Periodontal infection as a possible severity factor for rheumatoid arthritis.
OBJECTIVE Clinical effects of periodontal treatment on biochemical and clinical markers of disease severity in rheumatoid arthritis ( RA ) patients with periodontal disease were evaluated . METHODS Forty-two patients were assigned to two groups , G1 ( n=16 ) and G2 ( n=26 ) . G1 patients were su bmi tted to oral hygiene instruction and professional tooth cleaning and G2 patients additionally had full-mouth scaling and root planing ( SRP ) . Clinical periodontal measurements were obtained at baseline and 3 months after periodontal treatment . A Health Assessment Question naire ( HAQ ) was used to evaluate their performance on daily living . Rheumatoid factor ( RF ) , erythrocyte sedimentation rate ( ESR ) and drug therapy were assessed . RESULTS Both groups presented a full-mouth improvement in all periodontal clinical parameters ( p<0.05 ) , with the exception of clinical attachment level ( CAL ) and probing pocket depth ( PPD ) > 6 mm for G1 . G2 showed greater mean reductions on PPD > 4 mm than G1 ( p<0.001 ) . HAQ analyses showed a reduction on the degree of disability of G2 , but not statistically significant . ESR was significantly reduced for G2 after SRP although RF did not show statistical reductions . CONCLUSION The data suggest that periodontal treatment with SRP might have an effect on the ESR reduction
REVIEW OBJECTIVE The objective of this systematic review is to identify and synthesis e the best available evidence to examine whether periodontal disease is a risk factor for rheumatoid arthritis .
BACKGROUND Rheumatoid arthritis ( RA ) is a chronic inflammatory disease of unknown aetiology and has a complex multifactorial pathogenesis affecting joints and other tissues .
The natural history of rheumatoid arthritis is poorly defined ; its clinical course fluctuates and the prognosis unpredictable .
Rheumatoid arthritis affects up to 1 - 3 % of the population , with a 3:1 female preponderance disappearing in older age .
There is also evidence of a genetic predisposition to the disease .
Rheumatoid arthritis is characterised by progressive and irreversible damage of the synovial-lined joints causing loss of joint space , bone and function , leading to deformity .
Extracellular matrix degradation is a hallmark of rheumatoid arthritis which is responsible for the typical destruction of cartilage , ligaments , tendons , and bone .
Rheumatoid arthritis is characteristically a symmetric arthritis ( symmetrical swelling of the joints ) .
Articular and periarticular manifestations include joint swelling and tenderness to palpation , with morning stiffness and severe motion impairment in the involved joints .
Extra-articular signs can involve pulmonary , cardiovascular , nervous , and reticuloendothelial systems .
The clinical presentation of rheumatoid arthritis rheumatoid arthritis varies , but an insidious onset of pain with symmetric swelling of the small joints is the most frequent finding .
Rheumatoid arthritis onset is acute or subacute in about 25 % of patients .
Early rheumatoid arthritis is characterised by symmetric polyarthritis involving the small joints of the h and s and feet with no radiologic changes .
Rheumatoid arthritis most frequently affects the metacarpophalangeal , proximal interphalangeal and wrist joints .
Although any joint , including the cricoarytenoid joint , can be affected , the distal interphalangeal , the sacroiliac and the lumbar spine joints are rarely involved , which is peculiar because these are some of the most typical targets of seronegative spondylarthropathies , such as psoriatic arthritis and ankylosing spondylitis .
The clinical manifestations of rheumatoid arthritis vary , depending on the involved joints and the disease stage .
The clinical features of synovitis are particularly apparent in the morning .
Morning stiffness in and around the joints , lasting at least 1 hour before maximal improvement is a typical sign of rheumatoid arthritis .
It is a subjective sign and the patient needs to be carefully informed as to the difference between pain and stiffness .
Morning stiffness duration is related to disease activity .
Progression of rheumatoid arthritis can be measured by laboratory tests and clinical evaluation ( question naires of disease activity and physical examination ) .
Laboratory tests include blood tests for Rheumatoid factor ( RF ) and Acute-phase reaction tests while clinical evaluation can be measured by the Disease activity using the Disease Activity Score ( DAS ) .
Periodontitis is a destructive inflammatory disease of the dental supporting tissues which leads to erosion of bone around teeth result ing in tooth loss .
Severe periodontitis affects about 5 - 15 % of the adult population .
In periodontitis , the clinical findings of bone resorption and loss of clinical attachment level around tooth are a result of inflammatory mediated alterations to the bone remodelling balance .
The inflammatory infiltrate present between the plaque biofilm , bone and connective tissues regulate the host immune response to the bacteria .
The host produces proteases and substances that de grade the extracellular matrix , and lead to resorption of the alveolar bone , result ing in irreversible loss of tissue attachment .
Bone is a dynamic tissue and bone homeostasis involves the opposing events of resorption and apposition ; dissolution of the existing bone mineral , resorption of the extracellular matrix , and formation of a new matrix .
Bone homeostasis mechanisms maintain bone integrity in the alveolar bone ( regulates periodontal bone loss ) and , elsewhere in the body .
It also functions to regulate the calcium balance within the body ; this is an important ion as it is involved in the clotting of blood , formation of gl and ular secretions and regulation of the cardiac pacemaker .
Rheumatoid arthritis and periodontitis are arguably the most prevalent chronic inflammatory diseases in humans and associated with significant morbidities .
Both rheumatoid arthritis and periodontitis present an imbalance between pro-inflammatory and anti-inflammatory cytokines , which is thought to be responsible for the tissue damage .
In this sense , both conditions are associated with destruction of bone , mediated by inflammatory cytokines such as interleukin-1 , tumour necrosis factor and prostagl and in E2.Several studies have suggested a relationship between periodontitis and rheumatoid arthritis ; rheumatoid arthritis may have a negative impact on periodontal condition and vice versa .
Mercado et al. in 2001 reported a significantly high prevalence of moderate to severe periodontitis in individuals with rheumatoid arthritis .
In addition , the converse is true : periodontitis patients have a higher prevalence of rheumatoid arthritis compared to the general population .
One hypothesis that links rheumatoid arthritis and periodontitis is the recently published " two-hit " model that attempts to link experimental evidence from animal models and is supported by evidence from human clinical studies .
In this theory , the first " hit " involves the periodontopathic subgingival biofilm and its microbial products , such as endotoxin .
The second " hit " involves a medical systemic disease , such as rheumatoid arthritis , which increases biomarkers of systemic inflammation in the circulation , including C reactive protein ( CRP ) , cytokines ( e.g. IL-6 ) , prostanoids ( e.g. PGE2 ) , and matrix metalloproteinases ( e.g. MMP-9 ) , and tumour necrosis factor alpha ( TNF- α ) .
These cytokines are thought to stimulate resident cells in the synovium and the periodontium to produce MMPs mediating connective tissue destruction , and induce the differentiation and activity of osteoclasts to destroy bone In particular , TNF-α , also promotes bone resorption : ( i ) by up-regulating inducible nitric oxide synthase ( iNOS ) and the production of nitric oxide ( NO ) ; and ( ii ) by modulating the receptor activator of nuclear factor _ B ( NF_B ) lig and ( RANKL ) in osteoblasts , and its antagonist osteoprotegerin ( OPG ) , thus altering the RANKL/OPG ratio , which enhances osteoclast activity , and finally , lead to periodontal breakdown .
Aggressive periodontitis is rapid progression of periodontal disease with severe periodontal breakdown .
As no systematic review has been identified as been either published or underway on this topic , the aim of this systematic review is to identify and synthesis e the best available evidence of periodontal disease as a risk factor for rheumatoid arthritis