Authors

  • Shodikulova Gulandom Zikriyayevna
    Professor, Samarkand State Medical University, Samarkand, Uzbekistan
  • Gulomov Jahongir Ibrokhimovich
    Assistant, Samarkand State Medical University, Samarkand, Uzbekistan
  • Pulatov Ulugbek Sunatovich
    PhD, docent, Samarkand State Medical University, Samarkand, Uzbekistan
  • Khasanov Oybek Gafurovich
    Assistant, Samarkand State Medical University, Samarkand, Uzbekistan

DOI:

https://doi.org/10.37547/ijmscr/Volume04Issue08-03

Keywords:

Osteoarthritis (OA) femoral hip joint COVID-19

Abstract

Osteoarthritis (OA) is one of the most common chronic degenerative joint diseases, significantly affecting the quality of life of patients. The COVID-19 pandemic has revealed the long-term effects of the SARS-CoV-2 virus, including the development of OA. The object of this study is the impact of COVID-19 on the clinical, immunological, and genetic features of OA. The article discusses the mechanisms leading to inflammatory processes in the joints, as well as genetic aspects that may be associated with cartilage regeneration. Patients after COVID-19 have more pronounced OA symptoms, which confirms the need for further study of this relationship to develop effective approaches to treatment and rehabilitation.


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Volume 04 Issue 07-2024

23


International Journal of Medical Sciences And Clinical Research
(ISSN

2771-2265)

VOLUME

04

ISSUE

07

P

AGES

:

23-28

OCLC

1121105677
















































Publisher:

Oscar Publishing Services

Servi

ABSTRACT

Osteoarthritis (OA) is one of the most common chronic degenerative joint diseases, significantly affecting the quality

of life of patients. The COVID-19 pandemic has revealed the long-term effects of the SARS-CoV-2 virus, including the

development of OA. The object of this study is the impact of COVID-19 on the clinical, immunological, and genetic

features of OA. The article discusses the mechanisms leading to inflammatory processes in the joints, as well as genetic

aspects that may be associated with cartilage regeneration. Patients after COVID-19 have more pronounced OA

symptoms, which confirms the need for further study of this relationship to develop effective approaches to

treatment and rehabilitation.

KEYWORDS

Research Article

CLINICAL FEATURES AND IMMUNOLOGICAL MECHANISMS OF
DEVELOPMENT OF OSTEOARTHRITIS OF THE FEMORAL HIP JOINT

Submission Date:

Aug 02, 2024,

Accepted Date:

Aug 07, 2024,

Published Date:

Aug 12, 2024

Crossref doi:

https://doi.org/10.37547/ijmscr/Volume04Issue08-03


Shodikulova Gulandom Zikriyayevna

Professor, Samarkand State Medical University, Samarkand, Uzbekistan

Gulomov Jahongir Ibrokhimovich

Assistant, Samarkand State Medical University, Samarkand, Uzbekistan

Pulatov Ulugbek Sunatovich

PhD, docent, Samarkand State Medical University, Samarkand, Uzbekistan

Khasanov Oybek Gafurovich

Assistant, Samarkand State Medical University, Samarkand, 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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Osteoarthritis (OA), COVID-19, SARS-CoV-2 virus, femoral hip joint, interleukin-6 (IL-6) and interleukin-8 (IL-8), tumor

necrosis factor-alpha (TNF-

α), non

-steroidal anti-inflammatory drugs (NSAIDs).

INTRODUCTION

Osteoarthritis (OA) is one of the most common chronic

degenerative joint pathologies, significantly affecting

patients' quality of life and ability to work. The COVID-

19 pandemic caused by the SARS-CoV-2 virus has shown

that the infection can have long-lasting effects on

various div systems. Recent studies show the impact

of COVID-19 on the clinical, immunological, and genetic

features of OA development in patients with this

infection. This literature review aims to deepen our

understanding of the pathogenesis of the disease and

to search for possible mechanisms of COVID-19's

influence on osteoarthritis.

Impact of viral infections on the immune system:

Recent studies have shown that COVID-19 can cause

various immune system disturbances, including

activation of inflammatory processes. SARS-CoV-2

causes an enhanced immune response accompanied

by increased levels of cytokines and inflammatory

markers. This inflammatory response may contribute

to the development and progression of OA in COVID-19

patients.

Clinical manifestations of OA after COVID-19:

Observations show that COVID-19 patients present

with osteoarthritis with some peculiarities compared

to normal OA. These patients have more severe pain,

limitation of mobility and joint inflammation. This may

be due to the effect of the virus on cartilage tissues as

well as surrounding structures and joints.

Genetic aspects of OA after COVID-19: There is

evidence of abnormalities in genetic mechanisms

related to cartilage regeneration and metabolic

processes in joints in patients with OA after COVID-19.

Some genes associated with cartilage formation and

destruction may play a role in the pathogenesis of OA

after infection. Genetic predisposition studies help to

identify risk groups and understand the molecular

mechanisms involved in the pathogenesis of OA after

COVID-19.

Despite the relative novelty of the problem, existing

studies point to possible clinical, immunological, and

genetic features of OA in COVID-19 patients. Continued

research in this area is important to better understand

the molecular mechanisms and to develop tailored

treatment and rehabilitation strategies to prevent or

delay the development of OA after COVID-19.


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Risk factors and metabolic disorders: To understand

the etiopathogenesis of the disease, it is important to

consider risk factors such as age, obesity, diabetes

mellitus, hypertension, and dyslipidemia. One

mechanism explaining the association between

metabolic disorders and OA is chronic inflammation

associated with metabolic diseases. Inflammatory

cytokines such as interleukin-

1β (IL

-

1β) and tumor

necrosis factor-alpha (TNF-

α) activate destr

uctive

processes in cartilage and promote its degeneration.

Traumatic osteoarthritis: Mechanisms associated with

the development of traumatic osteoarthritis include

damage to joint structures, cartilage, and synovial

membrane, inflammation, and immune cell activation.

Traumatic injury causes inflammatory processes that

lead to the release of cytokines such as interleukin-6

(IL-6) and interleukin-8 (IL-8) that activate destructive

processes in cartilage and promote cartilage

degeneration.

Effect of drugs: Drugs play an important role in the

treatment and management of osteoarthritis.

Different classes of drugs have different effects on the

pathogenesis and symptoms of osteoarthritis. For

example, non-steroidal anti-inflammatory drugs

(NSAIDs) are widely used to relieve pain and

inflammation in OA, but their long-term use can cause

serious side effects. Glucosamine and chondroitin

sulfate may have a positive effect on cartilage tissue

and reduce OA symptoms, but their effectiveness

requires further research.

Genetic disorders: Genetic factors play an important

role in the development of osteoarthritis. Several

genes related to the metabolism of cartilage

components, collagen structure, and proteoglycans

are of potential importance in the development of the

disease. For example, polymorphisms in the COL2A1

gene encoding type II collagen may contribute to

impaired cartilage structure and increased risk of

osteoarthritis.

Genes

encoding

matrix

metalloproteinases (MMPs) and tissue inhibitors of

metalloproteinases (TIMPs), as well as cytokines such

as IL-

1β and TNF

-

α, may also play a role in the

pathogenesis of osteoarthritis. Alterations in these

genes may affect the activity of cartilage-related

enzymes and joint inflammation.

Thus, the etiopathogenesis of osteoarthritis is a

complex and multifaceted process involving various

risk factors, metabolic disorders, traumatic injuries,

drug effects, and genetic factors. Age, gender, obesity

and occupational factors significantly influence the

development of the disease. Metabolic disorders,

especially those associated with metabolic syndrome,

also play an important role in the pathogenesis of

osteoarthritis. Traumatic osteoarthritis may result

from joint injuries leading to inflammatory and

degenerative processes. Medications such as NSAIDs,

glucosamine and chondroitin sulfate may have a


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positive effect on osteoarthritis symptoms but require

further

research.

Genetic

factors,

including

polymorphisms of genes related to cartilage

metabolism and inflammation, also play an important

role in the development of osteoarthritis.

Etiopathogenesis of COVID-19 and its musculoskeletal

complications: COVID-19, caused by the SARS-CoV-2

coronavirus, has become one of the most serious

public health problems in world history. Since the start

of the pandemic in late 2019, the disease continues to

spread and affect various div systems. The main

symptoms of COVID-19 are related to the respiratory

system, but a growing div of research points to

possible complications in other systems, including the

musculoskeletal system.

Etiopathogenesis of COVID-19: The SARS-CoV-2

coronavirus enters div cells via angiotensin-

converting enzyme 2 (ACE2) receptors widely

distributed in various tissues, including lungs, heart,

kidneys, blood vessels, and musculoskeletal tissues.

Infection causes systemic inflammation and activation

of the immune system, leading to a complex set of

molecular and cellular responses.

Complications of COVID-19 in the musculoskeletal

system are:

1. Myalgia and arthralgia: One of the most common

symptoms of COVID-19 is muscle pain (myalgia) and

joint pain (arthralgia). These symptoms may be caused

by systemic exposure to the virus or the div's

response to a viral infection. Studies show that myalgia

occurs in 45% of patients with COVID-19. These

symptoms can cause significant discomfort and limit

mobility.

2. Joint inflammation: In some patients, COVID-19 may

cause joint inflammation, leading to arthritis-like

symptoms. Research suggests that the virus may cause

inflammatory processes in the joints, leading to

rheumatic symptoms. This may cause pain, swelling,

and limitation of joint motion.

3. Myopathies: COVID-19 may cause musculoskeletal

disorders such as myopathies. These disorders may be

caused by the direct effect of the virus on the muscles

or by inflammatory processes caused by the div’s

immune response. Patients may experience muscle

weakness, pain, and limitation of motion.

4. Thrombosis and embolism: COVID-19 is associated

with an increased risk of thrombotic complications

such as vascular thrombosis and pulmonary embolism.

These complications may be due to hypercoagulability,

inflammatory changes, and damage to the vascular

wall.

CONCLUSION

Thus, studies show that osteoarthritis (OA) may be

exacerbated in patients after COVID-19 due to immune

system disorders, clinical manifestations, and genetic


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factors. The SARS-CoV-2 virus activates inflammatory

processes, which may accelerate the development of

OA. In this case, specific clinical symptoms are

observed, such as increased pain and limited joint

mobility. Genetic mechanisms associated with

cartilage regeneration may also play an important role

in the pathogenesis of OA in patients after COVID-19. It

is important to consider risk factors such as age,

comorbid diseases, and metabolic disorders, which can

aggravate the course of the disease. This emphasizes

the need for further research to develop specific

therapeutic strategies and rehabilitation measures.

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НА ПРОБЛЕМУ АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИИ У

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И

КЛИНИКО

-

ГЕНЕТИЧЕСКИЕ ОСОБЕННОСТИ ДИСПЛАЗИИ

СОЕДИНИТЕЛЬНОЙ ТКАНИ У ЛИЦ УЗБЕКСКОЙ

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Chow YY, Chin KY. The Role of Inflammation in the Pathogenesis of Osteoarthritis. Mediators Inflamm. 2020 Mar 3;2020:8293921. doi: 10.1155/2020/8293921. PMID: 32189997; PMCID: PMC7072120.

Endstrasser F, Braito M, Linser M, Spicher A, Wagner M, Brunner A. The negative impact of the COVID-19 lockdown on pain and physical function in patients with end-stage hip or knee osteoarthritis. Knee Surg Sports Traumatol Arthrosc. 2020 Aug;28(8):2435-2443. doi: 10.1007/s00167-020-06104-3. Epub 2020 Jun 18. PMID: 32556438; PMCID: PMC7299668.

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Khella C. M. et al. An evidence-based systematic review of human knee post-traumatic osteoarthritis (PTOA): timeline of clinical presentation and disease markers, comparison of knee joint PTOA models and early disease implications //International Journal of Molecular Sciences. – 2021. – Т. 22. – №. 4. – С. 1996.

Kijima H. et al. The differences in imaging findings between painless and painful osteoarthritis of the hip //Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders. – 2020. – Т. 13. – С. 1179544120946747.

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Molnar V. et al. Mesenchymal stem cell mechanisms of action and clinical effects in osteoarthritis: a narrative review //Genes. – 2022. – Т. 13. – №. 6. – С. 949.

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Trivanovic D. et al. Immune and stem cell compartments of acetabular and femoral bone marrow in hip osteoarthritis patients //Osteoarthritis and Cartilage. – 2022. – Т. 30. – №. 8. – С. 1116-1129.

Zikriyayevna S. G. et al. HEART RHYTHM DISTURBANCES IN CONNECTIVE TISSUE DYSPLASIA //International Journal of Medical Sciences And Clinical Research. – 2024. – Т. 4. – №. 06. – С. 32-39.

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Пулатов У. С., Суюнов А. Ф. ПОЛИМОРФИЗМ ГАПТОГЛОБИНА У БОЛЬНЫХ С РЕВМАТОИДНЫМ АРТИРОМ //" Conference on Universal Science Research 2023". – 2023. – Т. 1. – №. 2. – С. 120-123.

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Пулатов У. С. и др. ОСОБЕННОСТИ ЛЕЧЕНИЯ ПРИ ХПН //INNOVATIVE DEVELOPMENTS AND RESEARCH IN EDUCATION. – 2023. – Т. 2. – №. 23. – С. 303-305.

Шодикулова Г. З. и др. СОВРЕМЕННЫЙ ВЗГЛЯД НА ПРОБЛЕМУ АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИИ У БОЛЬНЫХ С ПОДАГРОЙ И БЕССИМПТОМНОЙ ГИПЕРУРИКЕМИЕЙ //Journal of cardiorespiratory research. – 2023. – Т. 1. – №. 1. – С. 28-33.

Шодикулова Г. З., Мирзаев О. В., Саматов Д. К. РАСПРОСТРАНЕННОСТЬ И КЛИНИКО-ГЕНЕТИЧЕСКИЕ ОСОБЕННОСТИ ДИСПЛАЗИИ СОЕДИНИТЕЛЬНОЙ ТКАНИ У ЛИЦ УЗБЕКСКОЙ ПОПУЛЯЦИИ //Journal of cardiorespiratory research. – 2023. – Т. 1. – №. 1. – С. 94-98.

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