Ricardo P. Teles, DDS, DMSc

The focus of the Periodontology Department in the past decades has been the identification of the microbiota associated with periodontal disease. These efforts have resulted in a clearer picture of the putative periodontopathogens. In response to this bacterial challenge, the host releases a series of inflammatory mediators, which modulate tissue destruction and disease progression. The purpose of Dr. Teles' research is to develop methods to quantify such mediators in the gingival crevicular fluid (GCF) and determine how they correlate with the microbial burden and the clinical manifestations of the disease.

Periodontal diseases are infections that result in the destruction of the apparatus of support of the teeth. The etiological agents of such infections are bacteria, for the most part, belonging to the indigenous flora of the mouth. However, periodontal diseases are multifactorial and depend on other conditions such as: the immune response of the susceptive host, the local environment and time. As a result, the great variability in disease severity and distribution cannot be accounted for by differences in the microbial composition only. In fact, several lines of evidence demonstrate that immune mechanisms are responsible for the tissue destruction characteristic of the disease. Therefore, it is imperative that, in order to understand the pathogenesis of these infections, the host response to the periodontal flora be investigated in depth.

Such knowledge also carries practical repercussions. Periodontal diseases progress through periods or 'bursts' of destruction, followed by periods of remission. Being able to distinguish sites and/or individuals that are undergoing active progression has obvious therapeutic implications. Thus far, there are no clinical means of establishing which areas are active. In this context, the gingival crevicular fluid (GCF), a transudate that flows from the capillary vessels within the gingival tissues and ends up in the gingival crevice, provides us with a diagnostic tool to investigate the inflammatory mediators released during disease progression. By studying the composition of this fluid, one can infer possible immunological mechanisms that take place within the tissues in a non-invasive manner.

Several immune mediators and products resulting from the disease process have been determined as components of the GCF, and their levels associated with the disease status of sites and individuals. Nevertheless, most studies using GCF as a diagnostic tool suffer from limitations such as: small number of sites and or subjects investigated, lack of longitudinal data and lack of evaluation of the microbial burden. In order to overcome such limitations, Dr. Teles proposes the application of the checkerboard immunoblotting (CBIB) technique in the identification of several components of the GCF in large numbers of samples. A similar approach, using DNA-DNA hybridization, has been applied in our laboratory for the past 10 years, in the characterization of the microflora associated with these infections. This technology puts our laboratory in a strategic position to combine the data generated through the CBIB characterizing the GCF components, with microbiological data offered by the DNA-DNA hybridization technique.

The CBIB approach offers several advantages over other immunological methods currently used in the identification of antigens: It is relatively simple and involves inexpensive apparatus (readily available in our laboratory); the volume and amount of reagents required is small; multiple (over 2,000) reactions can be examined simultaneously, with highly reproducible results available within 24 hours. The proposed technique should provide a more complete picture of the inflammatory mediators and byproducts of tissue destruction present in GCF. In addition, it would allow us to correlate these data with the microbial burden in specific sites and follow the changes in composition and concentration of such mediators in GCF longitudinally.

Selected Publications

Teles RP, Patel M, Socransky SS, Haffajee AD. 2008. Disease progression in periodontally healthy and maintenance subjects. J. Periodontol. 79(5):784-94.

Bogren A, Teles RP, Torresyap G, Haffajee AD, Socransky SS, Wennstrom JL. 2008. Locally Delivered Doxycycline During Supportive Periodontal Therapy: A 3-Year Study. J Periodontol. 79(5):827-835.

Teles RP, Bogren A, Patel M, Wennstrom JL, Socransky SS, Haffajee AD. 2007. A three-year prospective study of adult subjects with gingivitis II: microbiological paramaters. J Clin Periodontol. 24(1)7-17.

Teles RP, Haffajee AD, Socransky SS. 2006. Microbiological goals of periodontal therapy. Periodontol. 2000 42(1):180– 218.

Haffajee AD, Teles RP, Socransky SS. 2006. The effect of periodontal therapy on the composition of the subgingival microbiota. Periodontol. 2000 42(1) :219– 258.

Colombo AP, Teles RP, Torres MC, Rosalem W, Mendes MC, Souto RM, Uzeda M. 2005. Effects of non-surgical mechanical therapy on the subgingival microbiota of Brazilians with untreated chronic periodontitis: 9-month results. J. Periodontol. 76(5) :778–784.

Sorciano de Souza CAS, Teles RP, Souto R, Chaves MAE, Colombo APV. 2005. Endodontic therapy associated with calcium hydroxide as an intracanal dressing: Microbiologic evaluation by the checkerboard DNA-DNA hybridization technique. J. Endod. 31 (2):79–83.

Castro GF, Souza IPR, Lopes S, Stashenko P, Teles RP. 2004. Salivary IgA to Cariogenic bacteria in HIV-positive children and its correlation with caries prevalence and levels of cariogenic microorganisms. Oral Microbiol. Immunol. 19(5):281–288.

Colombo AP, Teles RP, Torres MC, Souto R, Rosalem WJ, Mendes MC, Uzeda M. 2002. Subgingival microbiota of Brazilian subjects with untreated chronic periodontitis. J. Periodontol. 73(4):360– 369.

Gilad JZ, Teles R, Goodson M, White RR, Stashenko P. 1999. Development of a clindamycin-impregnated fiber as an intracanal medication in endodontic therapy. J. Endod. 25(11):722–727.

Stashenko P, Teles R, D'Souza R. 1998. Periapical inflammatory responses and their modulation. Crit. Rev. Oral Biol. Med. 9(4) :498–521.

Teles R, Wang CY, Stashenko P. 1997. Increased susceptibility of RAG-2 SCID mice to dissemination of endodontic infections. Infect. Immun. 65 (9) :3781– 3787.