|Rompola, Eirini: Effektivität von Schmelzmatrixproteinen in der chirurgischen Behandlung von gingivalen Rezessionen |
Enamel matrix protein derivatives (EMDOGAIN®), which mainly consists of amelogenins, have been used clinically to regenerate bony defects due to chronic inflammatory periodontal disease for several years. It is suggested that during periodontal wound healing, enamel matrix protein derivatives reactivate odontogenetic processes, which promote the formation of cementum with inserting fibers. The aim of our study was to investigate long-term effects of EMDOGAIN® on regeneration of non-inflammatory marginal recessions. For root coverage, application of EMDOGAIN® was combined with a coronary positioned flap in a surgical procedure. Measurements of recession depth and width, clinical attachment level and pocket probing depths were performed to evaluate the effect of EMDOGAIN® on promoting periodontal wound healing qualitatively and quantitatively.
The study was designed as a randomized, longitudinal (12 months), intra-individual, placebo-controlled double blind study. 22 patients between 24-64 years old were included. 44 buccal recession defects, at least 3mm deep, which were located contralateral of same jaw (Split-Mouth-Design) were treated. EMDOGAIN® consists of two components, a sterile lyophilized and resorbable protein mixture (derivative of the enamel matrix proteins) and a vehicle (Propylenglycolalginat). Test teeth were treated with EMDOGAIN® strictly according to the producers (Biora) protocol. Same surgical procedure was performed in control teeth, but vehicle was applied instead (placebo). Coverage of both teeth was performed in one visit. Every 1 and 3 weeks, 3, 6 and 12 months patients came for recall visits. Then, wound healing was documented photographically and by clinical measurements. Changes of recession depth and width, width of keratinized gingiva, attachment level, pocket probing depth and alveolar bone margin were recorded.
Our results showed that both methods resulted in a significant increase of attachment level and recession coverage following 12 months. A mean recession depth of initially 4.5 mm in test and 4.4 mm in control group was reduced to 1.5 mm in both groups. These values are representing a mean coverage of 71,7% in the test and 73,6 % in the control group.
72The attachment gain was .09 mm for test and 3.02 mm for control group. Probing pocket depths stayed stable throughout the study period compared to baseline measurements. Both treatment modalities showed a significant alveolar bone gain. With regard to clinical parameters differences between the two groups were not significant. However, in the test group there is a clear tendency that left recession depths stay stable throughout 6 and 12 months postsurgically. This has to be confirmed in the future.
To sum up our data, after 12 months EMDOGAIN® combined with the coronary positioned flap procedure shows similar results in recession coverage compared with the coronary positioned flap alone. Further investigations may elucidate if EMDOGAIN® may have a positive impact on the coverage of marginal recessions 24 or 36 months postsurgically.
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