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In 1976, Walter J. Loesche⁴¹ described the specific plaque hypothesis, postulating that dental caries was a bacteria-specific infection, particularly originated by Streptococcus mutans, and that acute necrotizing ulcerative gingivitis was caused by specific intermediate-sized spirochetes, as well as Bacteroides melaninogenicus (known today as Prevotella melaninogenica).

The specific plaque hypothesis was further developed in the 1970s and 1980s, when more advanced culture and bacterial identification techniques were developed.^44,45 Key periodontal pathogens related to severe and aggressive periodontal diseases were identified, such as Aggregatibacter actinomycetemcomitans, P gingivalis, T forsythia, or T denticola.^32,46,47 In light of the increased microbiologic understanding, it became evident that periodontal destruction was not only influenced by quantity, but also by the qualitative composition of bacterial plaque.⁴¹