I special _ endo-implant algorithm andtheperi-implantenviron- ment. A bacteria-proof seal, the lack of micro-movement associated with a friction grip interface and a minimally inva- sive second-stage surgery (where in- dicated) without any major traumatotheperiostealtissues are also important factors in preventing cervical bone loss. The literature suggests that the stability of the implant- abutmentinterfacemayhavean important initial role to play in de- termining crestal bone levels.52 Tarnow’s seminal study on crestal bone height support for the inter- dentalpapillaeclearlydemonstratedtheinfluenceof the bony crest on the presence or absence of papil- lae between implants and adjacent teeth.53 Twenty years later, logic dictates that anticipated early cre- stal bone loss and diminished, albeit continual, loss in successive years of function ought to have been engineered out of the substitution algorithm for peri-implant tissues.54 _Platform switching: By default or by design Thereisnologicalwaytothediscoveryofelemental laws. There is only the way of intuition, which is helpedbyafeelingfortheorderlyingbehindtheap- pearance. —Albert Einstein Platform switching theorises that by using an abutmentdiameterofalesserdimensionthanthe peripheryoftheimplantfixture,horizontalreloca- tion of the implant-abutment connection will re- duce remodelling and resorption of crestal bone af- ter insertion and loading. The concept implies that peri-implant hard tissue stability will engender soft tissueandpapillapreservation.Maedaetal.reported thatstresslevelsinthecervicalboneareaperipheral to a fixture were greatly reduced when a narrow di- ameter abutment was connected, in comparison to asizecommensuratewiththefixturediameter.55 The authors concluded that the biomechanical advan- tageofshiftingstressconcentrationsawayfromthe cervical area will diminish their impact on the bio- logical dimension of hard and soft tissue extending apically from the FAI (Figs. 11a–c). The inherent dis- advantage is that this shifts stress to the abutment screw with the potential for loosening or fracture. Ericssonetal.56 detectedneutrophilicinfiltratein theconnectivetissuezoneattheimplant-abutment interface. The facility by which platform switching/ shiftingreducesbonelossaroundimplantshasbeen investigated by Lazzara etal.57 The authors hypoth- esisedthatiftheabutmentdiametermatchesthatof the implant, the inflammatory cell infiltrate will be formed in the connective tissue at the micro-gap createdattheFAI.Ifanabutmentofnarrowerdiam- eter is connected to a wider neck implant, the FAI is shifted away from the outer edge of the implant, thus distancing inflammatory cell infiltrate away from bone. Hypothetically, less crestal bone loss is 16 I implants2_2011 Fig. 11bFig. 11a Fig. 11c Fig. 11a_The composition of bio- logical width around implants: sulcus depth (SD), distance from peri- implant mucosal margin (PM) to the most coronal point of junctional epithelium (cJE); junctional epithe- lium (JE), distance from cJE to most apical point of the junctional epithe- lium (aJE); connective tissue zone (CT), distance from aJE to the first bone to implant contact (BC).63 Fig. 11b_When a matching implant- abutment diameter is used, the inflammatory cell infiltrate is located at the outer edge of the implant-abut- ment junction close to crestal bone; this close proximity may explain in part, the biological and radiographi- cal observations of crestal bone loss or saucerisation around restored implants. This is not peri-implantitis or mucositis; however, any area of bacterial accumulation and stasis, inaccessible to normal hygiene proto- cols, is a risk factor for exacerbation.