G. Heden et al., Periodontal tissue alterations following Emdogain (R) treatment of periodontal sites with angular bone defects - A series of case reports, J CLIN PER, 26(12), 1999, pp. 855-860
The aim of the present study was to assess the predictability of probing at
tachment gain and probing pocket depth reduction following Emdogain(R) trea
tment at sites with deep angular bone defects.
Material and Methods: 108 consecutively-treated periodontal patients (mean
age 55.8 years) were included. Each subject exhibited at least 1 deep inter
proximal intrabony defect that could be identified as an experimental site
based on the inclusion criteria: (i) probing pocket depth greater than or e
qual to 5 mm, (ii) probing attachment loss greater than or equal to 6 mm, (
iii) radiographic evidence of an interproximal bone defect with a greater t
han or equal to 3 mm intrabony component. A total of 145 defects met the cr
iteria for inclusion. All subjects received non-surgical periodontal therap
y. This included subgingival instrumentation in all parts of the dentition.
At least 6 months after the completion of this treatment, a baseline exami
nation was performed to characterise the experimental site. Reconstructive
therapy was subsequently performed. Full-thickness periodontal flaps were e
levated, and the root surface scaled and planed. No bone recontouring was p
erformed. A gel containing 24% EDTA was applied on the exposed root and was
kept in place for 2 min. A preparation of enamel matrix proteins was appli
ed to the root surface and adjacent defect space. The flaps were replaced a
nd closed with sutures. The experimental sites were re-examined 12 months a
fter reconstructive surgery.
Results: The re-examination demonstrated that a treatment including the app
lication of enamel matrix proteins at periodontal sites with angular defect
s resulted in a mean probing attachment level gain of 4.6 mm and a probing
pocket depth reduction of 5.2 mm. 87% of all sites treated exhibited a prob
ing attachment gain of >2 mm. One site suffered probing attachment loss. Th
e radiographic assessments revealed that the bone defect had been reduced i
n depth by 2.9 mm on average. The reduction in defect size corresponded to
an average bone fill of 69% of the original defect. In 43% of the defects,
the bone fill amounted to greater than or equal to 80%.
Conclusion: The overall probing pocket depth reduction, probing attachment
level gain, and soft tissue recession, that results following Emdogain(R) t
herapy, is similar to the corresponding outcome variables following GTR.