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- Publisher Website: 10.1034/j.1600-051X.2003.00390.x
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- PMID: 12956661
- WOS: WOS:000185114900011
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Article: Periodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy program
Title | Periodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy program |
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Authors | |
Keywords | Alveolus and palate Cleft lip Periodontal disease progression Supportive periodontal therapy (SPT) |
Issue Date | 2003 |
Publisher | Blackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPE |
Citation | Journal Of Clinical Periodontology, 2003, v. 30 n. 9, p. 840-845 How to Cite? |
Abstract | 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-six subjects not enrolled in a supportive periodontal therapy (SPT) program were examined in 1979, 1987 and 1993. PD progression was assessed as increase in pocket probing depth (PPD in mm) and probing attachment loss (PAL in mm). Results: Extensive plaque accumulation and high frequencies of gingival units bleeding on probing were observed at all three examinations. A statistically significant increase in mean PPD of 0.57 ± 0.21 mm (SD) in both groups as well as a statistically significant loss of PAL of 1.85 ± 0.23 mm (SD) in the CLAP group and of 1.72 ± 0.21 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 14 years, however, PPD increased 1.72 ± 1.08 mm (SD) at cleft sites versus 0.72 ± 1.14 mm (SD) at control sites (p < 0.05), and PAL amounted to 3.19 ± 1.35 mm (SD) at cleft sites versus 2.41 ± 1.52 mm (SD) at control sites (p < 0.05). Conclusion: Both the CLAP and the CL/CP subjects are at high risk for PD progression if no SPT program is provided. This also suggests that alveolar cleft sites in subjects with high plaque and gingival inflammation scores underwent more periodontal tissue destruction than control sites over a 14-year period. |
Persistent Identifier | http://hdl.handle.net/10722/154261 |
ISSN | 2023 Impact Factor: 5.8 2023 SCImago Journal Rankings: 2.249 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Salvi, GE | en_US |
dc.contributor.author | Brägger, U | en_US |
dc.contributor.author | Lang, NP | en_US |
dc.date.accessioned | 2012-08-08T08:24:16Z | - |
dc.date.available | 2012-08-08T08:24:16Z | - |
dc.date.issued | 2003 | en_US |
dc.identifier.citation | Journal Of Clinical Periodontology, 2003, v. 30 n. 9, p. 840-845 | en_US |
dc.identifier.issn | 0303-6979 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/154261 | - |
dc.description.abstract | 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-six subjects not enrolled in a supportive periodontal therapy (SPT) program were examined in 1979, 1987 and 1993. PD progression was assessed as increase in pocket probing depth (PPD in mm) and probing attachment loss (PAL in mm). Results: Extensive plaque accumulation and high frequencies of gingival units bleeding on probing were observed at all three examinations. A statistically significant increase in mean PPD of 0.57 ± 0.21 mm (SD) in both groups as well as a statistically significant loss of PAL of 1.85 ± 0.23 mm (SD) in the CLAP group and of 1.72 ± 0.21 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 14 years, however, PPD increased 1.72 ± 1.08 mm (SD) at cleft sites versus 0.72 ± 1.14 mm (SD) at control sites (p < 0.05), and PAL amounted to 3.19 ± 1.35 mm (SD) at cleft sites versus 2.41 ± 1.52 mm (SD) at control sites (p < 0.05). Conclusion: Both the CLAP and the CL/CP subjects are at high risk for PD progression if no SPT program is provided. This also suggests that alveolar cleft sites in subjects with high plaque and gingival inflammation scores underwent more periodontal tissue destruction than control sites over a 14-year period. | en_US |
dc.language | eng | en_US |
dc.publisher | Blackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPE | en_US |
dc.relation.ispartof | Journal of Clinical Periodontology | en_US |
dc.subject | Alveolus and palate | - |
dc.subject | Cleft lip | - |
dc.subject | Periodontal disease progression | - |
dc.subject | Supportive periodontal therapy (SPT) | - |
dc.subject.mesh | Adult | en_US |
dc.subject.mesh | Alveolar Process - Abnormalities | en_US |
dc.subject.mesh | Cleft Lip - Complications | en_US |
dc.subject.mesh | Cleft Palate - Complications | en_US |
dc.subject.mesh | Dental Plaque - Complications | en_US |
dc.subject.mesh | Disease Progression | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Follow-Up Studies | en_US |
dc.subject.mesh | Gingival Hemorrhage - Etiology | en_US |
dc.subject.mesh | Gingivitis - Etiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Periodontal Attachment Loss - Etiology - Prevention & Control | en_US |
dc.subject.mesh | Periodontal Pocket - Etiology | en_US |
dc.title | Periodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy program | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lang, NP:nplang@hkucc.hku.hk | en_US |
dc.identifier.authority | Lang, NP=rp00031 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1034/j.1600-051X.2003.00390.x | en_US |
dc.identifier.pmid | 12956661 | - |
dc.identifier.scopus | eid_2-s2.0-0346364809 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0346364809&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 30 | en_US |
dc.identifier.issue | 9 | en_US |
dc.identifier.spage | 840 | en_US |
dc.identifier.epage | 845 | en_US |
dc.identifier.isi | WOS:000185114900011 | - |
dc.publisher.place | Denmark | en_US |
dc.identifier.scopusauthorid | Salvi, GE=35600695300 | en_US |
dc.identifier.scopusauthorid | Brägger, U=7005538598 | en_US |
dc.identifier.scopusauthorid | Lang, NP=7201577367 | en_US |
dc.identifier.issnl | 0303-6979 | - |