Biologic Width: How Do We Apply this to Implant Dentistry?

Dr. RJ, You are exactly right with regards to implant design. When we are speaking of biologic with respect to implants we are really looking at the distance between the most apical attachment of the soft tissue complex and the abutment/implant interface. This complex varies in make-up(epithelial vs connective tissue) and width depending on design(collar or not) and whether platform switching is utilized. This is different from natural teeth not only in make-up, but orientation of the connective tissue fibers. From a restorative viewpoint, we always look at what we wish to accomplish with the final restoration and then plan our surgery from there. Therefore, I will decide whether I will place my implant platform at the crest, below it, or above it. My soft tissue needs and esthetic desires will predict my use of platform switching or not. Hope this helps a bit-

‘Biologic width’ is used to described the connective and epithelial tissue about natural teeth. We need to be careful in relating this to dental implants. There has not been a true definition for dental implant ‘biologic width'. There is only a epithelial attachment to dental implants. Therefore, the tissue is very susceptible to infection. The true dental literature has been very clear about this.

Don, True-- it is not really a true biologic width. But the body does establish the complex in some respect like a "biological width". The soft tissue complex behaves differently with respect to implant design, vertical position related to the osseous crest and the adjacent teeth. These tendencies are pretty well established in the literature and seem to be influenced even more by the surounding hard tissue position than the implant itself

Dr RJ The fact that different implant systems have different degrees of crestal bone loss associated with them is associated with implant design and implant placement, not biologic width. You are associating biological width with implant crestal bone resorption, when in reality, the implan-gingival complex is physiologically determined with stable dimensions. The degree of crestal bone remodeling around implants is influenced by things such as: 1- implant placement in relation to the crestal bone level 2- the type of surface at the implant collar (polished, machined, blasted, laser etched, etc...) 3- Micro movement of the abutment-implant connection. 4- The abutment-implant connection design, which includes things such as platform switching, internal vs external connection, morse taper, antirotation, etc... You definitely need to take into account the established dimensions of the implant-gingival attachment complex when planning your surgery, but as you have observed, you choice of implant design will also influence the results. Thanks, for a great question.

The concept of the biologic width is as poorly understood around teeth as it is around implants.Most of our knowledge of biologic width around teeth stems from research on cadavers in the 60s by Garguilo & Orbans,which enabled us to ascribe a numerical value to the combined width of epithelium and connective tissue around teeth,ABOVE the crest of bone.We need to understand that these figures proposed by the mentioned names were AVERAGE figures and don't necessarily hold up around teeth as we know from Kois's work in the late 90's and 2000 and three relationships ie. normal,high and low crest relationships occur around teeth and the soft tissue measurements above the crest of bone can vary from 3-6mm on account of the dynamic attachment of gingival sharpey's fibres to tooth cementum.This sort of an arrangement is currently not possible around implants irrespective of surface characteristics. In this scenario, the best way to describe biologic width around implants is the minimum thickness of soft tissue-epith &C.t. that's required to PROTECT osseointegration and a lot of papers have shown this by means of a vertical measurement of 2.5-3mm,which is the reason why bone loss occurs with crestal and subcrestal placement. Perhaps a more rational approach would be to look at the VOLUME of the biologic width,which is probably one of the mechanisms by which platform switching works. Assesssing the soft tissue volume prior to placement is probably the most rational way to proceed with regard to contemplating on the surface characteristics of the implant CREST.3mm and greater- textured/rough collar ,crestal placement should not result in any crestal loss.)0.5mm smooth collar placed supracrestal in this situation will also not result in crestal loss.

"Biologic width" as I understand it( please correct me if I am wrong), was a term borrowed from prosthodontics. It denotes the observed resultant distance that develops between the crown-abutment margin of a natural tooth and the crestal bone level when the margin is placed less than 2mm to the crestal bone level. The observed distance or "biological width" is about 2mm. It means that if we place the crown-abutment margin less than 2mm distance to the crestal bone level, the bone level will resorb or die-back until there is at least a 2mm gap distance to the crown-abutment margin. It was labelled biologic or biological because it was observed as a "natural"(sic) biological response of the bone tissue to the crown-abutment margin. This response was attributed to the irritation that the margin inflicts on the bone for some reason. And this is the reason that we extrude a class 3 fractured tooth so that when we build a post crown, the distance between the crown margin and the bone level can be increased to at least 2mm to prevent further resorption of the bone and subsequent exposure of the crown margin. This term was borrowed into implant dentistry to explain why bone always seem to resorb back at least 2mm away from the abutment-fixture margin. The resorption was attributed often to microorganisms finding a snug home in the microgap. With the advent of "platform switching" and morse tapering the microgaps became non-existent or too small for the microorganisms to squeeze in any more and thus the dieback stopped! Or is it because the margin was designed away from the bone? In many morse taper designed implants, it was observed that bone grew over the abutment-fixture margins! So the former reason may be correct. Recently, after a marathon lecture by Carl M. I am almost convinced that inadequate attention to the biomechanics of the bite may also be part of the cause of the dieback of bone. Still learning, guys. Maybe we should try one pieces more often because then we do not have to bother with the abutment-fixture margins and therefore no diebacks but liveons!

Dr. Chow, Thanks for the explination.

Saddoun from France has addressed this question and it's worthwhile looking at some of his comments. Certainly, if the transgingival component of the implant (implant+ titanium abutment) is properly designed, there is no microgap leakage and the restorative element(eg crown) doesn't invade this area, then there is no such thing as a minimal or maximum "biologic width" for implants. If these parameters are understood and not abused, then you will get good gingival stability. If you place atrocities such as gold UCLA abutments,flared abutments,significantly sub gingival crowns, or don't seal the microgap, then you will not get good gingival stability. Depending on the tissue type, the gingival interface can be very thick or very thin,and if the rules are obeyed, then the gingival stability should be ensured, assuming adequate oral hygiene.

Hi,Lots of academic papers out there.Basically in practical terms you don't want bone loss!!This creates a pocket situation, with a rough threaded surface perfect for bacterial colonisation. Exacerbating therefore bone loss. Pocket elelination surgery aims to reestablish 'normal biological width'so we don't have an uncontrolled situation.Raise a flap curvilinear in design and debride and get rid of the granulation and fibrous tissue. Some people advocate preparing the implant surface with copious irrigation, obvious care needs to be taken not to damage the internal connection (think-reversal tool!)Values for biological width vary but in health we have less than 2mm vertical loss in the first year and less than .2mm annually thereafter. Chapel talks about the range of connective tissue between 2-9mm around teeth and implants to be the ideal. The nature of the tissue, and its tight intercellular connections (hemi-desmosomes) make it resistant to mechanical and microbial challenge. So with this layer of attached gingivae we maintain an ideal biological width which can thus vary greatly over the time from placement and thereafter.

Biological width in one stage for at the time of implant placement, while in 2 stage implant start at the time of abutment or crown installation, at the beginning of its formation is composed almost of connective tissue and less epithelium for this more resorption found at early healing wound period due to forceful connective tissue formation that push the crestal bone downward, while the later on more epithelium formed and the percentage of connective tissue become less for this we have some how less bone resorption after word, this is what I have found from my research, that I need to publish it, if some one can offer me to help me in this, my e0mail can be taken from the web site fro further contact, thank you

Dr. Chow provides an excellent rendition of the proper use of the term "biologic width" as it applies to teeth with crowns and subgingival margins. The term should have been left to describing that relationship only. Its use in implant dentistry simply created an atmosphere of confusion since the bone/epithelial atachment to the implant/abutment complex is not the same. What is known about implants and bone preservation is that the bone undergoes a resorptive process "down to the first thread" in platform abutment/implant systems due to the bacterial cesspool that develops in the microgap. This gap opens and cloles in functin as stresses rock the abutment side-to-side on the implant and creating a pumping of endotoxins into the peri-implant tissues. Morse taper systems can solve this problem, but not all Morse tapers ar created equally. The micro gap of a Morse taper can be smaller than any bacteria of dental significance. But when these systems are continuously loaded with off axis stress, only systems with long taper contact dimensions, greater than 2 mm, will withstand the forces and maintain the integrity of the microgap. No microgap = no bacterial cesspool and significantly less bone loss. Other factors influence bone loss such as depth of implant placement. Small Morse taper contact lengths, in the order of .7-1.0 mm will not resist abutment displacement over time since the retaining screw still does all the work for retaining the abutment to the implant. The bending causes screws to stretch, microgaps develop, and eventually the system integrity is compromised. Platform swithcing is nothing more than a technique to move the bacterial cesspool inboard from the implant periphery by using a smaller diameter abutment than the implant proper, but does nothing for the rocking of the abutment and the platform gap opening and closing. This helps protect the bone in the crestal area, but does not eliminate the problem.