Abnormal pocket depth and pocket-free gingival recession have been recognized as two separate periodontal phenotypes (albeit under different names) at least since the 18th century. With abnormal pocket depth – referred to here as destructive periodontal disease – the alveolar bone loss is associated with abnormally deep periodontal pocketing, which can be associated with signs of clinical inflammation and periodontal abscesses. With pocket-free gingival recession – which we will refer to as periodontal atrophy – the alveolar bone loss is associated with gingival recession and often presents without signs of clinical inflammation. In the 1970s, it was decided to label these two clinically distinct periodontal phenotypes as one and the same disease, namely chronic periodontitis, under the hypothesis that both are caused by plaque. After 30 years, this speculation, and therefore the rationale of the diagnostic classification, has remained unsubstantiated. The evidence for plaque contributing to either has remained surprisingly sparse and contradictory; indeed, available evidence suggests that distinctive etiologies are responsible for each phenotype. Furthermore, destructive periodontal disease and periodontal atrophy have different treatments and therefore economic implications, different anthropological and comparative medicine features, and possibly different outcomes in terms of quality of life and tooth loss.
The continued failure to distinguish destructive periodontal disease from periodontal atrophy may be a rate-limiting step in understanding the incidence, etiology, prognosis, and treatment of the different periodontal phenotypes. We will suggest that both phenotypes should once again, after a 30-year hiatus, be recognized as distinct entities and we will also explore criteria to define when pockets are abnormal.
Periodontol 2000. 2005;39:22-9. Link to article on publisher's site
Available at: http://works.bepress.com/barry_saver/37/