website: 86th General Session & Exhibition of the IADR

ABSTRACT: 2156  

Periodontal disease progression in cleft lip, alveolus and palate subjects

G. HUYNH-BA1, N.P. LANG1, M.A. KRAEHENMANN2, U. BRÄGGER1, and G. SALVI1, 1University of Berne, Switzerland, 2University of Zurich, Switzerland

Objectives: (i) To assess the overall and (ii) cleft-associated rate of periodontal disease (PD) progression in subjects with cleft lip, alveolus and palate (CLAP) and (iii) to compare these rates with those of subjects with cleft lip (CL) and cleft palate (CP).

Material and methods: Twenty subjects who were not enrolled in a supportive periodontal therapy (SPT) program were examined in 1979, 1987, 1993 and 2004. PD progression was assessed as increase in pocket probing depth (PPD) and probing attachment loss (PAL) in mm.

Results: Extensive plaque accumulation and high frequencies of gingival units bleeding on probing were observed at all four examinations. In the CLAP group, an increase in mean full-mouth PPD of 0.09±0.11mm (SD) was observed, which was not statistically significant. However in the CLP group, a statistically significant increase in mean full-mouth PPD of 0.35±0.12mm (SD) was reported (p<0.05). In the CLAP group a statistically significant loss of full-mouth PAL of 1.52±0.12 mm (SD) and of 1.66±0.15 mm (SD) in the CL/CP group occurred over the observation period (p<0.05). In subjects with CLAP, statistically significant increases in PPD and loss of PAL were recorded over time at sites adjacent to the cleft as well as at control sites (p<0.05). Over 25 years, however, PPD increased 0.92±0.23 mm (SD) at cleft sites versus 0.07±0.14 mm (SD) at control sites (p<0.05), and PAL amounted to 2.71±0.27mm (SD) at cleft sites versus 1.99±0.21 (SD) at control sites (p<0.05).

Conclusion: Both the CLAP and the CL/CP subjects were at high risk for PD progression when no SPT program was provided. This also suggested that alveolar cleft sites in subjects with high plaque and gingival inflammation scores underwent more periodontal tissue destruction than did control sites over a 25-year period.

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