




































Art of Medicine           Volume-1 

International Medical Scientific Journal       Issue-2 
10.5281/zenodo.5517719 

103 

    



Art of Medicine           Volume-1 

International Medical Scientific Journal       Issue-2 
10.5281/zenodo.5517719 

104 

 

Art of Medicine International Medical Scientific journal 

 

Founder and Publisher Pascual Izquierdo-Egea 

Published science may 2021 year. Issued Quarterly. 
Internet address: http://artofmedicineimsj.us 

E-mail: info@artofmedicineimsj.us 

11931 Barlow Pl Philadelphia, PA 19116, USA +1 (929) 266-0862 

 

 
 
  



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FEATURES OF TRAUMATIC INJURIES OF THE ORAL MUCOSA: 

LITERATURE REVIEW 
 

Kamalova Mekhriniso Кilichevna
1
., Sharipova Gulnihol Idievna

2
. 

1
DSc., Associate Professor of the Department of Surgical Dentistry of the Abu Ali ibn Sina 

Bukhara State Medical Institute, Uzbekistan 

mexriniso.stomatolog@mail.ru 
2
independent candidate of the Department of Therapeutic Dentistry of the Bukhara State 

Medical Institute named after Abu Ali ibn Sina, Uzbekistan 

gulniholsharipova@mail.ru 

 

 Abstract Among the various pathological conditions of oral mucosa in 
children, traumatic injuries are quite widespread, which can be the result of 

mechanical, thermal, chemical, electrical and radiation exposure. Diagnosis of 

traumatic injury to oral mucosa in children is often difficult, due to the variety of 
their manifestations in the oral cavity and the similarity of the clinical picture of 

diseases of different etiology and pathogenesis.Knowledge of the etiology, 

pathogenesis, features of the clinical course, the possibilities of prevention and 

adequate treatment is necessary for a dentist to carry out timely diagnosis and provide 
qualified assistance to children with traumatic injuries of the oral mucosa. 

 Keywords: traumatic lesions, young children, inflammation, oral mucosa, 

prevention, diagnostics, treatment. 
 

 Relevance. Depending on the origin, traumatic lesions of the oral mucosa 

(OOM) are usually divided into mechanical, chemical, physical, electrical, and 

radiation. Trauma can be acute (single exposure to a damaging factor) and chronic - 
with prolonged exposure to a stimulus of insignificant strength [2, 12]. 

 Starting to study specific sections, the student should know the following 

basic general provisions: 
• Traumatic lesions of the mucous membrane as a result of the action of various 

factors (mechanical, physical, chemical) occur if the intensity of their influence 

exceeds the physiological margin of safety of the mucous membrane (RM). 

• The degree of damage and clinical manifestations depend on the nature of the 
stimulus, time, strength of its impact, localization, individual characteristics, general 

condition of the body and the age of the patient. 

• The mucous membrane of the oral cavity has high protective and regenerative 
abilities. 

• Traumatic damage to the oral cavity is quickly accompanied by its infection. 

 Mechanical traum. Acute mechanical trauma (trauma mechanicaacuta) 

Etiology: Acute mechanical trauma CO (usually household, transport, sports) occurs 
accidentally when biting, hitting or injured by various objects. Most often, CO of the 

tongue, lips and cheeks along the line of closing of the teeth suffers. 

mailto:mexriniso.stomatolog@mail.ru
mailto:gulniholsharipova@mail.ru


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 Clinic: Clinically, it can proceed without violation of the integrity of the CO 

(edema, hyperemia, hemorrhage) or in violation (erosion, excoriation, ulcer), which 
determines the severity of the course of the disease. First, pain appears, and at the site 

of contact, a hematoma, excoriation, erosion or ulcer may form [3, 11]. Often their 

size, shape and localization on the SO coincide with those of the traumatic agent. 
Hematomas and superficial injuries (excoriation, erosion) disappear relatively quickly 

(within 1-3 days). In case of secondary infection, erosion can turn into a long-term 

non-healing ulcer. The base of the ulcer on palpation is painful, infiltrated. 

 Diagnostics: As a rule, it is not difficult, the cause is easily identified after 
taking anamnesis, and an objective examination allows you to establish the 

localization and depth of damage to the tissues of the oral cavity. 

Treatment: 

  In case of severe pain, apply, irrigate or rinse 0.5 - 1% solution of novocaine, 
0.5 - 1% solution of lidocaine, if necessary, stop bleeding using 0.5 - 1% solution of 

hydrogen peroxide , 5% solution of aminocaproic acid. For deep wounds, surgical 

treatment - stitches. It is enough to treat shallow lesions with ordinary non-irritating 
warm antiseptic agents (0.5% solution of chlorhexidinebigluconate, 0.2% solution of 

furacilin, 0.5% solution of etonium, 1% solution of  Dimexidum, 1% solution of 

hydrogen peroxide, etc.)and prescribe rinsing the mouth with artificial lysozyme, 

potassium permanganate solution, and in the presence of erosion - add applications 
with keratoplastic agents (colanchoe juice, aloe juice, "Ektericid", oil solution of 

vitamins A, E and etc.) [7, 22]. 

 If the wound is already covered with plaque, there is an infiltration, then its 
course is delayed. For treatment, application of solutions of proteolytic enzymes 

(solution of trypsin or chymopsin) is used for 8-10 minutes, after which necrotic 

tissue or fibrinous plaque is removed mechanically, and the ulcer or erosion is treated 

with antiseptics.With the advent of pure granulations, drugs are used that improve the 
reparative properties of tissues (Solcoseryl dental adhesive paste) and keratoplastic 

agents. It is necessary to examine the dentition and, in order to prevent chronic 

trauma, to treat caries and its complications, restoring the anatomical shape of the 
crown of the affected tooth or polishing its sharp edge [1, 9, 18]. 

 Chronic mechanical trauma (trauma mechanicachronica. Etiology and 

pathogenesis: It occurs quite often, especially among the elderly who use plate 

prostheses. The plate prosthesis transmits chewing pressure not only to the teeth, but 
also to CO, delays the self-cleaning of the oral cavity, which leads to a violation of 

the established balance between different types of microorganisms, and changes the 

analyzing function of CO receptors.These changes are often the starting point for the 
development of CO pathology and neurostomatological diseases or exacerbation of 

chronic foci that were in remission. Chronic mechanical trauma is caused by sharp 

edges of the teeth when they are damaged by caries or pathological abrasion, in the 

absence of teeth and malocclusion, poorly manufactured or worn out orthopedic 
structures, orthodontic appliances, dental calculi, bad habits, etc [10]. 

 Chronic mechanical trauma is observed more often in the elderly due to a 

decrease in the height of the bite, dysfunction of the temporomandibular joint, the 



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presence of terminal defects in the dentition, periodontitis of the II-III degree, a 

decrease in mucosal turgor, and a slowdown in the processes of epithelial 
regeneration. Thus, a long-term traumatic factor triggers and maintains a chronic 

focus of inflammation with the formationcongestive hyperemia, edema, at the site of 

which erosion may occur, and then an ulcer, which is called decubital, or traumatic. 
With a prolonged course, the edges and base of the ulcer become denser, its depth is 

different up to the muscle layer, malignancy is possible [19]. 

 Clinic: The presence of a chronic traumatic lesion of the oral mucosa without 

violating its integrity (edema, hyperemia, hemorrhage) may not disturb the patient, 
but in the presence of an ulcermost of them complain of a burning sensation, 

swelling, discomfort, soreness in a certain place, aggravated by eating and talking. 

The clinical course in older people is more severe than in young people. Such an 

ulcer is localized more often on the tongue, on the lips, cheeks along the line of 
closing the teeth, as well as within the prosthetic field. As a rule, it is solitary, painful, 

surrounded by an inflammatory infiltrate, its bottom is covered with fibrinous bloom. 

Regional lymph nodes are enlarged, painful on palpation, mobile. Inflammation can 
be focal and diffuse. It is accompanied by edema and hyperemia of CO, against the 

background of which hemorrhages, erosion and hyperplasia of CO in the form of 

granularity are possible, which is a prognostically unfavorable sign. In addition, at the 

site of injury to the CO by the edge of the prosthesis along the transitional fold, a 
proliferative process and the development of lobular fibroma, which has the form of 

several folds, may occur,parallel to the edge of the prosthesis, and with a poorly fitted 

prosthetic bed on the upper jaw, papillomatosisof the palate occurs. With the habit of 
biting or sucking lips, tongue, cheeks, the CO (mainly along the line of closing the 

teeth) takes on a peculiar appearance: it swells, has a white macerated surface in the 

form of spots or large indistinctly limited areas or a fringed appearance (as if eaten by 

a moth) due to many small shreds of unevenly eaten epithelium. The lesion has an 
asymptomatic course, but with deep biting, erosions are formed, painful when 

exposed to chemical stimuli. Synonyms: "mild leukoplakia", "cheek biting".  

 Differential diagnosis: Chronic trauma due to the habit of biting CO should 
be differentiated from candidiasis (absence of fungi of the genus Candida at 

microscopic examination), white cancellous nevus of Cannon, which manifests itself 

from early childhood and progresses over the years: CO of the cheeks looks 

thickened, with deep folds, spongy. Stopping CO biting leads to spontaneous 
recovery [4, 20]. Chronic traumatic ulcer of OOPR should be distinguished from 

cancerous ulcer, trophic ulcer, tuberculous ulcer, hard chancre. 

 Traumatic ulcers are characterized by the presence of an irritating factor, the 
presence of a painful infiltrate, and the absence of specific changes in cytological 

examination. Elimination of the traumatic factor, as a rule, leads to the healing of the 

ulcer in 5 to 6 days. 

With prolonged existence of an ulcer, its base and edges can become denser 
("infiltrative shaft") due to chronic inflammation; CO around the ulcer is edematous, 

hyperemic, the bottom of the ulcer becomes bumpy, covered with a bloom [15]. 

Soreness persists on palpation of the ulcer. Lymph nodes are enlarged, painful, 



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mobile. Long-termnon-healing ulcers can become infected with fusospirochetes, 

Candida, and also become malignant [8]. 
 A cancerous ulcer differs from a traumatic one by a greater density of edges 

and bases, by the presence of growth along the edges (in the form of cauliflower) and 

sometimes by their keratinization. After elimination of the irritant, healing does not 
occur. Cytological or histological examination of cancerous ulcers reveals atypical 

cells. Lymph nodes are painless on palpation, soldered in the form of conglomerates, 

motionless. 

 Tuberculous ulcers are characterized by soreness, soft, undermined 
"creeping" edges, their bottom is granular (Treel's grains are microabscesses), 

yellowish. They are not epithelized after removal of the stimulus. In a cytological 

study, epithelioid cells and giant cells of Pirogov-Langhans are found, in a 

bacterioscopic study - mycobacterium tuberculosis (Koch's bacillus). 
 A hard chancre differs from a traumatic ulcer by the presence of a dense 

cartilaginous infiltrate that surrounds the ulcer, with smooth edges, a smooth meat-

red bottom with a "greasy" coating, painless on palpation. The surrounding chancre is 
unchanged. Regional lymph nodes are enlarged, painless, indurated (scleroadenitis) 

[14, 16]. The diagnosis is clarified by the detection of pale treponema in the 

discharge of the ulcer. The Wasserman reaction (as well as RIF, and later RIBT) 

becomes positive 3 weeks after the onset of a hard chancre. 
 A trophic ulcer differs from a traumatic one by a longer existence, a sluggish 

course, mild signs of inflammation, the presence of general diseases in the patient 

(most often - of the cardiovascular system). Elimination of the alleged traumatic 
factor does not cause the ulcer to heal [2, 12]. 

 Treatment: provides for the mandatory elimination of the traumatic agent, 

treatment of the oral cavity and ulcers with antiseptic solutions, pain relief. If necrotic 

tissues are present, they are removed mechanically under anesthesia or with the help 
of proteolytic enzymes. Pure erosion and ulcers are treated with keratoplastic 

preparations ("Regenkur", "Dibunol", "Sanguirithrin", rosehip oil, sea buckthorn oil, 

vitamin A oil solution, kolanchoe juice,"Solcoseryl", "Olazol", "Hyposol-N", etc.). 
Treatment of the lobular form is surgical. The basis for suspicion of malignancy of 

traumatic injury are traumatic ulcers with infiltration at the base, which do not heal 

within 2 - 3 weeks after elimination of the causative factor. Prevention of traumatic 

injuries consists in the elimination of irritating factors in the oral cavity and its timely 
sanitation. 

 Chemical trauma (trauma chymica. Chemical damage occurs when 

chemicals come into contact with OCPR. It can be acute or chronic. Acute chemical 
damage occurs when high concentrations of chemicals enter the OCP. Most often this 

happens when they are mistakenly used in everyday life, at work, when attempting 

suicide, during an appointment with the dentist. OCD burns can occur upon contact 

with acids,alkalis, the use of arsenic paste, phenol, formalin, formalin-resorcinol 
mixture, silver nitrate. The clinical picture of the lesion (hyperemia, edema, erosion, 

necrosis, ulcer) depends on the nature of the chemical, its amount, concentration and 

duration of action, the structure of CO in the contact area. 



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 A burn with acids leads to the appearance of coagulation necrosis - a dense 

brown film - from sulfuric acid, yellow - from nitric acid, gray-white - from other 
acids. The phenomena of inflammation with edema and hyperemia are expressed near 

the film. 

 A burn with alkalis leads to colliquation necrosis of the OAS without the 
formation of a dense film, the process spreads over the surface and into the depths. 

From the action of alkalis, the lesion is deeper than with acid burns, and captures all 

layers of the OAS. After rejection of necrotic tissue, very painful erosive or ulcerative 

surfaces are exposed, which heal very slowly. 
 Treatment. It is necessary to quickly remove the damaging chemical and 

rinse the mouth with a weak solution of a neutralizing agent. For acid burns, soapy 

water, 1% lime water, burnt magnesia, 0.1% ammonia solution (15 drops per glass of 

water) are used. Alkalis are neutralized with a 0.5% solution of acetic or citric acid, 
as well as with a solution of hydrochloric acid (10 drops per glass of water) and 

thereby stop the further penetration of the chemical into the tissues.To reduce the 

absorption of concentrated solutions of silver nitrate, a 2 - 3% solution of sodium 
chloride or Lugol's solution is used, while insoluble silver compounds are formed. 

When affected by phenol, CO is treated with castor oil or 50% ethyl alcohol. Further 

treatment of patients with chemical burns of OOPR is carried out according to the 

example of treatment of an acute nonspecific inflammatory process: pain relievers are 
prescribed, weak solutions of antiseptic agents in the form of oral baths, rinses, drugs 

that accelerate epithelization (1% citral solution in peach oil, methyluracil ointment, 

vitamins A and E , "Tsigerol", "Hyposol-N") [10, 11, 13, 18]. 
 Physical trauma (trauma physica. The most common injuries of the OSR 

caused by physical factors are thermal (effects of high and low temperatures), electric 

shock (burns, electrochemical - galvanosis) and radiation injuries (with the localized 

effect of large doses of ionizing radiation). 
 CO burns can be caused by hot food, steam, hot objects, fire, hot air. Under 

the influence of hot water or steam, acute catarrhal stomatitis develops, which is 

accompanied by pain. CO is getting dramaticallyhyperemic, maceration of the 
epithelium is noted. With a severe burn, the epithelium sloughs off in thick layers or 

bubbles appear, in the place of which extensive superficial erosion or ulcers form. 

The accession of a secondary infection and the action of local irritating factors 

complicates the course and slows down the epithelialization of the affected areas 
[17]. 

 Treatment. The area of the CO burn should be anesthetized with local 

anesthetics, antiseptic treatment should be carried out, enveloping and anti-
inflammatory drugs should be prescribed along with antimicrobial agents. In the 

dehydration phase, keratoplastic agents are used [14]. 

 With the effect of low and ultra-low temperatures on the OSR, the doctor 

meets mainly during cryotherapy of various lesions of the CO and periodontal. In this 
case, a sharp acute catarrhal inflammation immediately occurs in the focus of 

cryotherapy - a bubble,which after 1 - 2 days passes into necrosis. In the 

postoperative period, in the first hours after cryodestruction, oral baths or rinsing with 



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antiseptic agents are prescribed, and with the development of necrosis, therapy is 

carried out as in ulcerative necrotizing stomatitis [6]. 
 CO electrical injury is often associated with electrotherapy (galvanization, 

electrophoresis) or the development of galvanism in the oral cavity. A galvanic burn 

is formed at the site of contact of the active electrode with CO in violation of the 
electrophoresis technique. Clinically defined continuous painful erosion, surrounded 

by reactive inflammation of adjacent tissues, accompanied by a painful reaction of 

regional lymph nodes [2, 13]. 

 Galvanism is the occurrence of registered electrochemical potentials in the 
oral cavity in the presence of heterogeneous metal inclusions, without pronounced 

subjective and objective signs (this is a phenomenon) [21]. The presence of dissimilar 

metal inclusions contributes to the occurrence of electrochemical reactions, the 

accumulation of electromotive force at the interface between the metal and the oral 
fluid, which ensures the emergence of galvanic pairs. 

 According to T.E. Nikitina, the value of the electrochemical potential (ECP / 

microvolt) 120 -140 µV is the conditional rate of electric current, over 140 µm is the 
risk of developing galvanosis and its complications. The significant content of metals 

in the oral fluid determines their accumulation in CO, soft tissues of the oral cavity, 

jaw bones and their constant entry into the gastrointestinal tract, which leads to their 

spread throughout the body and the emergence of sensitization to metals, metabolic 
disorders, and chronic diseases [1]. 

 Galvanosis - pathological changes of a local and general nature that arise as a 

result of electrochemical interaction between metal inclusions in the oral cavity (this 
is a symptom complex). 

 Galvanosis contributes to the development of glossalgia, leukoplakia, lichen 

planus, and is also an aggravating factor in the already existing pathology of oral 

mucosa and can lead to microbial imbalance and the development of oral candidiasis. 
 Clinical picture: Clinical manifestations of galvanosis of OCPD depend on 

current strength, time of its influence and individual tissue sensitivity. With 

galvanosis, patients complain of a metallic taste in the mouth, perversion of taste 
sensitivity, burning or tingling sensation, pain in the tongue, cheeks, dryness or 

hypersalivation, slight irritability, headache, weakness. 

 Galvanic currents can cause hyperkeratosis or burns that occur on the tip, 

lateral and lower surfaces of the tongue, much less often on the cheeks, lips, palate. 
Clinically manifested by catarrhal or erosive-ulcerative lesions. With catarrhal 

lesions, bright hyperemia, edema and burning sensation occur. The foci of 

inflammation are clearly demarcated from the unchanged surface of the oral mucosa 
[6]. The erosive-ulcerative form is rare, characterized by focal or diffuse 

inflammation of CO with the formation of single or multiple erosions (sometimes 

ulcers or blisters), covered with a whitish-gray coating. 

 Diagnostics. To establish a diagnosis of galvanosis, at least 5 criteria must be 
met: 

1) the presence of a metallic taste in the mouth; 



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2) subjective symptoms, more pronounced in the morning and persisting 

throughout the day; 
3) the presence of two or more metal inclusions in the oral cavity; 

4) determination of the potential difference between metallic 

inclusions(registration); 
5) improvement of the patient's well-being after removal of prostheses from the 

oral cavity. 

 To detect galvanic phenomena in the oral cavity, the Lira-100 device is used. 

 Treatment. Etiotropic therapy of CO galvanosis is reduced to the removal of 
prostheses and fillings from heterogeneous metals from the oral cavity. In addition, 

protease inhibitors are used in the early stages of catarrhal oral mucosa lesions, anti-

inflammatory and antiseptic agents. The lesion is treated with 5% Unithiol solution. 

Galvanic burns, which occur with erosions, ulcers, blisters and are accompanied by 
severe pain, are treated with antiseptic agents together with local anesthetics (4-10% 

anesthesin oil solution, 10% alcoholic propolis solution with glycerin (1: 1), 20-40% 

solution DMSO). In the first phase of the wound process, it is advisable the use of 
nitacid, which has a high osmotic activity and a wide range of antimicrobial action. 

Anesthetic and anti-inflammatory effect has a tincture of plantain, green tea, nettle 

leaves. To improve the epithelialization of the affected areas, use "Hyposol-N", 

"Solcoseryl" (ointment, jelly), "Erbisol", "Spedian" liniment, "Vinilin", anti-burn 
liquid, etc. The drugs of choice are the following drugs (Barer G.M.) [11, 14, 21]. 

 For application anesthesi. Benzocaine / glycerin topically 5/20 g before each 

meal, until clinical improvement or Lidocaine, 2.5-5% ointment or 10% aerosol, 
topically before each meal, until clinical improvement. 

 For the treatment of the oral cavity and elements of mucosal lesions and 

preventing their infection Hydrogen peroxide, 1% solution, topically 1 - 2 times or 

Potassium permanganate, 0.02% solution, topically 1 - 2 times or 
Chlorhexidinebigluconate, 0.06% solution, topically 1 - 2 times or Ethacridine 

lactate, 0.05% solution, topically 1 - 2 times. For cleaning the surface of erosions and 

ulcers Trypsin 5 mg (in isotonic sodium chloride solution, 5.0 ml) topically 1 - 2 r / 
day.or Chymotrypsin 5 mg (in isotonic sodium chloride solution, 5.0 ml) topically 1 - 

2 r / day. If necessary, correction of the psychoemotional sphere (for example, with 

buccal biting) Vitamin B 1 20 - 30 mg. per day inside or 6% solution in / m 1 time 

per day. 1 - 2 ml., 10 days. Vitamin B 12 / m 1 - 2 ml. 1 time per day, 10 days. 
Valerian rhizomes extract inside 1 tablet 1 - 2 r / day, long-term or Glycine 

sublingual 0.1 g 2 - 3 r / day, long-term "Diazepam" inside 5 - 15 mg 1 - 2 r / day, 4 

weeks.or "Medazepam" inside 10 mg 2 - 3 r / day., 4 weeks. 
To accelerate the healing of affected areas Sea buckthorn oil topically on a cleansed 

area of the affected mucous membrane 1 - 3 r / day, until clinical improvement or 

"Solcoseryl" ointment or dental adhesive paste, topically on a cleansed area of the 

affected mucous membrane 1 - 3 r / day, until clinical improvement or Rosehip oil 
topically on the cleaned area of the affected mucous membrane 1 - 3 r / day, until 

clinical improvement. 



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 As an anti-inflammatory, immunostimulating agent that improves tissue 

trophism Retinol acetate oil solution, topically on the affected areas 5 - 6 times per 
day, until clinical improvement. As an active antioxidant to stimulate protein 

synthesis, reduce capillary permeability Vitamin E, solution, topically on the affected 

areas 5 - 6 r / day, until clinical improvement. 
 In order to regulate redox processes, stimulate tissue regeneration, activate 

phagocytosis and antibody synthesis Ascorbic acid inside 50 - 100 mg 3 - 5 r / day or 

5% solution in / m 1 ml 1 r / day, 20 - 40 days. In order to normalize the metabolism 

of fatty acids, stimulate the formation of acetylcholine, steroid hormones, utilize 
amino acid deamination products 

 Calcium pantothenate inside 0.1 g 2 - 4 r / day or 5% solution locally in the 

form of applications for long-term non-healing erosion 2 - 4 r / day or 10% ppi / m 2 

ml 1 - 2 r / day, 20 - 40 days To activate the processes of hematopoiesis and 
maturation of erythrocytes, tissue regeneration Cyanocobalamin inside 0.00005 g 1 r / 

day, 20 - 40 days. Folic acid inside 0.0008 g 1 r / day, 20 - 40 days. In order to 

regulate tissue respiration, metabolic processes Riboflavin inside 0.005 - 0.01 g 1 r / 
day, 20 - 40 days In order to normalize metabolic processes and peripheral blood 

supply Nicotinic acid orally after meals 0.025 - 0.05 g 3 r / day, 20 - 40 days.or 1% 

solution i / v, i / m or under the lesion 1 ml 1 r / day, 10 - 15 days. 

 Radiation injury. Radiation injury is a lesion of the oral mucosa that most 
often occurs during radiation therapy of neoplasms of the maxillofacial region. When 

carrying out radiation therapy of neoplasms of the maxillofacial region, unaffected 

areas of the oral mucosa are also exposed to radiation. The response of different areas 
of the OAS to irradiation is not the same and has some clinical features depending on 

the type of radiation therapy, single and total radiation dose, tissue radiosensitivity 

and the state of the oral cavity up to irradiation. The first clinical signs of a violation 

of the OSS state appear in areas covered with non-keratinized epithelium (hyperemia, 
edema) and increase with increasing radiation dose. Then, due to increased 

keratinization, the OSS becomes cloudy, loses its luster, becomes denser, and 

becomes folded. With further irradiation, this keratinized epithelium is rejected in 
places, as a result of which erosions appear, covered with a sticky necrotic plaque 

(focal membranous radiomucositis). If the necrosis spreads to the adjacent areas, then 

the erosion merges and a drainage diffuse membranousradiomucositis occurs. 

 It is especially sensitive to CO irradiation of the soft palate: here radio-
mucositis immediately appears, without the keratinization phase. In the areas of the 

OAS, which are normally covered with keratinized epithelium, only focal 

desquamation of the epithelium or single erosions occur. Further development of the 
process is complicated by damage to the salivary glands, the epithelium of which is 

very sensitive to radiation. In the first 3 - 5 days, salivation can be increased, and then 

persistent hyposalivation quickly sets in. After 12 - 14 days, xerostomia develops, 

which is accompanied by dysphagia, perversion andloss of taste. Later, hyperemia of 
the tip and lateral surfaces of the tongue and atrophy of its papillae appear. Radiation 

changes in the oral cavity are largely reversible. After the termination of the 

irradiation, the OSR in 2 - 3 weeks returns to the relative norm. However, with a 



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large absorbed dose (5000 - 6000 rad), irreversible changes in the salivary glands and 

OSS (hyperemia, atrophy, radiation ulcers) may occur [1, 15]. 
 In the prevention of radiation injuries, the rehabilitation of the oral cavity is 

of great importance. It should be carried out in the following sequence: 

1) Removal of mobile and decayed teeth with chronic lesions in the 
periodontium, followed by suturing - no later than 3 - 5 days before the start of 

radiation therapy. 

2) Removal of supra- and subgingival calculus, curettage of periodontal pockets. 

3) Filling of all carious cavities. In this case, metal prostheses and amalgam 
fillings must be removed or made on the dentition rubber or plastic protective caps 

with a thickness of 2 - 3 mm and applied directlybefore a radiation therapy session.  

Instead of mouth guards, you can use tampons soaked in vaseline oil or 

novocaine. 10-30 minutes before irradiation, a cystamine hydrochloride 
radioprotector 0.2-0.8 g or mexamine 0.05 g orally for 30-40 minutes is prescribed. 

before irradiation. Immediately before irradiation, the OSS is irrigated with an 

adrenaline solution in isotonic sodium chloride solution (2: 100) or adrenaline is 
injected under the skin, and the OSS is treated with prednisone. At the initial 

manifestations of the radiation reaction, the OSS and gums are treated 4 - 5 times a 

day with weak solutions of antiseptics. 

 In the midst of a radiation reaction, a 1% solution of novocaine or trimecaine, 
a 1% solution of dicaine, a 10% oil emulsion of anestezin are used to anesthetize 

OSS, periodontal pockets are washed with a warm solution of antiseptic agents, 

enzymes are applied with antibiotics, and then OSS is treated with drugs such as 
Hyposol -N "," Sanguirithrin ", rosehip or sea buckthorn oil. At this time, the removal 

of teeth, tartar and curettage of periodontal pockets are contraindicated. Therapy of 

post-radiation reactions and complications is aimed at increasing the body's 

resistance, a decrease in tissue permeability, as well as the elimination of factors that 
negatively affect the OSR. Prescribe "Splenin", sodium nucleinate, batiol, rutin, 

nicotinic acid, vitamin B6, B12, "Aevit", calcium preparations, "Galascorbin". 

Relative normalization of the oral mucosa occurs in 2 - 3 months. 
 Radiation sickness. Radiation sickness is a disease that develops as a result of 

exposure to the body of ionizing radiation. Distinguish between acute and chronic 

forms of radiation sickness.  Acute radiation sickness (ARS) develops from a 

short-term (from several minutes to 1 - 3 days) exposure to the body - γ - rays and a 
neutron flux in doses exceeding 1 Gy (gray), and is characterized by a phasic flow 

and polymorphism of the clinical picture. In the ARS clinic, bone marrow (1 - 10 

Gy), intestinal (10 - 20 Gy), toxemic (20 - 80 Gy), cerebral (80 Gy) forms are 
distinguished. When irradiation is less than 1 Gy, one speaks of radiation injury. 

Ionizing radiation causes metabolic changes in stem cells, lymphocytes, small 

intestinal epithelium, etc. 

 There are five periods during the course of the disease: 
1) the period of the primary reaction to radiation; 

2) the latent period, or the period of imaginary well-being; 

3) the period of pronounced clinical manifestations or peak; 



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4) the period of the permit; 

5) the period of late complications and consequences of the lesion. 
 Clinic First period: general weakness, dizziness, headache, drowsiness, 

nausea, vomiting, diarrhea, nosebleeds, fever, loss of consciousness, flushing of the 

skin, injection of the sclera. Dryness, metallic taste appears in the oral cavity, the 
sensitivity of the oral cavity decreases; it swells, hyperemia appears, punctate 

hemorrhages may occur. In the teeth, no visible clinical changes are observed, 

however, already at this stage, inhibition of phosphorus-calcium metabolism occurs, 

which in the III period develops into structural and morphological changes. In the 
blood, neutrophilic leukocytosis, reticulocytosis, lymphopenia are found. The 

duration of the period of the primary reaction is up to 2 days. 

 The second period begins on the 3rd day after irradiation and lasts 2-4 weeks. 

It is characterized by a relative improvement in general condition. There are no 
changes in the oral cavity, but the number of leukocytes and lymphocytes continues 

to fall, and the inhibition of hematopoiesis is noted. 

 The third period is observed from 7 to 12 days after irradiation and lasts 3 to 
4 weeks. It is characterized by a severe general condition caused by hematological, 

gastrointestinal disorders, increased bleeding, fever, and multiple complications. 

Inhibition of hematopoiesis progresses. 

 In the oral cavity, there is a pronounced hemorrhagic syndrome. Necrotizing 
ulcerative gingivitis and stomatitis gradually develop. The mucous membrane of the 

lips, cheeks and tongue is covered with a whitish, viscous mucus. In severe cases, 

necrosis can spread with CO to the underlying soft tissues and bone, leading to 
sequestration and possible fractures of the jaws. Tonsils are covered with a dirty gray, 

hard-to-remove plaque, under which a bleeding surface opens. Swallowing food is 

almost impossible due to severe pain. A putrid odor comes from the mouth. Regional 

lymph nodes are enlarged and painful on palpation [2, 12]. 
 The fourth period begins on the 4th week after irradiation and lasts 1 - 3 

months. It is characterized by the slow reversal of disease symptoms. 

The fifth period begins from 5 - 6 weeks after exposure and lasts 3 or more months. It 
is characterized by residual ARS in the form of long-term hematopoietic disorders 

(leukopenia, thrombopenia, erythropenia). Transitions to leukemia (myelosis, 

reticuloendotheliosis) and various somatic pathologies in the oral cavity are possible. 

Changes in the hard tissues of the teeth are noted - chipped, as if pitted edges of the 
enamel, pathological abrasion. All this is combined with many cavities,localized 

mainly in the cervical region and on the approximal surfaces.  

 There is circular caries, clouding of the enamel and the appearance of dark 
spots on it. Areas of enamel demineralization are noted, dentin is easily removed in 

layers using an excavator. Generalized periodontitis of the I-III degree, oral 

dysbiosis, xerostomia, areas of hyperkeratosis, cyanoticity develop. The tongue is 

increased in size. Neurostomatological symptoms appear: intermittent tingling 
sensation, creeping creeps, burning sensation and intense pain in the oral cavity, 

reminiscent of attacks of trigeminal neuralgia [5]. 



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 Chronic radiation sickness (CRS) occurs with prolonged external exposure to 

small doses of ionizing radiation, usually develops in people who, by the nature of 
their activities, encounter radioactive radiation (radiologists, etc.) and violate safety 

regulations. Allocate mild (I degree), medium (II degree) and severe (III degree 

CRS). 
 Clinic: the initial manifestation of CRS is changes in the nervous system, 

which have the character of neurosis with autonomic disorders. 

In the future, disorders of neurogenic regulation, the cardiovascular system and the 

development of hemorrhagic syndrome join. In addition, there are dysfunctions of the 
gastrointestinal tract, liver, metabolism and the endocrine system. In the oral cavity, 

CRS manifests itself in grade III in the form of persistent gingivitis, bleeding gums, 

glossalgia and glossitis [21]. 

 CRS diagnosis is complex and is based on the study of peripheral blood and 
bone marrow. 

 Treatment ARS requires physical and mental rest, high-calorie food, plenty 

of fluids, sedatives, antiemetics, detoxification, antihemorrhagic drugs, plasma 
substitutes. Dairy and lactic acid products are recommended. Prevention of 

inflammation of the oral mucosa is aimed at increasing the body's resistance and 

eliminating factors that have a negative effect on CO (traumatic factors, infection.). 

Removal of teeth and tartar, curettage of periodontal pockets, use of cauterizing 
agents are contraindicated. It is advisable to prescribe ascorutin, nicotinic acid, 

"Aevita", vitamins B6, B12, calcium preparations. Recommended processingoral 

cavity with weak antiseptic solutions. To increase local immunity in the oral cavity, 
rinse with artificial lysozyme, "Immudon", is prescribed. For anesthesia, 1% solution 

of trimecaine, 2% solution of lidocaine, 10% suspension of anestezin in oil, oil 

solution of propolis, 1% solution of sodium mefenaminate are used. Shown are the 

applications of enzymes - trypsin, chymotrypsin (10 ml of 0.25% novocaine + 10 mg 
of the enzyme), as well as honsuride. On the treated surfaces, applications are made 

with anti-inflammatory and keratoplastic agents. Use pastes and periodontal dressings 

withantibiotics, glucocorticoids, sodium mefenaminate, prepared in rosehip oil and 
sea buckthorn oil, vitamins A and E. In the period of long-term consequences, a 

complete sanitation of the oral cavity is carried out. It is better to use glass ionomer 

cements. Movable and decayed teeth with chronic foci of infection at the apex are 

removed with subsequent suturing on the hole. Suturing of the hole is necessary due 
to increased bleeding and poor blood clotting. This must also be taken into account 

when removing dental plaque, especially subgingival calculus, periodontal surgery. 

 
  



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