Individuals with Down's syndrome (DS) have an increased prevalence of periodontal disease compared with otherwise normal, age-matched control groups and other mentally handicapped patients of similar age distribution. The exaggerated immune-inflammatory response of the tissues cannot be explained by poor oral hygiene alone and might be the result of an impaired cell-mediated and humoral immunity and a deficient phagocytic system. As far as the progression and severity of destruction, the oral manifestations of DS patients are consistent with the juvenile periodontitis (JP) disease pattern. The purpose of the present study was 1) to assess the periodontal clinical and microbiological status of 10 DS patients aged 20 to 31 years (mean: 26.3 years) relative to that of 11 patients with cerebral palsy (CP) aged 23 to 53 years (mean: 36 years) without defective immunological functions, and 2) to determine the effect of supragingival plaque control and oral hygiene instruction in these patient groups. Subsequent to the initial examination and a professional tooth cleaning program, clinical and microbiological parameters were monitored over a period of 12 weeks. The clinical examination included the recording of plaque index (P1), gingival index (GI), probing depth (PD), and clinical attachment level (CAL). Subgingival plaque samples were always obtained from the same pocket with the highest disease activity (deepest bleeding site at baseline examination) in each subject for a morphotype analysis by dark field microscopy and for identification and quantitation of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, Bacteroides forsythus, Fusobacterium nucleatum, Treponema denticola, and Campylobacter rectus by DNA probes. The results of the baseline examinations demonstrated that DS patients and patients with cerebral palsy had inflamed gingiva associated with a high amount of plaque. The mean probing depth and percentage of sites with probing depth> 4 mm corresponded to age and poor oral hygiene in CP patients. Deep pockets in DS patients demonstrated a high prevalence of periodontal disease compared with age-matched children with mental retardation and non-handicapped patients. Regarding the young age of onset, the severe destruction of periodontal tissues and pathogenesis of periodontitis in DS patients are consistent with the juvenile periodontitis disease pattern. The missing clinical benefit and alteration of the subgingival flora following supragingival plaque control in DS patients underlined the alteration in the immunological response.