Materiały źródłowe

• #1 Septic Arthritis: What Is It, Symptoms, Treatment & Causes

  https://my.clevelandclinic.org/health/diseases/22418-septic-arthritis

  Septic arthritis (also known as infectious arthritis) happens when an infection spreads to one or more of your joints and causes inflammation. The inflammation is in the surface of the cartilage (a type of connective tissue) that lines your joints and the synovial fluid that lubricates your joints. Bacteria, a virus or fungus may cause the infection, which usually comes from another part of your body and spreads to your joint through your blood. […] Septic arthritis is caused by an infection. It can be from bacteria, fungus, mycobacteria, a virus or other pathogens. In most cases, the infection begins somewhere else on or in your body and then spreads through your blood to your joint. More specifically, the following organisms can cause septic arthritis: […] Staphylococcus aureus, a type of bacteria, is the most common cause of septic arthritis in both children and adults. Approximately 37% to 56% of septic arthritis cases are caused by Staphylococcus aureus.

• #2 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  The possible entry points of bacterial inoculation in the joint include, three possible routes i.e. a) direct seeding due to recent arthroplasty surgery such as prosthetic implantation or fracture fixation or joint aspiration or intra-articular steroid injection, b) through the hematogenous route from a distant infection reservoir and c) due to extension of contiguous infection underlying bone infection in cases of osteomyelitis or prosthetic infected joint with involvement of biofilm bacteria. […] Among the etiology associated with SA, Staphylococcus aureus has been the predominant pathogen responsible for 40%-50% of the cases of septic arthritis and further 6% to 22% of S. aureus isolates being identified as MRSA, hinting towards the frequent involvement of MRSA in bone and joint infections and its rise among orthopedic settings.

• #3 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Septic arthritis is inflammation of the joints secondary to an infectious etiology such as bacterial, fungal, mycobacterial, viral, or other pathogens. […] Septic arthritis occurs when there is a bacterial invasion of the synovium and joint space followed by an inflammatory process. Inflammatory cytokines and proteases mediate joint destruction. Other factors which play a role in joint damage are bacterial toxins and microbial surface components like staphylococcal adhesins which promote the binding of the bacteria to intra-articular proteins. […] The highly vascularized joint synovium lacks a limiting basement membrane so is prone to infection via hematogenous seeding from systemic infection. Septic arthritis may also result from direct injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis may occur.

• #4 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  Staphylococcus aureus is the most commonly cultured organism. […] Antibiotic coverage should start in suspected cases when blood cultures and a serologic test and microscopic analysis of synovial fluid collected from the affected joint are the initial steps in diagnosing septic arthritis. […] Standard treatment consists of irrigation and debridement of the affected joint, followed by intravenous antibiotics. […] In order to limit the risk of lifelong disability, making a fast diagnosis and treatment plan for ASA patients is crucial. […] These topics continue to be the subject of debate among experts, and unfortunately, the literature has no consensus about the etiology, the best treatment, and the diagnosis method available for ASA patients. […] The primary routes of joint infection include: 1) Hematogenous spread: pathogenic bacteria of the infection foci in other parts of the body spread to the joint through the blood circulation; hematogenous spread of infection is the most common etiology of shoulder sepsis; 2) Adjacent infection: the pathogenic bacteria come from the skin and soft tissue infection around the joint or secondary intra-articular infection after osteomyelitis; 3) Iatrogenic: such as secondary infection following joint cavity puncture or medicament injection, or secondary intra-articular infection following joint replacement and per-articular fracture internal fixation and implantation; 4) Traumatic, including trauma, stab wounds, and animal bites, resulting in joint soft tissue or joint infection after articular sac injury.

• #5 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Septic arthritis is inflammation of the joints secondary to an infectious etiology such as bacterial, fungal, mycobacterial, viral, or other pathogens. […] Septic arthritis occurs when there is a bacterial invasion of the synovium and joint space followed by an inflammatory process. Inflammatory cytokines and proteases mediate joint destruction. Other factors which play a role in joint damage are bacterial toxins and microbial surface components like staphylococcal adhesins which promote the binding of the bacteria to intra-articular proteins. […] The highly vascularized joint synovium lacks a limiting basement membrane so is prone to infection via hematogenous seeding from systemic infection. Septic arthritis may also result from direct injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis may occur.

• #6 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  Pyogenic (septic) arthritis is a severe joint infection characterized by the invasion of microorganisms into the synovium, causing inflammation and joint destruction. This review article provides a comprehensive overview of pyogenic arthritis, focusing on etiology, pathogenesis, clinical manifestations, diagnosis, and management strategies. This review explores routes of microbial entry into joints, emphasizing the importance of prompt identification and treatment to prevent irreversible joint damage. […] A common mechanism of infection is via hematogenous spread to the vascular synovial membrane, and once infected, the cartilaginous matrix is rapidly destroyed. Bacterial inoculation of the synovial membrane can arise from penetrating trauma to the joint or from contiguous spread related to osteomyelitis or skin infection.

• #7 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response along with bacterial virulence factors damages articular surface and cartilage. […] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection. […] Determinants of hematogenous seeding: Well vascularized synovium, Absence of limiting basement membrane, Recent joint surgery, induces the production of host-derived extracellular matrix proteins (e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection, Virulence of microorganism, Susceptibility of synovial membrane for microorganism.

• #8 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties. […] Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. […] Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process. […] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction. […] After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response.

• #9 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response along with bacterial virulence factors damages articular surface and cartilage. […] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection. […] Determinants of hematogenous seeding: Well vascularized synovium, Absence of limiting basement membrane, Recent joint surgery, induces the production of host-derived extracellular matrix proteins (e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection, Virulence of microorganism, Susceptibility of synovial membrane for microorganism.

• #10 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Septic arthritis is inflammation of the joints secondary to an infectious etiology such as bacterial, fungal, mycobacterial, viral, or other pathogens. […] Septic arthritis occurs when there is a bacterial invasion of the synovium and joint space followed by an inflammatory process. Inflammatory cytokines and proteases mediate joint destruction. Other factors which play a role in joint damage are bacterial toxins and microbial surface components like staphylococcal adhesins which promote the binding of the bacteria to intra-articular proteins. […] The highly vascularized joint synovium lacks a limiting basement membrane so is prone to infection via hematogenous seeding from systemic infection. Septic arthritis may also result from direct injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis may occur.

• #11 Pulsenotes | Septic arthritis notes

  https://app.pulsenotes.com/surgery/orthopaedics/notes/septic-arthritis

  Septic arthritis arises when bacteria (or other pathogens) enter the synovium. […] Haematogenous spread is the most common mechanism by which bacteria infect the joint. Bacteria in the bloodstream seed into a joint and infection results. […] The synovium is a specialised membrane that is well vascularised and lacks a basement membrane. The lack of a limiting basement membrane makes it susceptible to infection. […] Bacteria colonise the synovial fluid and an inflammatory response is generated. In immunocompetent patients, the immune response may eliminate the pathogen and clear the infection. If the infection continues, inflammation leads to worsening joint effusion with a resulting rise in the intra-articular pressure impairing the vascular supply. Untreated, infection becomes systemic and joint destruction occurs.

• #12 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response along with bacterial virulence factors damages articular surface and cartilage. […] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection. […] Determinants of hematogenous seeding: Well vascularized synovium, Absence of limiting basement membrane, Recent joint surgery, induces the production of host-derived extracellular matrix proteins (e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection, Virulence of microorganism, Susceptibility of synovial membrane for microorganism.

• #13 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  Staphylococcus aureus is the most commonly cultured organism. […] Antibiotic coverage should start in suspected cases when blood cultures and a serologic test and microscopic analysis of synovial fluid collected from the affected joint are the initial steps in diagnosing septic arthritis. […] Standard treatment consists of irrigation and debridement of the affected joint, followed by intravenous antibiotics. […] In order to limit the risk of lifelong disability, making a fast diagnosis and treatment plan for ASA patients is crucial. […] These topics continue to be the subject of debate among experts, and unfortunately, the literature has no consensus about the etiology, the best treatment, and the diagnosis method available for ASA patients. […] The primary routes of joint infection include: 1) Hematogenous spread: pathogenic bacteria of the infection foci in other parts of the body spread to the joint through the blood circulation; hematogenous spread of infection is the most common etiology of shoulder sepsis; 2) Adjacent infection: the pathogenic bacteria come from the skin and soft tissue infection around the joint or secondary intra-articular infection after osteomyelitis; 3) Iatrogenic: such as secondary infection following joint cavity puncture or medicament injection, or secondary intra-articular infection following joint replacement and per-articular fracture internal fixation and implantation; 4) Traumatic, including trauma, stab wounds, and animal bites, resulting in joint soft tissue or joint infection after articular sac injury.

• #14 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  Expression of host-derived protein products meant to promote joint healing can inadvertently further promote bacterial colonization. Furthermore, low fluid within the enclosed joint space can further encourage bacterial infection. […] S. aureus and S. pneumoniae share virulence factors integral to joint infection. Such virulence factors include fibronectin-binding proteins (FNBPs). FNBP gene knockout models revealed that FNBP is required for full virulence, as exhibited by weight loss, organ abscesses, and joint infections. […] Joint bacterial infection stimulates the recruitment of immune cells and the production of pro-inflammatory cytokines. Murine synovial tissue samples of septic joints revealed a large influx of macrophages, neutrophils, tumor necrosis factors (TNF-), and interferons (IFN-).

• #15 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties. […] Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. […] Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process. […] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction. […] After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response.

• #16 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #17 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #18 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #19 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #20 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #21 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #22 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  There are three stages to the pathophysiology of septic arthritis: 1) serous exudation stage: after pathogenic bacteria enter the joints, synovial congestion and edema, leukocyte infiltration, and serous exudation, there is typically no obvious damage to articular cartilage at this stage; if active treatment is administered, the exudate can be completely absorbed, the articular cartilage will not be destroyed, and the joint function will not be compromised. 2) Serous fibrinous exudation stage: the disease progresses, the exudate becomes turbid, the number of white blood cells and pus cells increases dramatically, synovitis worsens, vascular permeability increases and fibrin deposition causes articular cartilage rupture, ulcers, and shedding. The cartilage is uneven, resulting in poor joint function. 3) Purulent exudation stage: Inflammation progresses, the articular cartilage is involved, the subchondral bone and synovium are also destroyed, the soft tissues surrounding the joints can also be involved in cellulitis, the exudate is purulent, and the process is irreversible and causes severe dysfunction. […] Septic arthritis is on the rise, associated with an aging population, an increase in the number of invasive procedures performed, and an increase in the number of patients receiving immunosuppressive therapy. More research is needed on the topic to reach a consensus on the epidemiology of ASA.

• #23 Septic Arthritis: Background, Etiology and Pathophysiology, Prognosis

  https://emedicine.medscape.com/article/236299-overview

  The term Septic Arthritis (SA) represents an invasion of a joint space by a variety of microorganisms, most commonly bacteria. Various types of viruses, mycobacteria, and fungi also may be involved. This discussion will focus primarily on the bacterial pathogens. Despite timely institution of appropriate treatment, SA continues to produce significant rates of morbidity and mortality. […] Organisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or most commonly, via the bloodstream. […] The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism’s pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host’s polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans.

• #24 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Septic arthritis is inflammation of the joints secondary to an infectious etiology such as bacterial, fungal, mycobacterial, viral, or other pathogens. […] Septic arthritis occurs when there is a bacterial invasion of the synovium and joint space followed by an inflammatory process. Inflammatory cytokines and proteases mediate joint destruction. Other factors which play a role in joint damage are bacterial toxins and microbial surface components like staphylococcal adhesins which promote the binding of the bacteria to intra-articular proteins. […] The highly vascularized joint synovium lacks a limiting basement membrane so is prone to infection via hematogenous seeding from systemic infection. Septic arthritis may also result from direct injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis may occur.

• #25 Septic Arthritis: Background, Etiology and Pathophysiology, Prognosis

  https://emedicine.medscape.com/article/236299-overview

  The term Septic Arthritis (SA) represents an invasion of a joint space by a variety of microorganisms, most commonly bacteria. Various types of viruses, mycobacteria, and fungi also may be involved. This discussion will focus primarily on the bacterial pathogens. Despite timely institution of appropriate treatment, SA continues to produce significant rates of morbidity and mortality. […] Organisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or most commonly, via the bloodstream. […] The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism’s pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host’s polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans.

• #26 Acute Infectious Arthritis – Musculoskeletal and Connective Tissue Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/infections-of-joints-and-bones/acute-infectious-arthritis

  Infecting organisms multiply in the synovial fluid and synovial lining. Some bacteria (eg, S. aureus) produce virulence factors (adhesins), which allow bacteria to penetrate, remain within, and infect joint tissues. Other bacterial products (eg, endotoxin from gram-negative organisms, cell wall fragments, exotoxins from gram-positive organisms, immune complexes formed by bacterial antigens and host antibodies) augment the inflammatory reaction. […] Neutrophils migrate into the joint and phagocytose the infecting organisms. Phagocytosis of bacteria also results in neutrophil autolysis with release of lysosomal enzymes into the joint, which damages synovia, ligaments, and cartilage. Therefore, neutrophils are both the major host defense system and the cause of joint damage. Articular cartilage can be destroyed within hours or days.

• #27 Acute Infectious Arthritis – Musculoskeletal and Connective Tissue Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/infections-of-joints-and-bones/acute-infectious-arthritis

  Infecting organisms multiply in the synovial fluid and synovial lining. Some bacteria (eg, S. aureus) produce virulence factors (adhesins), which allow bacteria to penetrate, remain within, and infect joint tissues. Other bacterial products (eg, endotoxin from gram-negative organisms, cell wall fragments, exotoxins from gram-positive organisms, immune complexes formed by bacterial antigens and host antibodies) augment the inflammatory reaction. […] Neutrophils migrate into the joint and phagocytose the infecting organisms. Phagocytosis of bacteria also results in neutrophil autolysis with release of lysosomal enzymes into the joint, which damages synovia, ligaments, and cartilage. Therefore, neutrophils are both the major host defense system and the cause of joint damage. Articular cartilage can be destroyed within hours or days.

• #28 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Due to rapid proliferation of bacteria predisposes to activation of host acute inflammatory response. […] Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium. […] Activation of acute phase reactants by Interleukins. […] Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system. […] Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide. […] As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immune system is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.

• #29 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties. […] Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. […] Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process. […] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction. […] After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response.

• #30 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  Among the bacterial factors that mediate adherence is the Microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). […] It was observed that mice which was infected with a mutant strain devoid for the collagen adhesin gene, showed 43% low occurrence of septic arthritis than in the corresponding wild type. […] These biofilm bacteria exhibit altered phenotypes called small colony variants (SCVs) that exhibit slow growth and such forms are capable of intracellular persistence within the osteoblasts, fibroblasts, neutrophils etc. […] This property enables the pathogen to evade the immune attack while displaying higher recalcitrance towards deployed antibiotics. […] Following a bacterial seeding, the bacterial products and toxins initiate the inflammatory cascade characterized by an influx of immune cells, neutrophils, activation of macrophages, and release of inflammatory cytokines such as IL-1, IL-6, TNF-, MIP-2, Granulocyte-macrophage colony-stimulating factor (GM-CSF).

• #31 Septic arthritis: immunopathogenesis, experimental models and therapy | Journal of Venomous Animals and Toxins including Tropical Diseases | Full Text

  https://jvat.biomedcentral.com/articles/10.1186/1678-9199-20-19

  Septic arthritis is an inflammatory disease of the joints that is started by an infection whose most common agent is Staphylococcus aureus. […] The initial focus of joint destruction is usually the cartilage-synovium junction, with pannus formation and subsequent cartilage and bone destruction. […] The speed and accuracy of treatment are decisive for the outcome of SA. […] Host and bacterial factors are considered to be of pathogenic importance during SA. […] The immunopathogenetic characteristics described below are all related to this etiological agent. […] It is well established that, in addition to bacterial virulence factors, the host immune response plays an important role in the joint-damaging process. […] One of the hallmarks of septic arthritis is the massive inflammation that precedes cartilage and bone erosion.

• #32 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  Expression of host-derived protein products meant to promote joint healing can inadvertently further promote bacterial colonization. Furthermore, low fluid within the enclosed joint space can further encourage bacterial infection. […] S. aureus and S. pneumoniae share virulence factors integral to joint infection. Such virulence factors include fibronectin-binding proteins (FNBPs). FNBP gene knockout models revealed that FNBP is required for full virulence, as exhibited by weight loss, organ abscesses, and joint infections. […] Joint bacterial infection stimulates the recruitment of immune cells and the production of pro-inflammatory cytokines. Murine synovial tissue samples of septic joints revealed a large influx of macrophages, neutrophils, tumor necrosis factors (TNF-), and interferons (IFN-).

• #33 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Due to rapid proliferation of bacteria predisposes to activation of host acute inflammatory response. […] Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium. […] Activation of acute phase reactants by Interleukins. […] Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system. […] Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide. […] As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immune system is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.

• #34 Septic arthritis: immunopathogenesis, experimental models and therapy | Journal of Venomous Animals and Toxins including Tropical Diseases | Full Text

  https://jvat.biomedcentral.com/articles/10.1186/1678-9199-20-19

  Cytokines released from macrophages such as TNF-, IL-1 and IL-6 have been classically indicated as the major players of the severe inflammation that precedes cartilage and bone destruction during SA. […] The contribution of SAg to SA has been clearly observed in experimental arthritis. […] The direct contribution of bacterial products to the recruitment of PMNs was demonstrated by Gjertsson et al. […] The elevated virulence of S. aureus compared to other infectious agents has been, at least partially, attributed to the many immune evasion strategies presented by this pathogen. […] The massive inflammation that precedes cartilage and bone erosion is a key feature of septic arthritis. […] The presence of CP5, in comparison to its absence, leads to a higher frequency of arthritis and also to a more severe form of the disease. […] The combination of a tumor necrosis factor inhibitor and antibiotic alleviates staphylococcal arthritis and sepsis in mice.

• #35 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Due to rapid proliferation of bacteria predisposes to activation of host acute inflammatory response. […] Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium. […] Activation of acute phase reactants by Interleukins. […] Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system. […] Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide. […] As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immune system is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.

• #36 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  This inflammatory reaction mounted by the host is protective and along with antibiotic therapy may help to contain the spread of infection further. […] But, if in case the infection is not cleared, there continues an ongoing battle of the host mounted an immune response against bacteria and the immune system exacerbates rather than ameliorates the outcome of septic arthritis. […] Soon, the T-cells also start to enter the joint cavity and get activated upon antigen presentation supported by host antigen-presenting cells (APCs). […] High levels of cytokines induce the release of host matrix metalloproteinases (stromelysin and collagenases) and lysosomal enzymes, which further worsen joint degradation. […] As the intra-articular pressure rises, the synovial vasculature may get compressed with thrombosis and further permanent damage to the articular cartilage impeding the blood and oxygen supply as well.

• #37 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Potent activation of immune system and release of cytokines and oxygen free radicals. […] Activation and release of Metalloproteinases, Lysosomal enzymes and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells. […] Further damage of joint by bacterial toxins. […] Infectious process and inflammatory response lead to joint effusion. […] Increased intra-articular pressure. […] Mechanical obstruction to the joint blood supply. […] Further destruction of bone and cartilage.

• #38 Septic arthritis of the hand: Current issues of etiology, pathogenesis, diagnosis, treatment

  https://www.wjgnet.com/2218-5836/full/v13/i7/622.htm

  Pathogenic microorganisms that have penetrated into the joint produce substances that promote their adhesion and protection from humoral and cellular immunity factors. […] The multiplication of bacteria leads to the spread of infection. […] The production of proinflammatory cytokines (interleukin 1-, interleukin-6, tumor necrosis factor-, etc.) begins along with the activation of the complement system. […] If it is impossible to eliminate the infection, the immunological response continues to develop with the formation of byproducts that lead to the release of matrix proteinases and lysosomal enzymes. […] They, in combination with bacterial toxins, cause the degradation of host collagen. […] The formed articular effusion disrupts the nutrition of chondrocytes, contributing to the occurrence of cartilage destruction.

• #39 Neutrophils: Beneficial and Harmful Cells in Septic Arthritis

  https://www.mdpi.com/1422-0067/19/2/468

  The role of neutrophils in the pathogenesis of septic arthritis is dual. On the one hand, they are indispensable in the early phase of disease for effective defense against bacteria and consequently for host survival. On the other hand, these leukocytes act as mediators of tissue-destructive events. The massive infiltration of neutrophils into the infected joint can contribute to cartilage and bone destruction by the release of free radicals and bacteria- and tissue-degrading enzymes, including products of the NADPH oxidase complex and proteolytic enzymes targeting collagen and/or proteoglycans. Permanent destruction of cartilage and subchondral bone loss can occur within three days after infection. Elimination of neutrophils from the site of inflammation is a prerequisite for resolution of the acute inflammatory response. This implicates that prolonged presence of neutrophils at the site of inflammation can lead to persistence of the inflammatory response, associated with complications such as tissue damage.

• #40 Neutrophils: Beneficial and Harmful Cells in Septic Arthritis

  https://www.mdpi.com/1422-0067/19/2/468

  The role of neutrophils in the pathogenesis of septic arthritis is dual. On the one hand, they are indispensable in the early phase of disease for effective defense against bacteria and consequently for host survival. On the other hand, these leukocytes act as mediators of tissue-destructive events. The massive infiltration of neutrophils into the infected joint can contribute to cartilage and bone destruction by the release of free radicals and bacteria- and tissue-degrading enzymes, including products of the NADPH oxidase complex and proteolytic enzymes targeting collagen and/or proteoglycans. Permanent destruction of cartilage and subchondral bone loss can occur within three days after infection. Elimination of neutrophils from the site of inflammation is a prerequisite for resolution of the acute inflammatory response. This implicates that prolonged presence of neutrophils at the site of inflammation can lead to persistence of the inflammatory response, associated with complications such as tissue damage.

• #41 Septic Arthritis: Background, Etiology and Pathophysiology, Prognosis

  https://emedicine.medscape.com/article/236299-overview

  As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection. […] The pathogen of Lyme disease, Borrelia burgdorferi, commonly produces a septic arthritis picture. […] This appears to result from ongoing synovial inflammation due to persistent vascular damage, and autoimmune processes that interfere with appropriate tissue healing.

• #42 Septic arthritis: immunopathogenesis, experimental models and therapy | Journal of Venomous Animals and Toxins including Tropical Diseases | Full Text

  https://jvat.biomedcentral.com/articles/10.1186/1678-9199-20-19

  Septic arthritis is an inflammatory disease of the joints that is started by an infection whose most common agent is Staphylococcus aureus. […] The initial focus of joint destruction is usually the cartilage-synovium junction, with pannus formation and subsequent cartilage and bone destruction. […] The speed and accuracy of treatment are decisive for the outcome of SA. […] Host and bacterial factors are considered to be of pathogenic importance during SA. […] The immunopathogenetic characteristics described below are all related to this etiological agent. […] It is well established that, in addition to bacterial virulence factors, the host immune response plays an important role in the joint-damaging process. […] One of the hallmarks of septic arthritis is the massive inflammation that precedes cartilage and bone erosion.

• #43 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Potent activation of immune system and release of cytokines and oxygen free radicals. […] Activation and release of Metalloproteinases, Lysosomal enzymes and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells. […] Further damage of joint by bacterial toxins. […] Infectious process and inflammatory response lead to joint effusion. […] Increased intra-articular pressure. […] Mechanical obstruction to the joint blood supply. […] Further destruction of bone and cartilage.

• #44 Septic arthritis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/bone-and-joint-infections/symptoms-causes/syc-20350755

  Septic arthritis is a painful infection in a joint that can come from germs that travel through your bloodstream from another part of your body. […] The lining of your joints has little ability to protect itself from infection. Your body’s reaction to the infection including inflammation that can increase pressure and reduce blood flow within the joint contributes to the damage. […] If treatment is delayed, septic arthritis can lead to joint degeneration and permanent damage. If septic arthritis affects an artificial joint, complications may include joint loosening or dislocation.

• #45 Septic Arthritis: Background, Etiology and Pathophysiology, Prognosis

  https://emedicine.medscape.com/article/236299-overview

  As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection. […] The pathogen of Lyme disease, Borrelia burgdorferi, commonly produces a septic arthritis picture. […] This appears to result from ongoing synovial inflammation due to persistent vascular damage, and autoimmune processes that interfere with appropriate tissue healing.

• #46 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  This inflammatory reaction mounted by the host is protective and along with antibiotic therapy may help to contain the spread of infection further. […] But, if in case the infection is not cleared, there continues an ongoing battle of the host mounted an immune response against bacteria and the immune system exacerbates rather than ameliorates the outcome of septic arthritis. […] Soon, the T-cells also start to enter the joint cavity and get activated upon antigen presentation supported by host antigen-presenting cells (APCs). […] High levels of cytokines induce the release of host matrix metalloproteinases (stromelysin and collagenases) and lysosomal enzymes, which further worsen joint degradation. […] As the intra-articular pressure rises, the synovial vasculature may get compressed with thrombosis and further permanent damage to the articular cartilage impeding the blood and oxygen supply as well.

• #47 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  MMPs represent important mediators in the synovial tissue destruction and pathogenesis of septic arthritis. […] MMP expression is elevated in septic and aseptic arthritis and this contributes to tissue destruction owing to their capability of degrading extracellular matrix (ECM). […] Therefore, one approach directed towards neutralization of key MMPs and studying the effect on disease progression seems worth exploring. […] The bacterial clearance was also higher from joint and spleen as seen in ST2-/- mice and the infection remained localized and this was possibly due to the fact that higher expression of iNOS and higher levels of nitric oxide (NO) was observed in ST2-/- mice. […] Thus, it was concluded that ST2 deficiency was associated with induction and enhancement of Th1 cell types leading to activation of neutrophils and macrophages with IFN- production, enhanced iNOS expression and improved bacterial killing resulting in effective resolution of infection thus suggesting that ST2 deficiency is beneficial in S. aureus-induced septic arthritis.

• #48 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  MMPs represent important mediators in the synovial tissue destruction and pathogenesis of septic arthritis. […] MMP expression is elevated in septic and aseptic arthritis and this contributes to tissue destruction owing to their capability of degrading extracellular matrix (ECM). […] Therefore, one approach directed towards neutralization of key MMPs and studying the effect on disease progression seems worth exploring. […] The bacterial clearance was also higher from joint and spleen as seen in ST2-/- mice and the infection remained localized and this was possibly due to the fact that higher expression of iNOS and higher levels of nitric oxide (NO) was observed in ST2-/- mice. […] Thus, it was concluded that ST2 deficiency was associated with induction and enhancement of Th1 cell types leading to activation of neutrophils and macrophages with IFN- production, enhanced iNOS expression and improved bacterial killing resulting in effective resolution of infection thus suggesting that ST2 deficiency is beneficial in S. aureus-induced septic arthritis.

• #49 Novel therapeutic interventions towards improved management of septic arthritis | BMC Musculoskeletal Disorders | Full Text

  https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-021-04383-6

  This inflammatory reaction mounted by the host is protective and along with antibiotic therapy may help to contain the spread of infection further. […] But, if in case the infection is not cleared, there continues an ongoing battle of the host mounted an immune response against bacteria and the immune system exacerbates rather than ameliorates the outcome of septic arthritis. […] Soon, the T-cells also start to enter the joint cavity and get activated upon antigen presentation supported by host antigen-presenting cells (APCs). […] High levels of cytokines induce the release of host matrix metalloproteinases (stromelysin and collagenases) and lysosomal enzymes, which further worsen joint degradation. […] As the intra-articular pressure rises, the synovial vasculature may get compressed with thrombosis and further permanent damage to the articular cartilage impeding the blood and oxygen supply as well.

• #50 Septic Arthritis: Background, Etiology and Pathophysiology, Prognosis

  https://emedicine.medscape.com/article/236299-overview

  As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection. […] The pathogen of Lyme disease, Borrelia burgdorferi, commonly produces a septic arthritis picture. […] This appears to result from ongoing synovial inflammation due to persistent vascular damage, and autoimmune processes that interfere with appropriate tissue healing.

• #51 Septic arthritis of the hand: Current issues of etiology, pathogenesis, diagnosis, treatment

  https://www.wjgnet.com/2218-5836/full/v13/i7/622.htm

  Experimental studies have shown that cartilage surface erosion, degeneration and necrosis of chondrocytes appear starting from 24 h after intra-articular injection of bacteria. […] Clinical studies indicate that delaying treatment by more than 10 days leads to the development of osteomyelitis. […] Undoubtedly, timely treatment is the most important factor preventing the occurrence of osteochondral destruction in purulent arthritis, which was proven by a study in which, with an average treatment delay of 5.4 d, osteomyelitis was not detected in any case.

• #52

  https://www.orthobullets.com/trauma/1058/septic-arthritis–adult

  Septic Arthritis is the inflammation of the joints secondary to an infectious etiology, most commonly affecting the knee, hip, and shoulder. […] Diagnosis is made with an aspiration of joint fluid with a WBC count 50,000 being considered diagnostic for septic arthritis. Lower counts may still indicate infection in the presence of positive gram stains or cultures results. […] Treatment is usually urgent surgical irrigation and debridement followed by culture directed IV antibiotics. […] 3 etiologies of bacterial seeding of joint: bacteremia, direct inoculation from trauma or surgery, contiguous spread from adjacent osteomyelitis. […] Septic arthritis causes irreversible cartilage destruction in an involved joint; cartilage injury can occur by 8 hours. […] Caused by release of proteolytic enzymes from inflammatory cells (PMNs). […] Most common pathogens is staphylococcus aureus (accounts for 50% of cases). […] Delayed diagnosis can lead to profound, extensive cartilage damage within 8 hours.

• #53 Septic arthritis | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/septic-arthritis?lang=us

  Septic arthritis can cause rapid chondrolysis and destructive arthropathy. Intra-articular infection usually manifests with severe pain and decreased range of motion. Prompt treatment can avoid permanent damage to the joint which may result in chronic deformity, mechanical arthritis and even death. […] In the absence of trauma or recent instrumentation of the joint, septic arthritis is usually secondary to hematogenous seeding. Staphylococcus aureus is the most commonly isolated agent and Streptococci spp. are common; both these organisms can cause rapid joint destruction. Other pathogens include Pseudomonas, Escherichia coli, and Serratus. […] If unrecognised and left untreated, septic arthritis can result in irreversible joint damage within 48 hours of the onset of infection due to the proteolytic enzymes of the white blood cells that flood the infected synovial space. Osteonecrosis is also an important sequela of septic arthritis due to effusion and an increase in intra-articular pressure which compromises blood circulation. […] The treatment principle for septic arthritis is prompt drainage of purulent fluid and appropriate antibiotics.

• #54 Septic Arthritis: Diagnosis and Treatment | AAFP

  https://www.aafp.org/pubs/afp/issues/2021/1200/p589.html

  Septic arthritis must be considered and promptly diagnosed in any patient presenting with acute atraumatic joint pain, swelling, and fever. […] A delay in diagnosis and treatment can result in permanent morbidity and mortality. […] Subcartilaginous bone loss, cartilage destruction, and permanent joint dysfunction can occur if appropriate antibiotic therapy is not initiated within 24 to 48 hours of onset. […] The reported incidence of septic arthritis is four to 29 cases per 100,000 person-years, and risk increases with age, use of immunosuppressive medications, and lower socioeconomic status. […] A joint is most commonly infected hematogenously from bacteremia. […] Septic arthritis is diagnosed through laboratory testing, particularly synovial fluid studies. […] Analysis of synovial fluid obtained via arthrocentesis is necessary to differentiate septic arthritis from other forms of arthritis and to determine the causative pathogen.

• #55 Septic Joint

  https://mobile.fpnotebook.com/Rheum/ID/SptcJnt.htm

  Hematologic seeding in most cases from Occult Bacteremia. Once joint seeding occurs, infection progresses rapidly. Joint is susceptable to hematogenous spread. Synovial lining lacks a protective basement membrane. […] Joint infection leads to rapid joint destruction. Inflammatory reaction directly associated with infection. Intra-articular pressure with secondary vascular compromise. Risk of permanent joint injury increases when appropriate Antibiotics are delayed 24-48 from onset.

• #56 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  These immunological mediators act on the joint and promote bone resorption by forming an infectious nidus. […] It has been proposed that the host’s inflammatory response against the pathogen results in collateral damage, increasing mortality rates, and joint destruction. […] Several risk factors contribute to the pathogenesis of pyogenic arthritis. The regression-variable analysis identified positive associations between smoking, increasing age, rheumatoid arthritis, skin infections, and extensive joint involvement with pyogenic arthritis. […] Proposed theories suggest that abnormal joint remodeling and neovascularization in OA and RA promote bacterial colonization of the subchondral bone and synovium. […] Joint arthroplasty procedures are another common cause of joint infections. […] Newly implanted joints undergo environmental remodeling through fibrinogen and fibronectin coating, with these host proteins serving as potential bacterial adherence points. […] These findings suggest the relevance of underlying joint disease and associated increased risk of joint infection.

• #57 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  These immunological mediators act on the joint and promote bone resorption by forming an infectious nidus. […] It has been proposed that the host’s inflammatory response against the pathogen results in collateral damage, increasing mortality rates, and joint destruction. […] Several risk factors contribute to the pathogenesis of pyogenic arthritis. The regression-variable analysis identified positive associations between smoking, increasing age, rheumatoid arthritis, skin infections, and extensive joint involvement with pyogenic arthritis. […] Proposed theories suggest that abnormal joint remodeling and neovascularization in OA and RA promote bacterial colonization of the subchondral bone and synovium. […] Joint arthroplasty procedures are another common cause of joint infections. […] Newly implanted joints undergo environmental remodeling through fibrinogen and fibronectin coating, with these host proteins serving as potential bacterial adherence points. […] These findings suggest the relevance of underlying joint disease and associated increased risk of joint infection.

• #58 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  These immunological mediators act on the joint and promote bone resorption by forming an infectious nidus. […] It has been proposed that the host’s inflammatory response against the pathogen results in collateral damage, increasing mortality rates, and joint destruction. […] Several risk factors contribute to the pathogenesis of pyogenic arthritis. The regression-variable analysis identified positive associations between smoking, increasing age, rheumatoid arthritis, skin infections, and extensive joint involvement with pyogenic arthritis. […] Proposed theories suggest that abnormal joint remodeling and neovascularization in OA and RA promote bacterial colonization of the subchondral bone and synovium. […] Joint arthroplasty procedures are another common cause of joint infections. […] Newly implanted joints undergo environmental remodeling through fibrinogen and fibronectin coating, with these host proteins serving as potential bacterial adherence points. […] These findings suggest the relevance of underlying joint disease and associated increased risk of joint infection.

• #59 Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11364462/

  These immunological mediators act on the joint and promote bone resorption by forming an infectious nidus. […] It has been proposed that the host’s inflammatory response against the pathogen results in collateral damage, increasing mortality rates, and joint destruction. […] Several risk factors contribute to the pathogenesis of pyogenic arthritis. The regression-variable analysis identified positive associations between smoking, increasing age, rheumatoid arthritis, skin infections, and extensive joint involvement with pyogenic arthritis. […] Proposed theories suggest that abnormal joint remodeling and neovascularization in OA and RA promote bacterial colonization of the subchondral bone and synovium. […] Joint arthroplasty procedures are another common cause of joint infections. […] Newly implanted joints undergo environmental remodeling through fibrinogen and fibronectin coating, with these host proteins serving as potential bacterial adherence points. […] These findings suggest the relevance of underlying joint disease and associated increased risk of joint infection.

• #60 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Infection of the sternoclavicular and sacroiliac joint often occur in patients with IV drug abuse and usually involve serratia and pseudomonas. […] Joints previously damaged especially in patients with rheumatoid arthritis are highly susceptible to infection. The organisms damage the articular cartilage along the lateral edges of the joint. Effusions are common and often associated with pain. […] The incidence of septic arthritis peaks between ages 2 and 3 years and has a male predominance. […] Despite antibiotic use, there is a 7% to 15% mortality rate for in-hospital septic arthritis. Morbidity from septic arthritis occurs in one-third of patients. Both morbidity and mortality increase with patient age, comorbid conditions including pre-existing joint disease, and prior synthetic intra-articular material. This underscores the need for a high index of suspicion, early diagnosis and prompt treatment for septic arthritis especially in patients with known predisposing risk factors and comorbid conditions.

• #61 Septic Arthritis: What Is It, Symptoms, Treatment & Causes

  https://my.clevelandclinic.org/health/diseases/22418-septic-arthritis

  Septic arthritis cannot go away on its own since its an infection. Bacterial infections need to be treated with antibiotics. […] Despite the use of antibiotics for treatment, theres a 7% to 15% mortality (death) rate for septic arthritis. […] Septic arthritis is a serious condition. Complications of septic arthritis can include: […] Osteomyelitis (inflammation or swelling in the bone). […] Septic arthritis is a rare but serious condition. The good news is that its treatable.

• #62 Septic Arthritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK538176/

  Infection of the sternoclavicular and sacroiliac joint often occur in patients with IV drug abuse and usually involve serratia and pseudomonas. […] Joints previously damaged especially in patients with rheumatoid arthritis are highly susceptible to infection. The organisms damage the articular cartilage along the lateral edges of the joint. Effusions are common and often associated with pain. […] The incidence of septic arthritis peaks between ages 2 and 3 years and has a male predominance. […] Despite antibiotic use, there is a 7% to 15% mortality rate for in-hospital septic arthritis. Morbidity from septic arthritis occurs in one-third of patients. Both morbidity and mortality increase with patient age, comorbid conditions including pre-existing joint disease, and prior synthetic intra-articular material. This underscores the need for a high index of suspicion, early diagnosis and prompt treatment for septic arthritis especially in patients with known predisposing risk factors and comorbid conditions.

• #63 Septic Arthritis: What Is It, Symptoms, Treatment & Causes

  https://my.clevelandclinic.org/health/diseases/22418-septic-arthritis

  Septic arthritis cannot go away on its own since its an infection. Bacterial infections need to be treated with antibiotics. […] Despite the use of antibiotics for treatment, theres a 7% to 15% mortality (death) rate for septic arthritis. […] Septic arthritis is a serious condition. Complications of septic arthritis can include: […] Osteomyelitis (inflammation or swelling in the bone). […] Septic arthritis is a rare but serious condition. The good news is that its treatable.

• #64

  https://www.orthobullets.com/pediatrics/4032/hip-septic-arthritis–pediatric

  Pediatric Septic Hip Arthritis is an intra-articular infection in children that peaks in the first few years of life. […] Etiology Mechanism direct inoculation from trauma or surgery (skin penetration) […] hematogenous seeding upper respiratory infection precedes about 80% of the cases […] extension from adjacent bone (osteomyelitis) can develop from contiguous spread of osteomyelitis […] Pathophysiology enzymatic destruction release of proteolytic enzymes (matrix metalloproteinases) from inflammatory and synovial cells, cartilage, and bacteria which may cause articular surface damage within 8 hours […] increased joint pressure may cause femoral head osteonecrosis if not relieved promptly.

• #65 Septic arthritis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/bone-and-joint-infections/symptoms-causes/syc-20350755

  Septic arthritis is a painful infection in a joint that can come from germs that travel through your bloodstream from another part of your body. […] The lining of your joints has little ability to protect itself from infection. Your body’s reaction to the infection including inflammation that can increase pressure and reduce blood flow within the joint contributes to the damage. […] If treatment is delayed, septic arthritis can lead to joint degeneration and permanent damage. If septic arthritis affects an artificial joint, complications may include joint loosening or dislocation.

• #66 Septic Arthritis | Children’s Hospital of Philadelphia

  https://www.chop.edu/conditions-diseases/septic-arthritis

  If septic arthritis is treated fast enough, long-term damage to the joint is usually minimal. However, the risk of permanent damage to the joint or surrounding tissues is increased if: There is knee, hip or shoulder involvement, Your child is younger than one year old when diagnosed, Your child’s symptoms were left untreated for too long. […] Permanent damage could lead to decreased mobility, growth problems, chronic pain, or increased risk of fracture.

• #67 Septic Arthritis | Children’s Hospital of Philadelphia

  https://www.chop.edu/conditions-diseases/septic-arthritis

  If septic arthritis is treated fast enough, long-term damage to the joint is usually minimal. However, the risk of permanent damage to the joint or surrounding tissues is increased if: There is knee, hip or shoulder involvement, Your child is younger than one year old when diagnosed, Your child’s symptoms were left untreated for too long. […] Permanent damage could lead to decreased mobility, growth problems, chronic pain, or increased risk of fracture.

• #68 Septic Arthritis | Children’s Hospital of Philadelphia

  https://www.chop.edu/conditions-diseases/septic-arthritis

  If septic arthritis is treated fast enough, long-term damage to the joint is usually minimal. However, the risk of permanent damage to the joint or surrounding tissues is increased if: There is knee, hip or shoulder involvement, Your child is younger than one year old when diagnosed, Your child’s symptoms were left untreated for too long. […] Permanent damage could lead to decreased mobility, growth problems, chronic pain, or increased risk of fracture.

• #69 Septic arthritis: immunopathogenesis, experimental models and therapy | Journal of Venomous Animals and Toxins including Tropical Diseases | Full Text

  https://jvat.biomedcentral.com/articles/10.1186/1678-9199-20-19

  Septic arthritis is an inflammatory disease of the joints that is started by an infection whose most common agent is Staphylococcus aureus. […] The initial focus of joint destruction is usually the cartilage-synovium junction, with pannus formation and subsequent cartilage and bone destruction. […] The speed and accuracy of treatment are decisive for the outcome of SA. […] Host and bacterial factors are considered to be of pathogenic importance during SA. […] The immunopathogenetic characteristics described below are all related to this etiological agent. […] It is well established that, in addition to bacterial virulence factors, the host immune response plays an important role in the joint-damaging process. […] One of the hallmarks of septic arthritis is the massive inflammation that precedes cartilage and bone erosion.

• #70 Septic Arthritis: Diagnosis and Treatment | AAFP

  https://www.aafp.org/pubs/afp/issues/2021/1200/p589.html

  Septic arthritis must be considered and promptly diagnosed in any patient presenting with acute atraumatic joint pain, swelling, and fever. […] A delay in diagnosis and treatment can result in permanent morbidity and mortality. […] Subcartilaginous bone loss, cartilage destruction, and permanent joint dysfunction can occur if appropriate antibiotic therapy is not initiated within 24 to 48 hours of onset. […] The reported incidence of septic arthritis is four to 29 cases per 100,000 person-years, and risk increases with age, use of immunosuppressive medications, and lower socioeconomic status. […] A joint is most commonly infected hematogenously from bacteremia. […] Septic arthritis is diagnosed through laboratory testing, particularly synovial fluid studies. […] Analysis of synovial fluid obtained via arthrocentesis is necessary to differentiate septic arthritis from other forms of arthritis and to determine the causative pathogen.

• #71 Septic Arthritis: Diagnosis and Treatment | AAFP

  https://www.aafp.org/pubs/afp/issues/2021/1200/p589.html

  Septic arthritis must be considered and promptly diagnosed in any patient presenting with acute atraumatic joint pain, swelling, and fever. […] A delay in diagnosis and treatment can result in permanent morbidity and mortality. […] Subcartilaginous bone loss, cartilage destruction, and permanent joint dysfunction can occur if appropriate antibiotic therapy is not initiated within 24 to 48 hours of onset. […] The reported incidence of septic arthritis is four to 29 cases per 100,000 person-years, and risk increases with age, use of immunosuppressive medications, and lower socioeconomic status. […] A joint is most commonly infected hematogenously from bacteremia. […] Septic arthritis is diagnosed through laboratory testing, particularly synovial fluid studies. […] Analysis of synovial fluid obtained via arthrocentesis is necessary to differentiate septic arthritis from other forms of arthritis and to determine the causative pathogen.

• #72 Frontiers | An update on recent progress of the epidemiology, etiology, diagnosis, and treatment of acute septic arthritis: a review

  https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1193645/full

  Staphylococcus aureus is the most commonly cultured organism. […] Antibiotic coverage should start in suspected cases when blood cultures and a serologic test and microscopic analysis of synovial fluid collected from the affected joint are the initial steps in diagnosing septic arthritis. […] Standard treatment consists of irrigation and debridement of the affected joint, followed by intravenous antibiotics. […] In order to limit the risk of lifelong disability, making a fast diagnosis and treatment plan for ASA patients is crucial. […] These topics continue to be the subject of debate among experts, and unfortunately, the literature has no consensus about the etiology, the best treatment, and the diagnosis method available for ASA patients. […] The primary routes of joint infection include: 1) Hematogenous spread: pathogenic bacteria of the infection foci in other parts of the body spread to the joint through the blood circulation; hematogenous spread of infection is the most common etiology of shoulder sepsis; 2) Adjacent infection: the pathogenic bacteria come from the skin and soft tissue infection around the joint or secondary intra-articular infection after osteomyelitis; 3) Iatrogenic: such as secondary infection following joint cavity puncture or medicament injection, or secondary intra-articular infection following joint replacement and per-articular fracture internal fixation and implantation; 4) Traumatic, including trauma, stab wounds, and animal bites, resulting in joint soft tissue or joint infection after articular sac injury.

• #73 Septic Arthritis: Diagnosis and Treatment | AAFP

  https://www.aafp.org/pubs/afp/issues/2021/1200/p589.html

  A white blood cell count less than 50,000 per L (50 109 per L) does not exclude septic arthritis. […] Other laboratory tests are being investigated for use in the diagnosis of septic arthritis. […] Septic arthritis caused by methicillin-resistant S. aureus requires drainage or debridement and three to four weeks of antibiotics. […] A large cohort study showed that the 90-day mortality rate for septic arthritis is 7% and increases to 22% to 69% in patients 80 years and older. […] Oligoarticular septic arthritis is associated with higher mortality compared with monoarticular septic arthritis. […] Poor functional outcomes such as amputation, arthrodesis, prosthetic surgery, and severe functional deterioration occur in about 24% to 33% of patients with septic arthritis and are more likely with older age, preexisting joint disease, and synthetic intraarticular material.

• #74 SciELO Brazil – Septic arthritis: immunopathogenesis, experimental models and therapy Septic arthritis: immunopathogenesis, experimental models and therapy

  https://www.scielo.br/j/jvatitd/a/DsNnVcSXmjynPCrJ7Jbgsfg/?lang=en

  The direct contribution of bacterial products to the recruitment of PMNs was demonstrated by Gjertsson et al. […] The contribution of metalloproteinases and a rapid systemic bone resorption have been well characterized in experimental arthritis. […] Even though it is well established that killing the bacteria is essential for controlling SA evolution, this treatment alone will not block the joint-destruction process. […] This realization prompted the association of antibiotics with substances able to counteract this exaggerated immune response.

• #75 Infectious (septic) arthritis: Causes, symptoms, treatment, and risks

  https://www.medicalnewstoday.com/articles/323049

  Having a weakened immune system or a history of other joint problems, such as gout, rheumatoid arthritis, lupus, or osteoarthritis, may also increase the risk as joints that are damaged may be more susceptible to infection. […] Septic arthritis causes severe inflammation that can break down tissue in the joint. This may lead to permanent damage to the cartilage and bone. […] Septic arthritis treatment options can vary depending on which pathogen is causing the condition. […] Because the condition can become severe rapidly, doctors prescribe antibiotics as soon as they suspect infectious arthritis. […] If the antibiotics are effective, the symptoms can improve within 48 hours. However, a person may need IV antibiotics for 24 weeks, depending on the severity of the condition. […] If a person does not receive early, robust treatment, infectious arthritis may cause permanent damage to the tissues and bones in the joint.

• #76 Septic Arthritis: Diagnosis and Treatment | AAFP

  https://www.aafp.org/pubs/afp/issues/2021/1200/p589.html

  A white blood cell count less than 50,000 per L (50 109 per L) does not exclude septic arthritis. […] Other laboratory tests are being investigated for use in the diagnosis of septic arthritis. […] Septic arthritis caused by methicillin-resistant S. aureus requires drainage or debridement and three to four weeks of antibiotics. […] A large cohort study showed that the 90-day mortality rate for septic arthritis is 7% and increases to 22% to 69% in patients 80 years and older. […] Oligoarticular septic arthritis is associated with higher mortality compared with monoarticular septic arthritis. […] Poor functional outcomes such as amputation, arthrodesis, prosthetic surgery, and severe functional deterioration occur in about 24% to 33% of patients with septic arthritis and are more likely with older age, preexisting joint disease, and synthetic intraarticular material.

• #77 AB0937 Clinical Profile and Etiology of Septic Arthritis in Filipino Children: A Three-Year Retrospective Study | Annals of the Rheumatic Diseases

  https://ard.bmj.com/content/74/Suppl_2/1212.4

  Septic arthritis is a joint inflammation caused by intra-articular and hematogenous infection, most common of which are bacterial pathogens. […] Although it accounts for only approximately 6.5% of all childhood arthritides, early diagnosis and prompt treatment are important to prevent permanent disability. […] Timely and appropriate management requires knowledge on the clinical profile of children with septic arthritis and on the current predominant pathogens causing it. […] The most common risk factor reported in pediatric septic arthritis were history of trauma (64.7%) and infection from other sites (52.9%). […] The most common presenting signs and symptoms were swelling (100%), fever (82.4%) and limitation of joint movement (76.5%). […] Culture studies yielded MSSA (33.3%) and MRSA (27.8%) which were sensitive to Oxacillin and Clindamycin respectively. […] Observed increased number of MRSA septic arthritis warrants alteration of first-line treatment from Oxacillin to Clindamycin.

• #78 Septic arthritis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Septic_arthritis_pathophysiology

  Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties. […] Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. […] Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process. […] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction. […] After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response.

• #79 Septic arthritis: pathophysiology, diagnosis, treatment and prevention in the current context

  https://www.medigraphic.com/cgi-bin/new/resumenI.cgi?IDARTICULO=119478

  septic arthritis is a pathology characterized by inflammation of the joints by an infectious agent, commonly bacterial, but also existing viral, mycotic, mycobacterial, and other etiologies. […] bacterial virulence and host immune response play an essential role in its pathophysiology, with the hematogenous route being the leading cause of the pathology. […] Its diagnosis is first of all clinical, through a clinical history and an adequate physical examination, and the use of paraclinical studies to diagnose the pathology is essential. […] Treatment should be based on intravenous antibiotic therapy and synovial fluid drainage. […] due to its incidence, rapid presentation, and complications, an established strategic plan should be developed for its prompt diagnosis and treatment.

• #80 Septic Arthritis and Tuberculosis Arthritis

  https://www.iomcworld.org/open-access/septic-arthritis-and-tuberculosis-arthritis-45637.html

  Once the synovial fluid (SF) is colonized, bacteria proliferate rapidly and generate an acute inflammatory response. Under these circumstances, the host produces inflammatory cytokines, such as interleukin 1- (IL-1) and interleukin 6 (IL-6), that promote opsonization and activation of the complement system. […] Progression of the infection generates joint effusion, which increases intra-articular pressure that may result in further cartilage and bone loss.

• #81 Septic Arthritis (Infectious Arthritis) in Children

  https://www.nationwidechildrens.org/conditions/health-library/septic-arthritis-infectious-arthritis-in-children

  Septic arthritis is an infection in the joint fluid (synovial fluid) and joint tissues. It occurs more often in children than in adults. The infection usually reaches the joints through the bloodstream. In some cases, joints may become infected because of an injection, surgery, or injury. […] Different types of bacteria, viruses, and fungi can infect a joint. The most common type of bacteria that cause septic arthritis is Staphylococcus aureus (S. aureus or staph). These bacteria can enter the body in many ways, such as: An infection that spreads from another place on the body, such as the skin or genitals. […] Septic arthritis needs treatment right away with antibiotics if bacteria are the source of infection. This can improve symptoms within 48 hours. […] If bacteria are the source of infection, quick treatment with antibiotics is needed to stop the risk for joint damage.

• #82 Septic arthritis | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/septic-arthritis?lang=us

  Septic arthritis can cause rapid chondrolysis and destructive arthropathy. Intra-articular infection usually manifests with severe pain and decreased range of motion. Prompt treatment can avoid permanent damage to the joint which may result in chronic deformity, mechanical arthritis and even death. […] In the absence of trauma or recent instrumentation of the joint, septic arthritis is usually secondary to hematogenous seeding. Staphylococcus aureus is the most commonly isolated agent and Streptococci spp. are common; both these organisms can cause rapid joint destruction. Other pathogens include Pseudomonas, Escherichia coli, and Serratus. […] If unrecognised and left untreated, septic arthritis can result in irreversible joint damage within 48 hours of the onset of infection due to the proteolytic enzymes of the white blood cells that flood the infected synovial space. Osteonecrosis is also an important sequela of septic arthritis due to effusion and an increase in intra-articular pressure which compromises blood circulation. […] The treatment principle for septic arthritis is prompt drainage of purulent fluid and appropriate antibiotics.

• #83 Septic arthritis of the hand: Current issues of etiology, pathogenesis, diagnosis, treatment

  https://www.wjgnet.com/2218-5836/coretip/v13/i7/622.htm

  Septic arthritis of the hand often occurs as a result of penetrating wounds. The most common causative agent is Staphylococcus aureus, often characterized by high antibiotic resistance. Delayed treatment of septic arthritis can lead to cartilage destruction and osteomyelitis. To achieve a positive result in the treatment of septic arthritis of the hand, timely surgery, adequate antibiotic therapy and early rehabilitation are necessary.

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