Volume 04 Issue 10-2024
48
International Journal of Medical Sciences And Clinical Research
(ISSN
–
2771-2265)
VOLUME
04
ISSUE
10
P
AGES
:
48-55
OCLC
–
1121105677
Publisher:
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Servi
ABSTRACT
Upper jaw sinus cysts are a very common disease, often an accidental clinical find upon radiography and computed
tomography of the paranasal sinuses. At the same time, there are few reports in the literature about the location of
cysts in the frontal and ponal cavities. It is especially difficult to diagnose the cysts of the wedge-shaped cavity, as
known radiographic arrangements do not allow them to be diagnosed. The problem of diagnosing paranasal sinus
cysts was solved by implementing computed tomography into practice.
KEYWORDS
Research Article
ASPECTS OF ETIOLOGICAL FACTORS OF CYST MAXILLO-FACIAL SINUSES
Submission Date:
October 02, 2024,
Accepted Date:
October 07, 2024,
Published Date:
October 12, 2024
Crossref doi:
https://doi.org/10.37547/ijmscr/Volume04Issue10-09
Mirzayev S.P.
Tashkent Medical Academy, Uzbekistan
Jabborov N.N.
Tashkent Medical Academy, Uzbekistan
Akhmedov S.E.
Tashkent Medical Academy, Uzbekistan
Botirov A.J.
Tashkent Medical Academy, Uzbekistan
Abdullaev U.P.
Tashkent Medical Academy, Uzbekistan
Akhundjanov N.A.
Tashkent Medical Academy, Uzbekistan
Journal
Website:
https://theusajournals.
com/index.php/ijmscr
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
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Sinusitis, upper humerus, cyst.
INTRODUCTION
Sinuses of odontogenic origin occupy a significant
place
among
inflammatory
diseases
of
the
maxillofacial region, and patients with odontogenic
maxillary sinusitis make up about 25.8% among patients
with inflammatory processes of the maxillary sinus and
about 7.6% of patients in maxillofacial hospitals, and
among dental and otolaryngological institutions - from
3 to 10% [2].
The disease is a serious general medical and economic
problem, as the majority of patients are young and
middle-aged people, and in recent years, there has
been an increase in the number of patients with
chronic obstructive pulmonary disease, ranging from
41% to 77% of all inflammatory processes in the
maxillary sinus [12, 17].
Depending on the etiology of the disease, rhinogenic,
odontogenic, traumatic and allergic sinusitis of the
upper jaw are distinguished. On average, one-third of
all maxillary sinusitis is represented by its odontogenic
forms [23, 34], which are mainly the result of prolonged
existence of a chronic peri-apical infection focus in the
area of small and large maxillary teeth (MZ) [4, 11] or
errors of doctors in the process of treatment and
removal of these teeth [3, 15, 17, 30].All of the above is
a pressing dental problem.
The purpose of this study is to analyze the current
state, epidemiology, etiology, and pathogenesis of
odotogenic maxillary sinusitis.
Despite the improvement of therapeutic and
diagnostic equipment, the frequency of CHF among
other inflammatory diseases of the maxillofacial region
increased from 4-4.2% in the 1970s to 7.6% in the 1990s,
and there is a steady trend towards an increase in the
number of patients with CHF in recent years [13, 21].A
statistical analysis conducted by F.I. Shulman (2003)
showed that over the period from 1997 to 2001, the
frequency of severe acute respiratory distress
syndrome (AVSR) developed as a result of filling
material penetration into the upper jaw cavity after
endodontic treatment of teeth increased tenfold,
indicating a significant impact of the iatrogenic factor
on the development and progression of this pathology.
According to literature data [5,9,35] 23.6 to 77.2% of
FVV are its perforated forms.
Depending on the etiology of the disease, rhinogenic,
odontogenic, traumatic and allergic sinusitis of the
upper jaw are distinguished. This division is conditional,
as rhinogenic upper jaw sinusitis, developed against
the background of acute respiratory disease, can lead
to exacerbation of the periapical focus of chronic
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odontogenic infection and secondary infection of the
upper jaw sinus mucosa [36]. Therefore, 62% of
patients with rhinogenic maxillary sinusitis exhibited
odontogenic infection foci [5, 24].
Emergency cases, like rhinogenic ones, are primarily
caused by a purulent infection. The leading infectious
agents are hemolytic streptococci, pneumococci,
staphylococci, as well as opportunistic intestinal
bacteria.
Several microbial agents, often a mixed flora: aerobic
flora: Staphylococcus anreus, Streptococcus Species,
Hemophylus influenrac, Pseudomonasaeru- ginosa,
Pseulomonas
mirabilis,
Moraxella
catarrhalis;
anaerobic non-clostridian flora: Bacteroidesiradillis,
Bacteroides melaninogenicus, Fusobacterium nucleus
peptococcus, Veptobacillus peptococcus; fungal flora:
Candida pss., Aspergilluss pp.
These microorganisms are sown in monoculture as well
as in various associations with each other - mainly
aerobic-anaerobic and bacterial-fungal [7, 22].
According to the literature, there are differences in the
microflora in different courses of the disease. S. Ziuzio,
W. Stepniewier (1980) found bacterial flora
predominantly homogeneous in acute sinusitis and
mixed in chronic sinusitis.
At the same time, it is important to identify the
microflora of the oral cavity and the upper jaw cavity
[27, 31].
Studies conducted by A. and Bogatov (1991) show that
the immediate cause of chronic periodontitis is often
acute and acute periodontitis (up to 50% of cases) or
various complications of therapeutic and surgical
interventions on teeth (up to 20% of cases).Radical
cysts and osteomyelitis of the dental cavities in contact
with the floor of the maxillary sinus are found in 13% of
cases with almost the same frequency. In his research,
A.I. Bogatov (2000) established that the source of
infection in the emergency room is often the first mol
(56.6% of cases). In a number of cases, premature or
poor sanitation of the oral cavity is a prerequisite for
the development of VVR.
Currently, there are numerous reports in the literature
regarding the development of VCH due to the
penetration of filling material into the VCH cavity after
endodontic treatment of upper jaw teeth (UJ) [3, 17,
29, 30].
One of the frequent causes of the development of VVR
is a cavity perforation, differing in etiology,
localization, size, and course. According to a number of
authors [12, 16, 35], the development of emergency
situations against the backdrop of existing guaranteed
communication occurs in 41.2% to 91.7% of cases. There
is information in the literature that the most frequent
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group of VCH sinus perforations occurs with the
removal of lateral VCH teeth [2, 5, 10]. In the literature,
the rarest causes of chronic kidney disease are delayed
eruption of third molars, as well as inflammation
around retinated and semi-retinated teeth [23]. There
are clinical facts indicating the development of VCR
after the operation to raise the bottom of the VCHP
with sub-intral augmentation [9, 33].
Patho-morphological changes in chronic obstructive
pulmonary disease generally correspond to the stages
of the inflammatory process: alterative-exudative,
productive, and fibrous. Due to the spread of infection
from the alveolar ridge of the tooth to the left
ventricle, there is mucous-purulent discharge,
irreversible morphological changes in the mucous
membrane and the formation of necrotic tissues [7, 13].
Later on the ciliary activity of the ciliary epithelium
suffers, i.e. it is blocked. Meanwhile, the average
number of functioning glands in the mucous
membrane is significantly reduced, and general and
local cellular immunogenesis is disrupted [22]. In the
development of the pathological process against the
background of CHD, there is constant irritation of the
mucous membrane of the oral cavity with oral fluid,
and the mucous membrane begins to react with
productive inflammation. This process is often
localized, affecting the lining only in the area of the
alveolar bucket, it occurs weakly, asymptomatically,
therefore it is not always diagnosed.
Factors of a general nature contribute to the
development of maxillary sinusitis (MS): a decrease in
the div's immunological reactivity, the impact of
adverse environmental conditions [13]. The prolonged
exposure of microorganisms, products and the vital
activity of isodontogenic lesions, as well as
autoinfection of the oral cavity, penetrating into the
oral cavity, play a certain role in reducing
immunological reactivity in the maxillary sinus after its
perforation.
Microbial effects on the whole organism and on the
already altered, pre-sensitized mucosa of the maxillary
sinus from the focus of odontogenic infection
determine
the
further
development
of
the
inflammatory process [24]. Chronic granulating and
granulomatous periodontitis contribute to the
development of odontogenic chronic periodontitis [24,
27].
The bone barrier between the IVC floor and the
pathological focus due to inflammation of the bone
tissue of the dental alveolus undergoes resorption, in
fact, the integrity of the IVC floor is disrupted, which
can occur long before the tooth is removed [26, 30, 32].
In the majority of patients with chronic modontogenic
perforating VCH with the presence of a persistent
fistula at the bottom of the maxillary sinus, thickening
and polypoid transformation of the maxillary sinus
mucosa are observed [1, 10, 20].
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According to S.Z. Piskunov and co-authors. (2004),
productive changes in the VCH membrane in chronic
odontogenic sinusitis, unlike rhinogenic ones, are
localized in the area of the alveolar cavity and the
anterior sinus wall at the initial stage.
It has been established that in odontogenic VCH with
puncture of the sinus floor, inflammatory changes of a
chronic nature are detected in the mucous membrane,
which may be caused by frequent exacerbations,
inflammation in the area of the peri-apical lesions of
the teeth adjacent to the floor of the VCH. Another
important factor influencing the development of VCHP
is the size and throughput of the VCHP natural joint.
According to modern concepts, this factor is leading in
the pathogenesis of sinusitis [18]. As a result of nasal
mucosal edema and VCHP, the permeability of the
natural opening of the nasal cavity is disrupted, and the
ventilation and drainage function of the nasal cavity is
reduced. With complete obturation of the oxygen
membrane, due to the absorption of oxygen by the
mucous membrane into the VCHP, negative pressure is
created, veins are dilated, and stagnation of the
mucous membrane occurs. This exacerbates the
swelling of the tissue. As a result of pressure drop,
hypoxia and hypercapnia, conditions are created for
the growth of aerobes and facultative anaerobes [14].
Thus, a vicious circle is formed that determines the
outcome of the disease. If it is not torn, irreversible
changes develop in the mucous membrane [8, 25, 28].
CONCLUSIONS
Thus, summarizing the above, the following
conclusions can be drawn:
Currently, VCH is one of the most common dental
diseases, one of the causes of which is a perforation of
the upper jaw due to errors in the technique of removal
and endodontic treatment of VCH premolaries and
molars, and it is a serious general medical problem, as
the majority of patients are of working age.
The main etiological factors in the development of
VCHD are bacterial and fungal microflora with diseases
of the upper jaw teeth (chronic periodontitis, radicular
cysts, pubic osteomyelitis, periodontitis), foreign
bodies in the VCHD and reconstructive operations on
the VCHD, as well as sensitization of the div.
Topographic anatomical relationships between VCH
and VCHP teeth are the prerequisites for the
development of VCHS.
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