Bacterial biofilms are regarded to be the primary aetiological factor in the initiation of
gingival inflammation and subsequent destruction of periodontal tissues (Offenbacher 1996)
and three major specific pathogens have been repeatedly identified as etiologic agents,
namely Aggregatibacter (Actinobacillus) actinomycetemcomitans (Aa), Porphyromonas gingivalis
(Pg) and Tannerella forsythia (Tf) (Socransky et al. 1998).
Medicine is an ever-changing science. Every day we are encountered with the new developments and knowledge in the pathogenesis, mechanism of disease, newer diagnostic modalities, treatment options and new challenges in the management of the various diseases. The same holds true for respiratory diseases with the emergence of new respiratory pathogens having significant impact on the respiratory system.
The biological changes underlying the transition process from gingival health to early
inflammatory changes involve local increase in vascular permeability, edema and the
recruitment and activation of polymorphonuclear neutrophils (PMN) (Delima and Van
Dyke 2003). Acquired immune response becomes involved once antigen-presenting cells
interact with immunocompetent cells, such as T and B lymphocytes, leading to the
expansion of antibody-secreting plasma cells and the development of the chronic lesion
(Gemmell and Seymour 2004).
Periodontitis is one of the most common oral diseases and is characterised by gingival
inflammation and alveolar bone resorption (Savage et al. 2009). Periodontitis is a
multifactorial irreversible and cumulative condition, initiated and propagated by bacteria
and host factors (Kinane 2001). More than 500 different bacterial species are able to colonise
the oral biofilm and up to 150 different species of bacteria are possible in any individual’s