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PATHOPHYSIOLOGICAL MECHANISMS OF THE INFLUENCE OF RENAL
FAILURE ON INFLAMMATORY PROCESSES IN PERIODONTAL TISSUES
Azizbek Gofurov
assistant at the Fergana Medical Institute of Public Health.
Annotation:
Chronic renal failure (CRF) is a systemic disease characterized by
accumulation of uremic toxins, impaired microcirculation, and activation of systemic
inflammation. These processes have a significant impact on periodontal tissues, enhancing
inflammatory responses and leading to destruction of connective and bone tissue. This
article reviews the pathophysiological mechanisms linking CRF with inflammatory
periodontal diseases, including the role of uremic toxins, calcium-phosphorus imbalance,
and oxidative stress. Promising therapeutic approaches, including the use of biomarkers ,
new-generation antioxidants, and regenerative technologies, are also discussed. This work
highlights the need for an interdisciplinary approach to the diagnosis and treatment of
patients with CRF to minimize negative consequences on the periodontium.
Keywords:
chronic renal failure, inflammatory periodontal diseases, uremic toxins,
oxidative stress, biomarkers , regenerative technologies, systemic inflammation.
Introduction
The relevance of studying the pathophysiological mechanisms underlying the relationship
between renal failure and inflammatory processes in periodontal tissues is due to the high
prevalence of chronic renal failure (CRF), which, according to statistics, affects about 10%
of the adult population worldwide, as well as its systemic impact on the div. CRF is
accompanied by metabolic disorders, activation of systemic inflammation, and accumulation
of uremic toxins, which can significantly affect the condition of the periodontium.
Periodontal tissues, being highly sensitive to changes in microcirculation and inflammatory
processes, are subject to significant destructive changes under the influence of chronic
pathologies.
The aim of this review article is to summarize current data on the mechanisms linking renal
failure with inflammatory periodontal diseases, as well as to identify key pathogenetic links
that can serve as a basis for the development of new therapeutic approaches.
The main mechanisms of renal failure
Chronic renal failure (CRF) is a progressive impairment of renal function resulting in
accumulation of metabolites, electrolyte imbalance, and systemic changes in the div. The
main pathogenetic mechanisms are uremic intoxication, including accumulation of toxins
such as p- cresyl sulfate and indoxyl sulfate , activation of the renin-angiotensin- aldosterone
system (RAAS) accompanied by hypertension and vascular damage, chronic inflammation,
and increased oxidative stress, which disrupts normal endothelial and tissue functions.
Uremic toxins such as p- cresyl sulfate , indoylacetic acid, and guanidinosuccinate have
pronounced proinflammatory properties, increasing oxidative stress and damaging the
vascular endothelium.
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Activation of RAAS in CRF leads to vasoconstriction , increased systemic arterial pressure
and vascular hypertrophy, which in turn disrupts microcirculation and promotes the
progression of inflammatory processes. Chronic inflammation is one of the key links in the
pathogenesis of CRF and is accompanied by increased expression of proinflammatory
cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and C-reactive
protein (CRP). These mediators enhance destructive changes in tissues, including
periodontal structures.
The role of inflammatory processes in the pathogenesis of periodontal diseases
Periodontal diseases, including gingivitis and periodontitis, are inflammatory pathologies
that arise as a result of dysbiosis of the oral microbiota and a decrease in the div's defense
mechanisms. The main pathogenetic mechanisms include activation of innate and adaptive
immunity in response to lipopolysaccharides (LPS) of pathogenic bacteria, such as
Porphyromonas gingivalis
,
Tannerella forsythia
and
treponema denticola
. These
microorganisms stimulate the production of cytokines such as IL-1β, IL-6, IL-8 and TNF-α,
which promote collagen degradation, vascular permeability impairment and osteoclast
activation. The interaction of these cytokines activates immune cells such as macrophages
and neutrophils, which release reactive oxygen species and proteolytic enzymes that enhance
the inflammatory process. Increased levels of TNF-α stimulate the expression of adhesion
molecules on endothelial cells, promoting leukocyte migration into the tissue, which
increases local inflammation. IL-1β and IL-6, in turn, promote the production of
prostaglandins, which enhance the destruction of connective tissue and bone resorption.
An important role in the development of inflammatory processes is played by oxidative
stress, which leads to damage to periodontal cells, a decrease in their regenerative potential
and increased apoptosis. This, together with microcirculatory disorders, creates conditions
for chronic inflammation and progressive tissue destruction.
The relationship between chronic renal failure and periodontal disease
Numerous studies confirm that patients with CRF have an increased risk of developing and
progressing periodontal diseases. Uremic toxins circulating in the blood penetrate into
periodontal tissues, where they enhance inflammatory reactions. Chronic systemic
inflammation in CRF aggravates local inflammatory processes by increasing the level of IL-
6, TNF-α and other mediators. In addition, microcirculation disorders and endothelial
dysfunction characteristic of CRF prevent normal regeneration of periodontal tissues.
Of particular interest is the finding that hemodialysis patients have a significant deterioration
in periodontal health associated with high levels of proinflammatory cytokines and calcium-
phosphorus imbalance. Hormonal imbalances such as decreased vitamin D levels also
contribute to alveolar bone loss and connective tissue deterioration.
Discussion
The obtained data on the pathophysiological mechanisms of the influence of chronic renal
failure on inflammatory processes in periodontal tissues emphasize the relationship between
systemic inflammation and local pathological changes in the oral cavity. Uremic toxins
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circulating in the div during CRF initiate chronic inflammation in periodontal tissues due
to the activation of proinflammatory cytokines and increased oxidative stress. At the same
time, there is a pronounced violation of microcirculation in periodontal tissues, which
aggravates the inflammatory process and contributes to the progressive destruction of bone
and connective tissue.
Systemic changes associated with CRF, including activation of the renin-angiotensin -
aldosterone system and imbalance of calcium-phosphorus metabolism, have a significant
impact on the periodontium . Increased levels of interleukin-6 (IL-6) and tumor necrosis
factor-alpha (TNF-α) promote osteoclast activation, which leads to accelerated alveolar bone
resorption. Moreover, vitamin D deficiency, typical for patients with CRF, reduces the
regenerative potential of tissues, impairing their ability to recover from inflammatory
damage.
It is interesting that treatment of patients with CRF, including control of uremic toxins and
proinflammatory markers, improves the condition of the periodontium. Clinical studies
show that regular hemodialysis reduces the concentration of toxins, and vitamin D therapy
reduces the severity of inflammatory reactions. The introduction of new antioxidants, such
as N-acetylcysteine, and anti-inflammatory drugs has demonstrated a significant decrease in
inflammation markers in periodontal tissues. The most effective control methods are
hemodialysis, which reduces the concentration of uremic toxins, and correction of vitamin D
levels aimed at restoring mineral balance and reducing inflammatory reactions. In addition,
therapy with anti-inflammatory drugs and antioxidants, such as tocopherol and N-
acetylcysteine, has demonstrated a positive effect on reducing oxidative stress in periodontal
tissues. This confirms the need for an integrated approach, including both systemic and local
treatment methods for this category of patients.
Conclusion
Chronic renal failure and inflammatory periodontal diseases mutually reinforce each other
through complex pathophysiological mechanisms including systemic and local inflammation,
uremic intoxication, oxidative stress and microcirculation disorders. These interactions
highlight the need for a multidisciplinary approach to the treatment of patients with CRF,
including monitoring and therapy of inflammatory periodontal diseases. Future research
should be aimed at developing therapeutic strategies that take into account the systemic
nature of these diseases and their impact on periodontal tissues. It is important to study the
use of biomarkers such as IL-6 and TNF-α levels to predict the risk of inflammation, as well
as the development of innovative therapies, including the use of stem cells to restore
damaged periodontal tissues and nanomaterials for local drug delivery. Promising areas
include the use of biomarkers for early diagnostics of inflammatory processes in the
periodontium in patients with chronic renal failure, as well as the introduction of innovative
therapies, such as the use of anti-inflammatory biopreparations, new-generation antioxidants,
and regenerative techniques using stem cells. These approaches can significantly improve
clinical outcomes and minimize the negative impact of systemic diseases on the
periodontium.
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