The oral cavity harbors one of the most diverse microbiota of the human body, and bears an extraordinary ecological heterogeneity. Indeed, keratinized and non-keratinized mucosae, dental hard tissues, supra- and sub-gingival sites are all exposed to different nutrients, pH and redox conditions that create ecologically distinct niches. These niches differently support microbial growth, and dictate which microorganisms are able to persist in each ecosystem. In turn, the microbial colonization of an ecosystem alters the microenvironment, either directly by the action of excreted enzymes, or indirectly by the induction of an inflammatory response. In the subgingival ecosystem, the upsurge of inflammation typically causes a deepening of the sulcus that comes along more anaerobic conditions and an increased protein load in the gingival exudate. These changes foster a higher abundance of taxa with a periodonto-pathogenic potential, and prompt subgingival communities into a dysbiotic cycle that engages chronic inflammation, altered microecology and further taxonomic shifts. In other words, alteration of the subgingival microecology is a paramount culprit to the transition of a health-associated microbiota to a dysbiotic one. This chapter describes the ecological alterations that occur during an ongoing periodontal inflammation and while the pathological niche of the periodontal pocket is shaped.