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1. DENTAL DISEASES
(ODONTOGENIC , FUNGAL DISEASES)

2. DENTAL DISEASES
The nature disease damaged tissue disease
Non-inflammatory odontogenic infections hard tissues of the tooth Caries
Inflammatory odontogenic infections dental pulp
Periodontium
Periosteum
bone tissue
Soft tissues of the face and neck
Maxillary sinus
lymph nodes
Generalized infection
Pulpitis
Periodontitis
Periostitis
Osteomyelitis
Abscess, phlegmon
Sinusitis
Lymphadenitis
Sepsis
Inflammatory periodontal infections Periodontist
gum tissue
Periodontopathies
Gingivitis, pericoronitis
Inflammatory non-odontogenic infections mucous membrane
Major salivary glands
Skin and subcutaneous tissue
Stamotite
Mumps
Furuncle, carbuncle, erysipelas, abscess,
etc.

3. Odontogenic infections (OI) is a secondary infectious process , accompanied
by acute or chronic purulent-inflammatory diseases, caused by pathological
processes in the tissues of the tooth ( periodontium), due to incorrect or
untimely treatment of caries, pulpitis, periodontal disease, inflammation of the
bone tissue of the upper and lower jaws.
OI caused in most cases by microorganisms that are part of the usual biocenosis
of microbes of the skin of the face and oral mucosa, more often represented by
cocci;
- β-hemolytic streptococci
- peptostreptococci
- Staphylococcus aureus
- Fusobacteria .
Also bacteroids, actinomycetes, spirochetes, proteus, clostridia , candida can
be sown from the foci of infection . The microbial landscape in odontogenic
infections is usually mixed.

4. Odontogenic processes
Localized Common (progressive)
Pulpitis
Periodontitis
Alveolitis
Abscess
Phlegmon
Periostitis
Osteomyelitis
sepsis

5. Pathogenesis
 The development of an odontogenic infection is influenced by the virulence and the number of microorganisms
in the primary focus, as well as the state of the macroorganism . The spread of infectious pathogens from the
primary stomatogenic focus in most cases occurs by contact. Under certain conditions (a high degree of
pathogenicity, a decrease in local and general resistance), pathogens penetrate the lymphatic and bloodstream,
migrate throughout the body.
 In the area of the infectious focus in the oral cavity, conditions are created for the unhindered reproduction of
microorganisms (venous congestion, edema, tissue ischemia). Through the top of the tooth root, pathogens can
go beyond the focus through the intermuscular, subperiosteal , and cellular space. So there are odontogenic
periostitis, osteitis, sinusitis, osteomyelitis.
 In addition, microbial toxins cause an increase in vascular permeability, which, under conditions of good
vascularization , perimaxillary tissues facilitates the penetration of bacterial agents into the vascular bed. In this
way, perimaxillary abscesses and phlegmon are formed. Settling of microorganisms in the lymph nodes in
violation of the barrier function of the latter is accompanied by the development of regional lymphadenitis.

6. CARIES
Dental caries also known as tooth decay or a
cavity, caries is a biofilm dependent disease,
bacterial in origin, that causes demineralization and
destruction of the hard tissues of the teeth (enamel,
dentin and cementum).
It is a result of the production of acid by bacterial
fermentation of food debris accumulated on the
tooth surface. Bacteria that live in plaque produce
lactic acid, which demineralizes tooth hard tissues .
The most important in the pathogenesis of caries are
bacteria:
- acid formers - streptococci (the leading role
belongs to S. ( nutans ),
- lactobacilli ;
- proteolytic bacteria (Peptostreptococci , Bacteroids
and other asporogenic anaerobes).

7. INFLAMMATORY ODONTOGENIC INFECTIONS
 Pulpitis is an inflammation of the soft tissue
of the tooth (pulp), which is accompanied by
severe pain and can lead to tooth loss. It is
the most common consequence of caries. The
microflora usually corresponds to the nature
of pulpitis: with serous inflammation,
streptococci, lactobacilli, bacteroids are more
often found, with purulent - hemolytic
streptococcus and Staphylococcus aureus ;
with putrefactive - peptostreptococci ,
bacteroids, veillonella , protea, clostridia .

8. Periodontitis is a dental disease that affects the connective tissue between the bone of
the hole in which the tooth is located and the cementum of its root.
The main role in this process belongs to microorganisms that enter the periodontium
through the canal of the tooth from the inflamed pulp. Less commonly, they penetrate
between the wall of the alveolus and the root of the tooth (with periodontopathies ) or as
a result of hematogenous infection.
The microorganisms that cause this disease produce enzymes that destroy individual
components of the connective tissue ( hyaluronidase , neuraminidase, collagenase ) and
induce an inflammatory process.
Among the most common microbes, one can distinguish Staphylococcus aureus,
hemolytic and non- hemolytic streptococcus, spirochetes, fusobacteria , fungi.
In acute periodontitis, streptococci and spirochetes are often isolated, as they become
chronic anaerobes are the most important. In adults, periodontitis is dominated by gram-
negative anaerobes ( Porphyromonas gingivalis , Bacteroides forsythus , Prevotella
melaninogenica ), facultative anaerobes ( Actinobacillus actinomycetemcomitans ) and
treponema (T. denticola ).

9.  Periostitis and osteomyelitis of the jaw - inflammation, respectively, of the
periosteum and bone tissue; can be odontogenic or non- odontogenic (traumatic,
hematogenous).
The etiological moment of this disease is S. aureus, often streptococci, however,
anaerobic microflora prevails: peptococci (P. niger ), peptostreptococci , bacteroids.
In traumatic osteomyelitis, enterobacteria , S. aureus are more often found. and
Pseudomonas aeruginosa .
 Osteomyelitis of the jaw is an infectious purulent-necrotic process that develops
in the bone marrow, in all structural parts of the bone and its surrounding soft tissues.
It can be limited (within 2-3 teeth) and spilled (diffuse). It is often caused by pyogenic
Staphylococcus aureus.
 An abscess is a limited purulent-inflammatory process in the soft tissues of the
maxillofacial region. It can be caused by streptococci, staphylococci, pneumococci,
diplococci, Escherichia coli, fusobacteria and other anaerobic microorganisms.

10.  Phlegmon is a diffuse purulent-inflammatory process in the
soft tissues of the maxillofacial region (in the subcutaneous,
intermuscular, interfascial loose tissue).
 The direct cause of the purulent process in the vast majority of cases
are pathogenic microorganisms that penetrate into the cellular spaces
directly through a wound or abrasion, or through the lymphatic or
blood vessels. Most often, phlegmon develops under the influence of
Staphylococcus aureus, the second most common is streptococcus .
 The danger of the disease is determined by the proximity of the
brain, the visual analyzer, the initial section of the upper respiratory
tract and the digestive tract. The infection can spread along the
neurovascular bundles of the neck, pharynx, and esophagus into the
mediastinum.

11. Stomatitis is an inflammation of the oral mucosa .
There are: catarrhal ( superficial ); ulcerative gangrenous (deep)
in the development of catarrhal stomatitis as secondary etiological factors.
- with superficial stomatitis, staphylococci, neisseria, hemophilic bacteria,
opportunistic corynebacteria are detected
- with deep - fusobacteria and treponema Vincent , bacteroids, peptostreptococci ,
veillonella , actinomycetes (anaerobic microflora predominates).
In childhood, impetigious stomatitis is observed. The disease is characterized by
the appearance of superficial erosions on the mucous membrane of the lips,
cheeks, gums, hard palate and tongue, often merging together. Erosions are
covered with a yellowish-gray coating, when it is scraped off, bleeding occurs.
The gums, especially on the free edge, often ulcerate. Initially, streptococci
(usually Streptococcus pyogenes ) are isolated from the lesions , and staphylococci
( Staphylococcus aureus ) in later ones . Impetigo tends to spread purulent process
on the skin

12. Infectious diseases in humans caused by fungi are collectively
referred to as mycoses. Most fungal infections of the oral
mucosa are caused by saprophytic fungi, which are constantly
present in the composition of the resident microflora of this
biotope. With a decrease in the activity of immunobiological
resistance factors, metabolic disorders, or with irrational
antibiotic therapy, saprophytic fungi cause opportunistic
mycosis of the mucous membrane. Most fungal diseases of the
oral mucosa do not occur exogenously, but as a result of
autoinfection, which develops only when conditions unfavorable
for the body appear.
Mycoses

13. ORAL CANDIDIASIS IS an infectious disease caused by opportunistic yeast-like
fungi of the genus candida. It is often found in children (in the newborn and
infancy, at a young age) up to 10 years, as well as in the elderly (over 60), which is
associated with a decrease in immunity.
The disease is caused by yeast-like microorganisms of the genus candida , most
often candida albicans and candida tropicalis . Normally, they are present in the
human body constantly and do not harm in any way. however, under the influence
of certain factors, the fungi are activated, their concentration increases, which leads
to inflammation of the mucosa and the formation of a white cheesy plaque.

14. Yeast -like fungi are a combined group of conditionally
pathogenic microscopic fungi 6–10 µm in size that do not
have a typical mycelium and are capable of existing in the
form of single cells, pseudohyphae and hyphal forms .
do not belong to true dimorphic fungi, since both yeast cells
and hyphae can be detected in tissues. The transition to the
mycelial phase can be observed when cultivating at a lower
temperature (22-25 0 C) or when the nutrient medium is
depleted. The transition of the yeast phase to the mycelial
(mold) phase in vivo can be observed during germination in
body tissues.
 Etiology of candidiasis of the oral mucosa

15. - Acute pseudomembranous candidal stomatitis
- Acute erythematous candidal stomatitis
- Chronic hyperplastic candidal stomatitis ( candidal leukoplakia, multiple type
of chronic hyperplastic candidal stomatitis)
- Chronic atrophic candidal stomatitis (stomatitis under a removable denture
caused by candidal infection)
- Mucocutaneous candidiasis
- Candidal granuloma
- Angular cheilitis
- Other specified manifestations in the oral cavity
- Manifestations in the oral cavity, unspecified ( candidiasis stomatitis, thrush)
TYPES OF CANDIDIOSIS

16. It occurs more often in newborns (premature, with birth injuries) or in
adults with immunodeficiency. Initially, the mucosal patches become
darker and more lustrous (“lacquered mucosa”), then white or
yellowish creamy or “curdled” plaques appear on them, which can
coalesce to form large lesions (hence “thrush”). Plaques can be
localized on the tongue, soft and hard palate, gums, cheeks, tonsils,
pharynx. Plaques are easily removed, leaving bleeding erosion. With
the localization of lesions on the tongue, patients complain of a change
in taste sensations or an increase in sensitivity to spicy or hot food. The
lesion is often associated with diffuse erythema and increased dryness
of the mucous membrane. In severe immunodeficiencies, almost the
entire mucous membrane of the oral cavity, tonsils, pharynx,
esophagus, stomach, bronchi and lungs are affected.
Pseudomembranous candidiasis (thrush)

17. It develops as a result of wearing prostheses or in pathology mediated
by defects in T-lymphocytes. Manifested by damage to the skin and
oral mucosa in the form of cheilitis, seizures, glossitis.
Chronic candidiasis

18. On the mucous membranes, white confluent papules are formed.
Considered as a precancerous condition. In chronic
hyperplastic candidiasis, there is a slightly raised area of the mucous
membrane with clear boundaries in the form of a plaque that does
not separate from the underlying epithelium ( candidal leukoplakia).
histologically, with this form of candidiasis, the penetration of
fungal hyphae into the thickness of the epithelium is noted. If white
areas of the mucous membrane alternate with erythematous ones ,
they are referred to as the nodular form of candidal leukoplakia.
Hyperplastic candidiasis

19. microscopic method. They take a scraping from the mucous membrane, make a
smear on a glass slide. Microscopically unstained preparations stained according
to Gram, according to Romanovsky- Giemsa, methylene blue. The diagnosis is
based on the detection of elements of the fungus: single budding cells,
pseudomycelium, other morphological structures ( blastoconidia , pseudohyphae).
Microbiological diagnostics

20. Ulcerative necrotic gingivostomatitis Vincent
( fusospirochetosis )
Fusospirochetosis is an acute inflammation of the
gums with severe alterations. Ulcerative-necrotic
gingivitis develops against the background of catarrhal
inflammation. This disease occurs mainly in young
people, when as a result of SARS, tonsillitis, influenza,
hypothermia, stress, malnutrition, hypovitaminosis,
immunity decreases.

21. Among microorganisms, anaerobic forms
predominate - FUSOBACTERIA ( fusobacterium
plautii ), spirochetes ( treponema vincentii ). often
the development of the disease is preceded by
inflammation caused by staphylococci and
streptococci. The pathogenetic significance of
fusiform bacteria is associated with the presence of
histolytic enzymes such as collagenase, proteinase,
hyaluronidase, which cause destruction of connective
tissue. At the same time, nitrogen-containing low
molecular weight products formed as a result of the
breakdown of collagen can be absorbed by
spirochetes.
Ulcerative necrotic gingivostomatitis Vincent
( fusospirochetosis )

22. The development of ulcerative necrotic gingivitis of Vincent is
facilitated by poor individual oral hygiene, dental deposits, the
presence of carious, decayed teeth, and difficulty in the eruption
of a wisdom tooth (the presence of a "hood"). The patient
complains of pain in the gums, which makes it difficult to eat and
speak. During the examination, hyperemia, the presence of ulcers
and necrosis of the gums (grayish plaque), a significant amount of
soft plaque and hard dental deposits, there is an unpleasant smell
from the mouth. Often, lesions of the tonsils and larynx are
observed with the development of a condition known as
Simanovsky - Vincent - Plaut 's angina .
Ulcerative necrotic gingivostomatitis Vincent (fusospirochetosis)

23. confirm the diagnosis, a bacterioscopic
examination is of great importance: When
microscopy of the discharge of ulcers,
fusobacteria and spirochetes are found in large
numbers, therefore this disease is called
fusospirochetosis: fusobacterium
necrophorum, fusobacterium nucleatum +
treponema vincentii, t. denticola , t. orale , t.
macrodentium. .
Perhaps the presence of peptostreptococci and
bacteroids.
Laboratory diagnostics
The figure shows a pure culture of
Fusobacterium

24. Erysipelas, erysipelas, is an acute, often recurrent infectious
disease caused by group A beta-hemolytic streptococcus.
Lesions can be a continuation of inflammation on the skin of
the face or begin with small cracks and abrasions on the
mucous membranes of the mouth and pockets. Sometimes
erysipelas develops after surgical and orthopedic
interventions in the oral cavity. Serous-hemorrhagic
inflammation with severe edema develops on the oral
mucosa. Leukocyte infiltration develops in the deep layers of
the mucous membrane. The mucous membrane acquires a
dark crimson color. In severe cases, blisters and areas of
necrosis appear on it. Local manifestations are accompanied
by symptoms of general intoxication. In weakened
individuals, the process can be generalized with the
development of sepsis.

25. ANGULUS INFECTIOSUS
 Angulus Infectiosus is a disease of the mucous membrane and skin of the
corners of the mouth caused by streptococci (streptococcal zaeda) or yeast-
like fungi of the genus Candida (yeast, or candidamicotic zaeda).The disease
begins with the appearance in the corner of the mouth of a small
streptococcal pustule, which quickly transforms into erosion with fragments
of the epidermis along the edges. In the absence of treatment and non-
compliance with the basic rules of hygiene, as well as due to stretching of the
skin when opening the mouth and minor injuries, a crack forms in the center
of erosion, passing to the mucous membrane of the cheek. The crack bleeds
easily and becomes covered with a bloody or purulent crust. Increased
salivation and untidy oral maintenance contribute to the constant irritation of
streptococcal erosion, which can lead to streptococcal impetigo on the skin
of the face.