apart from the obvious pathological reasons, the  functional bone  remodeling  and turn over as the later was not usually functional for a while..

waiting for more expert views

This is a very in-depth topic and I'll try to respond by summarizing various points within the topic.

1) I don't think that function is the issue here -- initial peri-implant bone loss will occur in similar fashion around implants that are merely subjected to placement of healing abutments.  The focus here is on a number of things -- biologic width, and micromotion and microleakage at the IAJ -- and these things generally only come into play one the implant-supported componentry protrudes transgingivally.

2) Three rationales are generally provided for initial peri-implant bone loss:

-IAJ microleakage / inflammatory zone of the IAJ

-IAJ micromotion

-apical shift of biologic width

Hermann et al. performed a number of investigations from 1997 to 2011 that looked at initial peri-implant bone loss and factors such as one-piece (no IAJ) and two-piece (yes IAJ) fixtures, subcrestal vs. supracrestal placement of the IAJ and soldered vs. regular healing abutments (in an attempt to isolate micromotion from the presence of an IAJ) and with these papers combined, along with those by Abrahamsson in 1997 and 2003, the following conclusions were derived:

- bone is generally lost to 1.5-2mm from the IAJ when the abutments are dis/reconnected multiple times

-bone tends to be lost on smooth / polished surfaces up until the rough/smooth border when the smooth / polished surface is placed subcrestally

What defines "multiple times" is a good question still under consideration.  If abutments are dis/reconnected, the speculation is that introduction of bacterial products into the IAJ space generates a circumferential halo of inflammation that leads to bone loss.

3) Continually removing abutments also acts to disrupt the biologic width formation on the abutment.  Epithelial cells attach via hemidesmosomes to the abutment and connective tissue fibers align parallel to the abutment surface just apical to that while the most coronal aspect of the fixture is placed against bone in the osteotomy.  Biologic width can then form and remain supracrestally.  However, with repeated abutment dis/reconnection, the continually disrupted biologic width shifts apically to find a more stable location to develop and this will be the implant surface.  Bone loss is effected in order to make way for biologic width formation on the implant rather than the abutment.

4) Platform switching has been demonstrated to be favorable to this scenario.  Mean horizontal dimension of the influence of initial peri-implant bone loss was initially reported by Tarnow et al. 2000 as ~1.5mm, which generated the 3mm rule (1.5 + 1.5).  With platform switching, this value is diminished to ~0.7mm (Rodriguez-Ciurana 2009).  Mean vertical dimension of bone loss is similarly diminished when it comes to platform switching, also ~0.7 verses 1.5-2mm for platform matched (R-C 2009).

The explanation as to the basis for this improvement is as follows.  Exposed platforms due to platform switching provide greater surface area for biologic width formation, and so less bone loss due to apical shifting.  The IAJ -- source of microleakage / micromotion -- is placed onto the platform, recessed away from the margin of bone at the most coronal aspect of the osteotomy, and so its (the IAJ's) effect on bone is decreased.

5) In respect to Gaballah's post, I'd just like to comment that "bone remodeling" is an unfortunately poorly understood term and adds to confusion, really.  Check out the Wikipedia article on bone remodeling -- it's defined as the coupled process of bone resorption and deposition that continues throughout life and meant to counteract the cumulative effects of micro-damage, etc.  Post-extraction ridge resorptive processes is not related to this phenomenon.  It's much more closely related to bone modeling, which is how bone responds to trauma, but even that is somewhat of a stretch, because post-extraction ridge resorption is somewhat unique, following what may be explained according to Wolff's law and the functional matrix hypothesis (check out those on Wikipedia as well).

Anyway, there's lot's more to say, but that should provide a good starting point for discussion.

Thank you so much Dr. Gaballah for your response to my question and many thanks for Dr. Rosenbach for the valuable information that he provided us with. Yes a part of peri-implantitis as i mentioned in my question it was a bout crestal bone loss around functioning, healthy implant, I think what Dr. Gaballah meant by remodelling is that the adaptation of the implant to directionally different occlusal forces, including vertical and lateral forces. As the crestal bone around the implant is the thinnest part of the alveolar process and due to absence of periodontal ligament fibers which act as shock absorber so these forces will be transmitted directly to the bone and this will lead to resorption of the thin alveolar crest as part of adaptation to these forces and this explain why the majority of crestal bone loss happens during the first year of function. I also agree with Dr Rosenbach’s answer in respect to the biologic width preservation because both natural teeth and similarly with dental implants there must be a biologic width for epithelial attachment in case of implants and epithelial and fibrous attachment in case of natural teeth, as most of the implants are inserted with the level of the crestal bone therefore there should be at least 2 mm bone lose in order to provide a room for the epithelial attachment at the biologic width. Hope to hear more from you Sirs.

It is due to many factors which can be summarized as following

1- The stress of occlusion distribute mainly in the cortical bone which is usually thinner than the cancellous bone of the jaw. So as a response to this stress the bone resorbed and this resorption occur in the cortical bone because of it hard structure compared with cancellous bone .

2- This  occur in the first year of loading of implant the there is a response from the bone to adapt this situation. In this case there are two theories which may explain the bone response to stress ( Wolfs and Forst theories). This response leads to stop or decrease the bone resorption that why the resorption of the bone is very low after one year.

3- Functioning implant subjected to different degree of plaque accumulation which may play a role in bone resorption.      

Thank you Dr. gataa,now i got a lot of knowledge and great explanations for my question I Really appreciate your answers and this nice discussion together, hope i  hear more about the subject.

To add little to the above well described facts.:  stress shielding may also be one of the reason for crestal bone loss. None of the implant biomaterials has the modulus of elasticity [Titanium 110 Gpa , zirconia 210 Gpa Vs Cortical 15 Gpa]near or equal to the cortical or cancellous [PEEK is some how near to cancellous, but it has its own limitations]. Because of this stiffness, implants do not adequately strain the bone which can result in disuse atrophy and bone resorption. Together with biological compatibility, mechanical compatibility also plays an equal role.

Further check this article it gives further insight about crestal bone loss in healthy condition http://www.pesgce.com/pde/pdf/2009_12_crestal%20bone%20loss%20part3.pdf

together with IAJ microleakage, to better understand the "biologic" background behing the importance of dis/reconnection, you should consider also the quality of the cleaningness of the abutmetn. In fact, several studies have demonstrated that soft (and therefore HARD) tissue response depends on how dirty is the abutmetn and how strong is the connectiove tissue adhesion to this abutment

Simply, because it is where bone loss will start.

yes Dr. Ghuneim,,, but the question is why within the first year then it will settle down to minimum 

Some possible causes for peri-implant bone loss are presented in the literature: flap  detachment, biological width establishment, three-dimensional positioning of the implant and bacterial leakage at implant-abutment interface. 

Perhaps the anatomical differences at the interface such as lack of fibrous attachment at the interface renders less secure attachment between the implant and the surrounding mucosa,  thus bacterial leakage to osseointegration zone.

The lack of fibrous attachment could permit bacteria get at the IAJ, but if we don't have misfit at that interface, immunologic system can handle with that in healthy people. In patients with periodontal disease the risk is much bigger. As I said before, this is a multifactorial issue. 

Platform switching is of great value to reduce the risk of bone loss, since in that case biofilm is not close to the bone. 

check the occlusion, perhaps there are traumatic occlusion.

It is principally due to the diference in elastic modulous €;   of bone and titamium alloy almost 10 folds that 

thank you Dr. Guneim, , Natural tooth also much harder than the surrounding bone with a big difference in modulus of elasticity between them, although titanium is a metal and it should be very ridged 

Dear Prof Faraedon Mostafa Zardawi ,

The biomechanical behavior of dental implants is different from that of natural teeth. One of the main reasons is that these implants suffer from the absence of the function of the periodontal ligament. This is because the periodontal ligament material is a soft tissue that can function as an intermediate cushioning element to absorb the force of the impact and evenly transfer the occlusal forces to the bone surrounding. However, the bio-structure of the dental implant is directly related to the bone. This can cause non-uniform stress distribution in these two elements, which can lead to biomechanical overload leading to bone and implant failures.

I'm available for any further information you may need.

Best Regards

Pr. Ali MERDJI

Faculty of science and Technology,

University Mustapha Stambouli of Mascara,

B.P. 305, W. Mascara, Algeria.

E-mail: [email protected]

E-mail : [email protected]

Mobile phone: +213540540277