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Periodontal Status and Serum Antibody Responses to Oral Microorganisms in Sjögren's Syndrome
Author(s) -
Çelenligil Haviye,
Eratalay Kenan,
Kansu Emin,
Ebersole Jeffrey L.
Publication year - 1998
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1998.69.5.571
Subject(s) - medicine , antibody , periodontal disease , dentistry , immunology
S jögren's syndrome is an autoimmune disease characterized by keratoconjunctivitis sicca and xerostomia. Rapid bacterial plaque accumulation occurs in Sjögren's syndrome patients due to decreases in salivary flow rate. The purpose of this study was to evaluate the periodontal status of patients with Sjögren's syndrome and evaluate serum antibody responses to selected oral microorganisms, including major periodontopathogens, compared to healthy controls. Seventeen Sjögren's syndrome patients and 14 healthy subjects were included in the study. Plaque (PL), sulcular bleeding (SBI), periodontal index scores (PI), probing depths (PD), and total number of teeth were recorded. An ELISA was used to determine the serum IgG antibody level to a panel of 13 oral microorganisms. Significantly higher PL, SBI, PD, and PI scores, as well as an increased number of lost teeth were observed in patients with Sjögren's syndrome compared to healthy subjects ( P <0.0001). Antibody levels to Streptococcus oralis zwere significantly lower in Sjögren's syndrome patients than controls ( P <0.0002). These patients exhibited significantly elevated antibody levels to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis compared to controls ( P <0.006 to 0.0004). Our findings indicate that Sjögren's syndrome patients have established periodontal disease and serum antibody responses to oral microorganisms previously identified as periodontopathogens in systemically healthy subjects. These results suggest that Sjögren's syndrome may affect bacterial colonization in plaque and contribute to increased periodontal disease in this compromised population. J Periodontol 1998;69:571–577 .