Purpose: Periodontal tissue destruction is a host mediated immunoinflammatory lesion, triggered by the accumulation of a complex microbial ecology in biofilms juxtaposed to the tissues. Current evidence is providing substantive support that characteristics of the portfolio of responses of individual hosts, e.g. controlled by gene expression variation, may be more significant than the commensal microbial biofilm dissimilarities in explaining disparities in the expression and severity of disease across the population. We report our molecular approaches, including microarray technology, to describe the responses in local host tissues to infection by oral microorganisms.
Materials and Methods: We describe a murine calvarial model (MCM) and a rat oral infection model (ROIM). The MCM focused on gene expression patterns of soft tissue and bone following monoinfection with Porphyromonas gingivalis (P. gingivalis), Treponema denticola (T. denticola), or Tannerella forsythia (T. forsythia), or a polybacterial challenge with this consortium. The ROIM evaluated gene expression in gingival tissues following oral infection with each of the microorganisms.
Results: The MCM identified gene families and genes that demonstrated a significantly altered expression after local infection with the oral bacteria. Importantly, gene expression profiles were substantially different between soft tissue and calvarial bone, and the gene profiles with the polybacterial infection showed extensive differences from the monoinfections. The ROIM demonstrated for the first time the ability to successfully orally infect rats with members of this human pathogenic consortium. We noted significantly increased bone loss with the consortium, and variations in gene expression profiles related to the type of infection.
Conclusions: The results from both models supported a dramatically different pattern of gene expression than what might have been expected based upon previous ‘reductionist’ approaches. Microarray technology should better describe the range of host responses that occur in local tissue challenged with oral bacteria, and may provide a very different gene expression footprint of homeostasis versus critical molecular mechanisms that enable disease progression.
Keywords: microarray, polybacterial infection, animal models, gene expression.