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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

TitlePeriodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy program
Authors
Issue Date2003
PublisherBlackwell 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?
AbstractObjectives: (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 Identifierhttp://hdl.handle.net/10722/154261
ISSN
2015 Impact Factor: 3.915
2015 SCImago Journal Rankings: 1.848
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSalvi, GEen_US
dc.contributor.authorBrägger, Uen_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:24:16Z-
dc.date.available2012-08-08T08:24:16Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Clinical Periodontology, 2003, v. 30 n. 9, p. 840-845en_US
dc.identifier.issn0303-6979en_US
dc.identifier.urihttp://hdl.handle.net/10722/154261-
dc.description.abstractObjectives: (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.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPEen_US
dc.relation.ispartofJournal of Clinical Periodontologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAlveolar Process - Abnormalitiesen_US
dc.subject.meshCleft Lip - Complicationsen_US
dc.subject.meshCleft Palate - Complicationsen_US
dc.subject.meshDental Plaque - Complicationsen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshGingival Hemorrhage - Etiologyen_US
dc.subject.meshGingivitis - Etiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPeriodontal Attachment Loss - Etiology - Prevention & Controlen_US
dc.subject.meshPeriodontal Pocket - Etiologyen_US
dc.titlePeriodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy programen_US
dc.typeArticleen_US
dc.identifier.emailLang, NP:nplang@hkucc.hku.hken_US
dc.identifier.authorityLang, NP=rp00031en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1034/j.1600-051X.2003.00390.xen_US
dc.identifier.pmid12956661-
dc.identifier.scopuseid_2-s2.0-0346364809en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0346364809&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume30en_US
dc.identifier.issue9en_US
dc.identifier.spage840en_US
dc.identifier.epage845en_US
dc.identifier.isiWOS:000185114900011-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridSalvi, GE=35600695300en_US
dc.identifier.scopusauthoridBrägger, U=7005538598en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US

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