Possible to Cause Compression Necrosis by Tightening Too Much?

Hi Dr, theres every possibility of Osseocompression to occur in implant cases well i,ll suggest you to wait for few more days wat best i suggest is ask your pt for warm saline rinses at least 5-7times/day for a week to enhance natural healing in your case don worry it. Wish you a Luck Regards Dr.Abhi

Dr. I do not agree with the term Osseonecrosis in bone from overtightening an implant. If you talk with your orthopedic colleagues you will find they tighten their screws routinely over 200 ncms. If the bone was rock hard and marble like, I believe the problem is not overtightening, but bone the is too dense to recieve a dental implant. Hard bone without a trabecular space has very little regenerative ability and failures can occur routinely in this type of bone. I always overprepare these sites and fill with regeneration material. After new bone forms with a good blood supply, I place my dental implant. This seems to work well for me. If the implant fails. Remove the implant. Create a wider osteotomy. Fill the osteotomy with a regenerative material like Regenafil or Progenix. After the area has healed for 5 months place a new implant. I hope this helps, Dr. Robert Schroering

dear doctor your patient is suffering from burnt bone syndrome. The etiology was high torque used to install a dental implant and to faster tightening of implants. Prolonged pain for a week is ok, better responds to analgesics. But high torque exceeding 35NCm is deleterious to bone, and better not exceed 12 rotations per minute when using a ratchet to install implant. But be prepared for bone regenerative techniques as crestal bone loss is common when a torque you used.

Dr. Robert's technique of over preparing, inducing new bone using bone analogues and place implant after 5 months is what i feel is very aggresive and needs evidence based evaluation. Better use bone taps after final osteotomy and install implants. Added to this patients with D2 bone are good candidates for immediate loading.

Paolo Trisi has a very interesting lecture and research on this topic where he torques the implants to over 100 Nm with no ill effects. Possibly the type of Implant can have a varying effect ( taper or cylinder) but it would appear as though compression necrosis may be mere hearsay. Heat is a more important issue and agin is dependant on the type of drills utilized whether twist or internal irrigated cutting blades.Possibly these variables need to be ascertained.

Can compression cause resorption ? No question, compression can cause resorption. We see it in oral surgery all the time. Soft tissue, muscle pull, wins the battle over bone every day and twice on Sundays. No where is this more evident in fracture repair and orthognathic surgery. Poor release of the counter vector muscle components leads to relapse and resorption. Let's us dive into the late 80's early 90's with fracture repair. The eccentric dynamic compression plate for instance was the hot topic in trauma. It was designed to approximate fracture segments and with the eccentric drilling, place compression on the fracture line (putting compressive forces on the distal and proximal fractured bone segments). This was thought to improve healing and speed recovery. As the literature began coming out, it actually had longer healing times and higher complications (infection, fibrous and non-unions). You'll see that the fracture systems in hospitals now don't include the EDCP (eccentric dynamic compression plates). Champe and others have shown, correct repositioning on the fracture segments (with minimal gap) with rigid or semi-rigid fixation without compression yields the best results. The phases of fracture healing and implant healing are quite similar. However, certainly, temperature sustained over 43 C is another critical factor in implant success. That being said, no one quite knows at what torque a particular individual and/or individual implant will suffer pressure necrosis (pressure ischemia). It will vary from individual and site to site and have other variables such as prep time, trauma, temperature, etc that lead to the ultimate success or failure of the implant. Although a different physiological model, look what little force on the PDL can cause resorption on bone to allow tooth movement. However, to muddy the water, an ankylosed tooth with many kilograms ( exaggeration ) will move little or none at all. So the science of what pressure and how bone react is still not completely understood as we don't know how all the variables that lead to resorption interact and what individual variations are. Also of note, please look at SEM (electron microscopy) of bone implant interface. After you study that, you'll understand the term osseointegration should likely be renamed.

Is it the toque or does your patient you descripe as being frail and middle aged, uses medication. I will think about medication against osteoporosis, etc. These can alter the nerve endings and causing pain which in normal cases won't occur in the same settings. When using medications against osteoporosis or for middle aged things the bone becomes harder, but loses its elasticity and causing more crakcs when put under strain. This can cause pain as well. I can't give you an answer on what to do. Maybe give it some time

Sounds like trauma to the periosteum. This happens to my patients from time to time any time we traumatize the periosteum. This includes PDL injections, laying a flap, aggressively polishing a restoration below the gingiva, and packing retraction cord. The pain should spontaneously disappear approximately 2 weeks after it began, similar to a dry socket. Using a continuously tapered implant, I don't worry about overtorquing anymore.

Compression Ossteonecrosis is a term that derived shortly after Nobel introduced the Replace implant which is a tapering implant placed into a tapering osteotomy. In medium to dense bone this is a very difficult implant to screw down since it binds at the apex as it tightens into the conical apical portion (a wedging effect). This can happen even when dense bone drills are used. Early users found this implant design to behave very differently from the parallel-walled implants that they were used to. There were preliminary reports in using this implant, of seeing uniform early bone loss through the entire length of the implants. Without any research, this phenomenon was attributed to "compression osteonecrosis" and an arbitrary value of 35 newtons became the recommended insertion torque baseline. There is however still no research whatsoever that such a condition as compression ossteonecrosis actually exists or that high value insertion torque over 50 to 60 newtons or greater is deleterious to bone. I personally have not seen any consequences of installing implants with high insertion torque unless the implant wall fractures such as may happen with very narrow diameter implants or the fixture mount fails. Dr Fairbairn has quoted Dr Tristi as an knowledgable person with regards to bone compression effects and I believe both are quite correct in their assertions that this is a red herring when it comes implant installation. I have countless times inserted implants at values I am sure were much greater than 50 newtons and have not seen any negative effects and yes I often use torque measurement systems to make my insertions. Further, if implants are planned to be done in single stages, a technique which is becoming commonplace, then I believe primary fixation to be paramount in which case the implant surgeon will be needing to place implants with fairly high insertion torques of over 30 newtons to withstand the intraoral loading on a healing abutment. If indeed such a thing as compression ossteonecrosis actually exists, than I think it must happen at torque values well in excess of 100 to 200 newtons.

I have had many cases like this one in which a backed the implant up 1/2 turn and the pain magically went away. What we have to consider is whether your implant is a compression screw by design. A parallel walled implant cannot be a compresion screw so the amount of torque is meaningless. THis is why orthopedic surgeons can put in screws at 200ncm. Nobel Tapered Groovy however is a compression screw and has shown bone loss and failure that looks very much like avascular necrosis at torque above 45ncm. One must also ask if this patient is on bisphosphonates and for how long as osteonecrosis following oral surgery has been demonstrated on these patients with patients on the medication over 7 years being at high risk. I would bet money that your patient is on bisphosphonates as bone in these jaws tends to be very hard as you described. ID love to hear how things turn out.

May sound unorthodox but we keep our implants in the freezer until placement. In woodworking or tightening a screw into sheet metal, you can feel the heat created. Just kinda makes sense.

The comments about Replace are right, but the mistake was to indicate an implant that was developed originally for immediate postextraction placement and latter indicated by Nobel for all purposes in the whole mouth. Necrosis synthoms are pain, no swelling but a never totally healed gingiva. After 7-10 days pain will disappear and in two to three weeks radiolucency will be watchable in a periapical X Ray. My advice: never torque your implants over 35N/cm (yes, you can do it but there is no need to do such a thing). Use a parallel wall implant in dense bone (never tapered). If you are a Replace user and you still want to use tapered implants in hard bone, then use Replant (implant Direct LLC) instead of Replace as it is better self cutting and has a vertical groove in the tip. What to do: retrieve the implant. Wait for bone healing/remodeling /ie 3 months). Place another implant with new drills, good cooling, taping and dense bone drilled and never go over 35n/cm. If the bucal wall is still present there is no need for bone fillers. Hope this will give you some light. Best regards. P.P.

With the implant system that I use (BioMet-3i), I have always been able to place my tapering implants with very high insertional torque and I have not experienced "compression necrosis". It helps if you become experienced with a particular system and implant design, and then you will better understand the limitations/indications and tolerances which will vary. I personally know many experienced surgeons who use the system that I use with expertise, and whom have not witnessed any evidence of compression necrosis. I have over 15 years experience with all of the implant designs that BioMet-3i has developed over the years.

A nice collection of theories, but most are off the mark. The operative word here is NECROSIS. In a failed site where the implant and surrounding bone have been explanted, do we see a zone of necrotic bone? What we see is a fibrous encapsulation of the implant body. Now let's deconstruct the path leading to this event. An interrupted angiogenic response leads to fibrous tissue rather than bone contact with the implant surface. There are several reasons why this occurs. First is an inflammatory response. Bone that has even a slight pH drop (from neutral 7.4 to even 7.1) will completely inhibit osteoblast metabolism. Second is the catabolic phase of bone. Increasing the zone of microfracture as the implant is placed (as torque values increase) increases this catabolic phase. Osteoclastic activity is potentiated and bone is being resorbed in the early phases. Third is seating the implant well above it's designed torque value. As the implant bottoms out in the osteotomy, further torque on the implant results in the implant threads moving coronally while the implant remains stationary. This microfractures the intra-thread bone, compromising the microvasculature and accentuating the catabolic response. Last is the choice of implant surfaces. Some of them will actually increase the catabolic phase as well, leading to higher failure rates of some implant lines of the biggest implant manufacturers. Therefore, I believe that the term compression necrosis is a poor choice for explaining this phenomenon. Rather, we should be referring to compression microfracture. Our new paper comparing three of the leading implant surfaces (Calicum phosphate blasted, HF etched, and Calcium phosphate impregnated) leads us very clearly to the concept of LOWER insertion torque values, and a chemistry that eliminates the catabolic phase of bone, speeding up bone bonding by 500% within the first week (Ossean Surface - Intra-Lock International). RJM

Thank you Dr. Miller, this is a nice explination.

I appreciate the explanation Dr. Robert MIller's theory for unexpected implant failures in what would be considered ideal circumstances. I and many others would like to read the article on this subject.Where is it published?

Dr. Miller, I too would like to read the article.

For those clinicians who would like a PDF article of our study on comparing leading implant surfaces, please email me at info@robertmillerdds.com. RJM

To Richard Hughes: How are you doing? I think you need to add some more letters after your name, it's not qite enough. To Dr. Miller: A zone of necrotic bone is EXACTLY what we see in these over-tightened cases. Rather than just a small radiolucency around the implant indicative of fibrous encapsulation these cases show saucerization with destruction of bone up to and involving adjacent dentition. Sometimes the implant ends up floating in a soup of granulation tissue and necrotic bone. Interesting that this occurs far more often with a 6.0mm diameter implant than any other. Is this because the implant is tightened more? No it is because the 6.0mm osteotomy removes all of the microvasulature that supplies the cortical plates and the implant creates compression directly on the cortical plate itself with no intervening medullary bone. No blood supply + pressure = necrosis. It has nothing to do with "exceeding the torque limits" or "change in pH". The term "compression necrosis" is indeed a good choice of words for this phenomenon.

Did you do the histo on these cases? Or is this your empirical impression of what you think you see. That radioluscent area that you see around the implant is a soft tissue response. There are living cells in this zone, NOT necrotic tissue. When you extract the implant, do you find a bleeding soft tissue interface? A necrotic tissue zone does not bleed because there are no blood vessels in that zone. We have done the histo on explanted implants and find a soft tissue interface with inflammatory infiltrate. The change from bone to soft tissue is the very definition of the catabolic response and will not occur in a necrotic zone. Angiogensis is actually ENHANCED and you get a nice beet red zone of tissue. Necrosis is what you see in bone with a pathologically low oxygen tension (osteoradionecrosis and osteochemonecrosis). This bone does NOT bleed when prepared. I woould suggest a review of basic histology. RJM

I agree to Dr. Robert Schroering, If the bone was rock hard and marble like, I believe the problem is not overtightening, but bone the is too dense to recieve a dental implant. Hard bone without a trabecular space has very little regenerative ability and failures can occur routinely in this type of bone. Thanks for this blog I learned a lot. -heather-

Robert J. Miller, I think logic isn't correct there. In a stroke patient you will not find necrotic tissue inside their brain after few months. Problem would be that highly specialised cells couldn't survive without adequate blood supply and died, subsequently being replaced by scar tissue. I should think same principle applies in here. Naturally, you find [b]living[/b] cells, only it is basic non specialised cells - granulations. I agree with Dr.Levit in this matter.

Granulation tissue by definition is chronic inflammatory tissue. In this case it replaces bone during the inflammatory phase. The production of matrix metalloproteinases (collagenase, gelatinase, elastase) occurs during the catabolic phase of bone, breaking down the collagen matrix in bone. The slight decrease in pH completely turns off osteoblast metabolism. At the same time, osteoclastic activity is POTENTIATED. This is why excessive microfracture at high torque values results in failures of some implants and a finding of a fibrous interface rather than osseointegration. Necrosis results from a shutdown of microvasculature and cell death from low oxygen tension (i.e. stroke patient). Nothing that we see histologically gives any credence to the concept of compression necrosis. It is, rather, a substitution of tissue that occurs during an exaggerated inflammatory cascade. RJM

Just theoretically, when autogenous bone is processed with a mill you get macro- and microfractures, osteoclast activity is also much elevated, yet the new bone is formed. I dont think microfractures are the reason. But i agree with "a substitution of tissue that occurs during an exaggerated inflammatory cascade". The question remains: what started the inflammation?

You are right in your assessment of autogenous bone grafts ultimately forming new bone. But this occurs over several months, well after any inflammatory byproducts are gone. The question here is failure of an implant early in the healing process and the events leading up to the failure of osseointegration. Two different paradigms and two different pathways. However, the catabolic phase of bone actually ramps up when grafts are placed. If you did not get upregulaion of ostoclasts, your graft would never be resorbed and replaced with autogenous bone. There is a beautiful study measuring rate of osseointegration and average roughness (Ra) of dental implants. Osseointegration increases in rate as Ra reaches 3.13 and then starts to DECREASE as implants become more rough. This increased microfracture of bone as the implant is being turned through bone (osteoreduction)results in an exagerrated catabolic response and an interruption of angiogenesis. Microfacture of bone around implants has long been established as a leading cause of bone remodeling, whether caused bt roughness or excessive torque values. RJM

its obvious that we all agree that exceeding torque values isnt always safe, but ive seen many live syrgeries and videos people doing immediatte loading and overtighten the implant manualy and they donto get necrosis or failures. in my experience i have notice alot of coronaly bone loss from placement up to uncovery with xive that iam using (and over-torque)iam searching quite along time the reason for that, but qoing to an immediatte loading era iahavent seen enough evidence. iave notice that when in soft bone a value of 50 will not lead to coronal bone loss, while in lower jaw a value of 50 will destroy bone and i might loose implant. it seems that is not torque values alone but quality of bone?

I think we have to differentiate between immediate loading and traditional loading. In immediate loading higher torque is desired and it can be up to 100n/cm wih no osseointegration problem. This refers to survival of the implant, no uncovery flap is being done and probable dehiscences or circumferential bone loss can go unremarked unless soft tissue recession evolves. in traditional loading protocols, most people agree to stay below 35- 45 N/cm. More torque is meaningless anyway in these situations.

RJM is a very smart guy The rest of us have "clinical theorys" based on anecdotal experience...read and re read what he (RJM) writes Then re read your basic histo of osseo integration. Thanks RJM you have taught us a lot

Expect decrease in bone density around implant within 1 month and at end of 3 months there may be failure. I believe systemic disease also one of the cause if there is any. Please refer this article doi: 10.1902/jop.2009.080581