - in 20-30% of patients admitted to the PCLH hospital.
An abscess is a limited focus of purulent inflammation, leading to the melting of a piece of fiber or other tissue with the formation of a cavity.
Phlegmon is an acute diffuse purulent inflammation of the subcutaneous, intermuscular and interfascial tissue.
Sources of infection in abscesses and phlegmon of the maxillofacial region can be of odontogenic and non-odontogenic nature. More often, the entrance gates of infection are defects in the hard and soft tissues of the tooth and the marginal periodontium. Therefore, such abscesses and phlegmons are called odontogenic. If abscesses and phlegmons accompany odontogenic osteomyelitis and complicate its course, then they are called osteogenic or osteophlegmons. Abscesses and phlegmon resulting from infection of damaged skin face or oral mucosa, as well as complications of diseases such as furunculosis, sialadenitis, ulcerative stomatitis and others, are non-odontogenic.
It is customary to distinguish: abscess and phlegmon of the infraorbital region; abscess and phlegmon of the zygomatic region; abscess and phlegmon of the orbit; abscess and phlegmon of the buccal region; abscess and phlegmon of the infratemporal and pterygopalatine fossae; abscess and phlegmon of the temporal region; abscess and phlegmon of the parotid-masticatory region; abscess and phlegmon of the posterior maxillary region; abscess and phlegmon of the pterygomaxillary space; abscess of the maxillary-lingual groove; abscess and phlegmon of the peripharyngeal space; abscess and phlegmon of the chin area; abscess and phlegmon of the submandibular region; phlegmon of the bottom of the mouth; putrefactive-necrotic phlegmon of the floor of the mouth (anaerobic infection); abscess and phlegmon of the tongue; abscess of the hard palate.
Abscesses and phlegmons of the maxillofacial region are manifested by a number of general disorders, symptoms of purulent-resorptive fever, as well as local changes, largely due to the localization of the focus of purulent inflammation. The disease often begins suddenly. The phenomena of inflammation are growing rapidly. As a result of intoxication of the body, a headache appears, sleep, appetite are disturbed, and body temperature rises. In severe cases, chills occur, the general condition worsens sharply. In the peripheral blood, leukocytosis, neutrophilia are determined. C-reactive protein is detected in blood serum. Developing phlegmon is characterized by a diffuse painful infiltrate, covered from above with hyperemic skin or mucous membrane. With the further development of the inflammatory process, the infiltrate increases, in its central sections tissue melting appears - fluctuation. With deeply located abscesses, these local signs are less pronounced.
Most phlegmons are characterized by pain, impaired mobility of the lower jaw, increased salivation, difficulty in chewing, swallowing, speech and breathing. When the masticatory muscles are involved in the process, reduction occurs - contracture of the jaws. Manifestations of the disease depend on the localization of phlegmon in one, two, three or more cellular spaces.
Diagnosis is based on the data of anamnesis and objective examination. With a superficial location of purulent foci, the determination of the latter does not cause difficulties, while the recognition of deep abscesses often requires a diagnostic puncture. Abscesses and phlegmon of the maxillofacial region must be differentiated from the furuncle and carbuncle of the face in the initial stage of the disease; erysipelas; acute inflammation of the parotid and submandibular salivary glands; festering median and lateral cysts of the neck; specific chronic inflammatory processes; tumor formations.
With abscesses and phlegmon of the maxillofacial region, complex treatment. It includes surgical intervention (surgical treatment of the infectious and inflammatory focus in order to ensure the evacuation of pus and cleansing the purulent wound); antibacterial, desensitizing, detoxifying, immunocorrective, restorative therapy; physiotherapy (UHF, microwave currents). After subsiding of acute inflammatory phenomena and resorption of infiltrates, physiotherapy exercises are prescribed.