Periodontal breakdown primarily develops when the microbial load within a periodontal pocket overrules the local and systemic host defence mechanisms. Such an imbalance occurs in different situations, including an aspecific increase in the total amount of bacteria, an outgrowth/overgrowth of pathogenic species above a certain threshold level and/or a reduction in the efficiency of the immune response. Actinobacillus actinomycetemcomitans, Tanneralla forsythensis and Porphyromonas gingivalis are still considered key periopathogens, but species such as Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros, Fusobacterium nucleatum, Eubacterium nodatum, Streptococcus intermedius and spirochetes are also linked with periodontal destruction (American Academy of Periodontology, 1996; Slots and Rams, 1991; Socransky and Haffajee, 1992; Wolff et al, 1994). The efficiency of the host defence is partially hereditary (Kinane and Hart, 2003) but environmental factors such as bad oral hygiene, smoking, immunosuppressive medication, stress and so on can further impair the immune defence mechanism. Since, so far, the susceptibility of the host cannot be modulated at a clinical level, with the exception of anti-inflammatory medications, periodontal therapy is focused on the reduction/elimination of periodontopathogens in combination with the reestablishment, often by surgical pocket elimination, of a more suitable environment (less anaerobic) for beneficial microbiota. Several studies indeed indicate that the presence of the above-mentioned periodontopathogens (persisting or re-established after treatment) was associated with a negative clinical outcome of perioOne-Stage, Full-Mouth Disinfection: Fiction or Reality?