Periodontitis, a major cause of tooth loss, is a bacterially induced inflammatory disease that has been associated with certain bacterial species. The aim of this thesis was to identify the epithelial mechanisms activated by commensal and periodontal pathogens to determine which signalling pathways, transcription factors, and pro-inflammatory cytokine responses are associated with periodontitis. The H400 gingival epithelial cell line was infected with the health-associated Actinomyces naeslundii and periodontopathogens Fusobacterium nucleatum and Porphyromonas gingivalis. Differential pathway activation was observed between the three species. A. naeslundii induced phosphorylation of JNK and NF-κB, similarly to F. nucleatum which activated all MAPK pathways (including p38 and ERK1/2) and NF-κB. P. gingivalis induced minimal levels of p-JNK. Differential transcription factor activation was observed in response to the three bacteria. A. naeslundii and F. nucleatum induced activation of c-Fos and c-Jun, while P. gingivalis transiently activated binding of ATF-2. Notably, F. nucleatum was the most potent activator. Both A. naeslundii and F. nucleatum induced a pro-inflammatory response, together stimulating release of IL-1α, IL-1β, IL-6, GM-CSF and G-CSF. P. gingivalis was the least stimulatory bacterium, an observation supported by a lack of cytokine production, IL-8 down-regulation and a reduction in lactate dehydrogenase release (measure of damage). To determine the functional role of these signalling pathways in inducing effector responses, the MAPK and NF-κB pathways were inhibited. Results indicate that the p38 MAPK pathway is the main regulator of inflammatory responses in A. naeslundii and F. nucleatum infections while in P. gingivalis infections, the JNK pathway appears to be the major regulator of oral epithelial responses. Furthermore, the possible involvement of P. gingivalis virulence factors in the bacterium’s ability to prevent epithelial cell activation was investigated. It was observed that the Lys-gingipain (Kgp) of P. gingivalis plays a role in supressing activation of the MAPK and NF-κB pathways and the c-Fos transcription factors in oral epithelial cells. Overall, the data in this thesis suggests that epithelial cells recognise and respond differently to commensal bacteria compared to periodontal pathogens and that P. gingivalis Kgp may be a key virulence factor involved in immune subversion.