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The mucosal barrier following abutment dis/reconnection
Author(s) -
Abrahamsson I.,
Berglundh T.,
Lindhe J.
Publication year - 1997
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1997.tb00230.x
Subject(s) - abutment , dentistry , implant , connective tissue , junctional epithelium , beagle , medicine , materials science , orthodontics , pathology , surgery , engineering , civil engineering
In the present experiment, the effect on the marginal peri‐implant tissues following repeated abutment removal and subsequent reconnection was studied. 5 beagle dogs were used. The mandibular premolars were extracted and 2 fixtures of the Branemark System® were installed. 1 in each mandibular quadrant. 3 months later, abutment connection was performed. A 6‐month period of plaque control was initiated. Once a month during the plaque control period, the abutment of the right side (test) in each dog was disconnected, cleaned and reconnected to the fixture. Thus, each test abutment was removed and reconnected altogether 5X during this period. The contralateral abutment remained undisturbed for 6 months and served as control. 1 month after the last reconnection, the animals were sacrificed and tissue samples, comprising the implant and the surrounding soft and hard periimplant tissues, were obtained, decalcified, embedded in Epon and sectioned. The following landmarks were identified and used for linear measurements: PM (the marginal portion of the periimplant mucosa). aJE (the level of the apical termination of the junctional epithelium). B (the marginal level of bone to implant contact), A/F (the abutment/fixture border). The findings indicate that the dis‐ and subsequent reconnections of the abutment component of the implant compromised the mucosal barrier and resulted in a more “apically” positioned zone of connective tissue. The additional marginal bone resorption observed at the test sites following abutment manipulation may be the result of tissue reactions initiated to establish a proper “biological width” of the mucosal‐implant barrier.

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