The oral cavity is thought to be the window to the body because oral manifestations accompany many systemic diseases [1]. Periodontitis is a common disease worldwide that has a primary bacterial etiology and is characterized by dysregulation of the host inflammatory response which eventually results in soft and hard tissue destruction [2, 3]
Rheumatoid arthritis (RA) is a chronic destructive inflammatory disease characterized by the accumulation and persistence of an inflammatory infiltrate in the synovial membrane that leads to synovitis and the destruction of the joint architecture [2].
Rheumatoid arthritis (RA) occurs worldwide with prevalence of 1% in the population, most common in females [4], affecting women three times more than men [5, 6]. It is estimated that arthritis and other rheumatic conditions affect 42.7 million Americans [7] with prevalence of 0.5 to 1% in Western population [8].
While the etiology of these two diseases may differ, the underlying pathogenic mechanisms are remarkably similar and it is possible that individuals manifesting both periodontitis and RA may suffer from a unifying underlying systemic dysregulation of the inflammatory response [2]. There is almost universal acceptance that a variety of cytokines and matrix metalloproteinases (MMPs) are upregulated and intimately involved in the pathogenesis of both periodontitis and RA; many of these effector molecules appear to be common to both diseases [3]. High levels of proinflammatory cytokines, including IL-1b and tumor necrosis factor-alpha (TNF-a), and low levels of cytokines which suppress the immunoinflammatory response, such as IL-10 and transforming growth factor-b (TGF-b), have been detected in periodontitis as well as in Rheumatoid Arthritis [9].
Natural history studies of periodontal disease in humans indicate the presence of three distinct subpopulations: [10].
1) no progression of periodontal disease, in which around 10% of the population manifest very little or no disease which is of particular consequence to dentition; 2) moderate progression, affecting around 80% of the population and representing a very slowly progressing form of disease that generally can be easily managed via routine therapies; and 3) rapid progression, affecting approximately 8% of individuals whereby extensive periodontal destruction occurs which can be very difficult to control.
On the other hand, three types of disease manifestations can also be observed in RA populations:
1) Self-limited: in these cases, individuals originally presenting for RA have no evidence of disease 3 to 5 years later; [11].
2) Easily controlled: the disease is relatively easily controlled with only non-steroidal anti-inflammatory drugs (NSAIDs); [12]
3) Progressive: these patients generally require second-line drugs, which often still do not fully control the disease [13].
It must be recognized that periodontitis differs in one significant way from RA through our understanding that the subgingival biofilm is a key etiologic factor in periodontitis. Unlike periodontal disease, no specific bacterial etiology has been identified for RA. Thus, while host modifications of disease processes are possible for periodontitis, controlling the bacteria that cause periodontal infections remains a significant focus for periodontal treatment and prevention. Host modification can be only an adjunct treatment for periodontitis. However, until an etiologic factor can be found for RA, host modification remains the primary treatment [3].
Currently, the first line of treatment for RA is NSAIDs such as aspirin, naproxen, diclofenac, and ibuprofen. Their mechanism of action through the inhibition of Cyclooxygenase (COX) synthesis produces both analgesic and antipyretic properties. Although these medications are effective in reducing the pain symptoms in RA, they do not significantly alter its course [14].
The use of NSAIDs for the treatment of chronic periodontitis has been studied over the past 20 years [15]. While the results appear promising, the widespread clinical use of these medications to alter the course of periodontitis has not been universal. Their use for the management of periodontitis appears to be a ''rebound'' effect to baseline following a cessation of the medication [16].
With the discovery of two COX enzymes responsible for PGE2 production, designated COX-1 and COX-2, a variety of COX-2 inhibitors have been studied for their potential to stop or slow down bone resorption. One of the first COX-2 inhibitors developed, Tenidap, has been shown to inhibit not only cyclooxygenase and PGE2 production but also IL-1, IL-6, and TNF-a production. To date, the potential of COX-2 inhibitors to modify bone resorption in periodontitis have not been thoroughly studied [3].
In contrast to NSAIDS, which do not significantly alter the course of RA, a newer family of medications designated as disease-modifying anti-rheumatic drugs (DMARDs) has been developed. This medication has demonstrated an ability to change the course of RA for at least one year as evidenced by sustained improvement in function, decreased synovitis, and prevention of further joint damage [17]. Examples of these medications include parenteral gold salts, methotrexate, sulfasalazine, hydroxychloroquine (antimalarial drug), penicillamine, azathioprine, and leflunomide. A major drawback in the use of DMARDs is their considerable toxicity [18].
The use of DMARDs for the management of periodontitis has been restricted largely due to the toxicity issues. However, the use of gold salts in an animal model has shown reduced periodontal destruction [19]. Till now, no human studies have been performed.
The relationship between rheumatoid arthritis (RA) and periodontitis is controversial. Many studies that have been done present conflicting results regarding the relationship between periodontitis and RA. However, a significant association between these two common chronic diseases has been reported recently [20, 21].
RA is a common disease in Sudan, [22] and the literature correlating the severity of RA and the severity of periodontal disease is insufficient. This study was designed to investigate the periodontal status and in RA patients and to find if there is an association between RA and periodontal disease among patients in Khartoum State.
