Periodontitis

Periodontitis is infection and inflammation located within the space between the gum and teeth. It usually starts with gingivitis, which is infection-inflammation of the gums. Accumulation of bacteria at the gum line leading toward the development of plaque is the hallmark of gingivitis. In periodontitis, microorganisms invade the periodontal space, the area between the gum and teeth. A biofilm of bacteria sets up causing an immune and inflammatory response.Cytokines are substances released by cells and bacteria involved in the inflammatory process. A number of these cytokines can be destructive to tissue. In periodontitis, cytokines are released as a result of bacterialinvasion. Such causes tooth decay and bone loss in the maxilla (cheek bone) and mandible (jaw bone) where the teeth are inserted. This bone is referred to as alveolar bone. Complete loss of the tooth may result.

Periodontitis is recognized as a systemic disease. The disorder has been linked to atherosclerosis and heart disease, the development of diabetes, and eclampsia or preterm labor.2

Initial therapy of periodontitis involves removing plaque and calculus. Cleaning below the gum line called scaling is utilized. Sometimes surgery is required, which includes open flap debridement and osseous surgery such as bone grafting. Teeth replacement may be necessary.3

Osteoarthritis

Osteoarthritis or degenerative joint disease is a joint disorder characterized by cartilage breakdown with underlying bone. It is the most common type of arthritis with 27 million people affected in the United States. Before the age of 45, men are more commonly affected, but after 45, the disease is seen in more women.4The symptoms are joint pain that can become severe, joint stiffness, swelling, and diminished range of motion. Osteoarthritis is most commonly seen in the fingers and thumb, neck, lower back, knees, and hips. It is caused by mechanical stress and is somewhat genetic.

In the cartilage of the joint, there is a disruption of the collagen matrix and degradation of collagen fibers. Proteoglycan content decreases. A mild inflammatory reaction occurs further causing joint damage.5

Osteoarthritis can be diagnosed by history and physical exam. X-rays reveal joint space narrowing, sclerosis or increase bone formation haphazardly around the joint, and osteophytes or bony spurs. An MRI is not necessary to diagnose osteoarthritis.

Treatment begins with non-steroidal anti-inflammatory drugs (NSAIDS) like ibuprofen. Moderate exercise has been shown to be beneficial. If these measures are not working, then surgery may be indicated. Arthroplasty or resurfacing and total joint replacement are the surgical procedures performed.6

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease affecting the joints primarily. The disease may also involve the heart, lungs, eyes, and skin. About 1 percent of the population suffers from RA. It generally starts in middleage but can be found in younger patients. Multiple joints are usually affected, called polyarthritis.RA causes inflammation of the synovial membrane in the joint. Such inflammation causes the joint to be swollen, tender, warm, and very stiff. The inflammation results in erosion and destruction of the joint surface. The joint may deform, and range of motion is severely hampered.7

RA starts as a state of inflammatory cell activation. Autoantibodies (antibodies against self) are produced that exacerbates the inflammation. This is why RA is called an autoimmune disease. During the inflammatory process, Cytokines are secreted including interleukin-1 and 6and tumor necrosis factor-alpha (TNF-alpha). These substances break down the synovial membrane and cause bone erosion.8
Both genetic and environmental factors are causative of RA. The human leukocyte antigen (HLA) DR4 is associated with RA. Smoking seems to be the most significant environmental factor.

History and physical exam make the diagnosis. X-rays show joint space narrowing and thinning of the bone in the joint. Deformity can be visualized. An MRI may pick up early disease. The blood is tested for rheumatoid factor, which is a non-specific antibody. However, 15 percent of RA patients will be seronegative for rheumatoid factor. Anti-citrullinated protein antibodies will be tested for.9

Treatment is NSAIDs for pain. Steroids are used and can be effective for pain and swelling but do not alter the disease course. Disease-modifying anti-rheumatic drugs are a primary treatment for RA. Most patients are placed on methotrexate, sulfasalazine, or leflunomide. These drugs have been shown to slow the disease process. If methotrexate or the others are not effective, biologics are infused. TNF-alpha blockers such as infliximab are employed. Monoclonal antibodies against B-cells such as rituximab and tocilizumab have been shown to diminish disease or inflammation.10

For acute joint problems, NSAIDs and steroids are given. If the joint becomes severely affected, total joint replacement surgery is indicated.

Connection between Periodontitis and Arthritis

Evidence now supports a link between periodontitis, osteoarthritis, and RA.11,12,13,14Arthritis and periodontitis are both chronic, inflammatory conditions. The association with periodontitis and systemic diseases is not new. Periodontitis is linked to diabetes, atherosclerosis, heart attacks, and stroke.15,16. The pathogenesis of periodontitis seems to be a heightened immune or inflammatory response to certain pathogens or bacteria in the periodontal space. The possibility that arthritis patients acquire an infection that creates an exacerbated immune reaction or inflammation of the synovial membrane would explain a lot of clinical features of osteoarthritis and RA. So far, though, no specific pathogen or bacteria has been found to cause directly arthritis.No doubt, a variety of cytokines and matrix metalloproteinases (MMPs) are located in the inflammatory soup seen in both periodontitis and RA. The cytokines present in each are very similar. Both disorders possess high levels of interleukin-1, TNF-alpha, MMPs, and prostaglandin E2. 17 TNF-alpha and its associated proteins activate osteoclasts, which is the cell that breaks down bone.

One large study found an association with the development of RA in patients and periodontitis.18 This investigation examined 13,779 newly diagnosed patients with RA with a control group of 137,790 people. A statistically significant link was found between newly diagnosed RA and periodontitis. The high number of participants in this study creates strong evidence of a periodontitis-RA connection.

Bacterial Link

In 2012, a study examined synovial (joint) fluids of patients with osteoarthritis and RA for the presence of bacterial DNA.19 These patients also had periodontal disease.Almost 14 percent of the patients possessed bacterial DNA in their synovial fluids. Most importantly, many of the patients had periodontitis caused by the same bacteria found in the synovial fluid. Such findings support translocation of periodontal bacteria through the bloodstream to the joint space. The recommendation of the authors was to examine patients with arthritis for periodontal disease and to treat accordingly (antibiotics).

A more recent investigation revealed the presence of periodontal pathogens or bacteria in the knees of osteoarthritis patients undergoing joint replacement. There was no clinical evidence of joint infection in any of the patients. Bacteria from the mouth had evidentially gotten into the bloodstream and settled in the joints of these patients. Although the bacteria did not cause a frank, clinically detectable joint infection, the pathogens could cause a chronic, inflammatory state in the synovia. It is the inflammatory response and resultant cytokine production that cause tissue damage in arthritis and periodontitis.

Conclusion

There exists enough evidence that there is a link between arthritis and periodontitis. Both are chronic, inflammatory diseases that create tissue damage and bone loss. The destructive cytokines present in the periodontal space and joints are essentially the same. The disease progression between the two disorders is similar.Does one cause the other? The answer to that remains unknown. However, one large study found an association between periodontitis and newly diagnosed RA. Also, periodontal bacteria have been found in the joints of osteoarthritis and RA patients.

It can be argued that people with arthritis disability do not possess the dexterity to practice good oral hygiene or see a dentist regularly. There is evidence for that.However, poor hygiene would not explain the link between periodontitis and newly diagnosed RA patients.

Certainly, the evidence supports that patients with arthritis undergo a dental exam looking for any periodontitis. If periodontal disease is discovered, full and aggressive treatment should be instituted.

In the meantime, brush your teeth twice daily and floss. Your joint health may depend on it.

References

1. Temoin S, Chakaki A, Askari A, et al. “Identification of Oral Bacterial DNA in Synovial Fluid of Patients with Native and Failed Prosthetic Joints.” Journal of Clinical Rheumatology, 18(3): 117-121, 2012.
2. Savage A, Eaton K, Moles D, Needleman I. “A Systemic Review of Definitions of Periodontitis and Methods that have been Used to Identify this Disease.” Journal of Clinical Periodontology, 36(6): 458-467, 2009.
3. Ibid.
4. Berenbaum F, “Osteoarthritis is an Inflammatory Disease (Osteoarthritis is not Osteoarthrosis),” Osteoarthritis and Cartilage, 21(1): 16-21, 2013.
5. Majithia V, Geraci S. “Rheumatoid Arthritis: Diagnosis and Management.” American Journal of Medicine, 120(11): 936-939, 2007.
6. Ibid.
7. Ibid.
8. Ibid.
9. Mercado F, Marshall R, Klestov A, Bartold P. “Relationship between Rheumatoid Arthritis and Periodontitis.” Journal of Periodontology, 72: 779-787, 2001.
10. Kasser U, Gleissner C, Dehne F, et al. “Risk for Periodontal Disease in Patients with Longstanding Rheumatoid Arthritis.” Arthritis Rheum, 40: 2248-2251, 1997.
11. Gleissner C, Willershausen B, Kaesser U, Bolten W. “The Role of Risk Factors for Periodontal Disease in Patients with Rheumatoid Arthritis.” Eur J Med Res, 3: 387-392, 1998.
12. Mercado F, Marshall R, Klestov A, Bartold P. “Is there a Relationship between Rheumatoid Arthritis and Periodontal Disease?” J Clin Periodontol, 127: 267-272, 2000.
13. Beck J, Garcia R, Heiss G, et al. “Periodontal Disease and cardiovascular Disease.” J Periodontol, 67:1123-1137, 1996.
14. Yalda B, Offenbacher S, Collins J. “Diabetes as a Modifier of Periodontal Disease Expression.” Periodontol 2000, 6: 37-49, 1994.
15. Snyderman R, McCarty G. “Analogous Mechanisms of Tissue Destruction in Rheumatoid Arthritis and Periodontal Disease.” In: Genco R, Mergenhagen S, eds. Host-Parasite Interaction in Periodontal Diseases. Washington, DC: American Society for Microbiology; 354-363, 1982.
16. Chen H, Huang N, Chen Y-M, et al. “Association between a History of Periodontitis and the Risk of Rheumatoid Arthritis: A Nationwide, Population-Based Case-Control Study.” Annuals of the Rheumatic Diseases, 72: 1206-1211, 2013.
17. Temoin S, Chakaki A, Askari A, et al. “Identification of Oral Bacteria DNA in Synovial Fluid of Patients with Arthritis with Native and Failed Prosthetic Joints.” Journal Clinical Rheumatology, 18(3): 117-121, 2012.
18. Ehrlich G, Hu F, Sotereanos N, et al. “What Role do Periodontal Pathogens Play in Osteoarthritis and Periprosthetic Joint Infections of the Knee?” j Appl Biomater Funct Mater, 12(1): 13-20, 2014.
19. Dolan T, Peek C, Stuck A, Beck J. “Functional Health and Dental Service use among Older Adults.” J Gerontol A Biol Sci Med Sci, 53: 413-418, 1998.