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Ask UsMassive Bone Resorption: What Should I Do Now?
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Anon. asks:
My treatment plan was to extract #12, 13 and 14 [Ed. Maxillary Left First, Second Premolars and First Molar] atraumatically, place bone graft material and allow the graft sites to heal for 5 months. Then I was to place dental implants.
The extractions went well, no buccal plate fractures occurred and I grafted w/ Puros and then covered the graft with Gelfoam and sutured over the wound sites securely.
Patient returned at 5 months and presented with massive resorption at all sites. At that time the patient learned he had diabetes which was then being controlled with drugs. What happened? Was the resorption due to the diabetes? Did I not graft correctly? What should I do now?
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16 Responses to “ Massive Bone Resorption: What Should I Do Now? ”
I guess the resorbtion was due to patients high sugar level, as seen in most diabetics, resorbtion of bone & perio problems are common.Guess some medications prescribed for diabetics like diuretics also have a role to play , reducing the water & salts level in the body can cause irreparable damage.
control the diabetes should be the first priority.Study the degenerative changes over a period of time should be the next to follow before planning any further treatment.
Treat the patient on temporary treatment plans to save both time & money .
Read IJPRD 1/06 Nevins.
Sure you want to get the diabetes under control, but what caught my eye was the using of Gelfoam.
Gelfoam does not keep out the soft tissue. You will end up with more bone in your grafted areas if you use a membrane instead of Gelfoam.
For now, if there is not enough bone for implants, get a sinus lift done and your back in the game.
as of now if it is confirmed that the patient is suffering from diabetes, it is imperative to first take care of that, i mean get his/her Hb1ac test done which will show you the pattern of control & then only proceed with some other procedure such as sinus lift or so on. because there is no point lifting the sinus n then after some time again ending up with same outcome….
Some additional questions; First, did the resorption occur from crest down or was it congruent with apical resorption? Second, was there complete primary closure of the flap throughout healing? I concur with the comments regarding the use of gelfoam. It it not an occlusive material but rather a hemostatic agent that increases surface reactivity at a time needed for angiogenesis and osteoid formation.
There many factors involved, but the first is the material that was used. Puros has NO ability to form bone, you were asking the body to do all the regeneration. The job of the body is to repair!! I feel that you should have used a material that will aid the body in the regeneration process. The material you use is only a filler it does not make bone, it allows bone to form on the material
What happened? Bone resorption as usual after extraction.
Was the resorption due to the diabetes? It´s not the mosto important reason
Did I not graft correctly? NO. We can´t make graft in a decompensatewd diabetes. Puros is only a osteocondutive material.If the bone vascularization is compromised as you see in diabetes there is no indication for this kind of material. Gelfoam is only a haemostatic material.
What should I do now? Remove the graft, diabetic control and wait 6 months. Evaluation of the patient and boen graft if necessary.
Dr Callan,
Can you elaborate on the Puros having no bone forming ability
I would like to know if the patient was on any medications. I had a patient that I placed an implant in great bone and she forgot to mention that she had been on Zometa. Didnt integrate. No osteoclasts. You have to have them. A graft would have been a disaster. What Age was the patient? Osteoporosis? smoker? coffee drinker or soda addict? Perio? As far as the sx, if you put in a hemostatic agent, it hinders the blood supply. no blood, weather diabetes or otherwise, no bone. Might as well have been a clot. My first few grafts, I packed the bone more densely than now. I get pink bone in a few months. I use mineralized bone only (recommended by a periodontist I respect) and I AGGRESSIVELY scrape the socket for RAP until it has as much bleeding as I can muster before grafting. I havent been disappointed since. Many things work in a graft site and patients heal differently and make bone differently. With this patient, I agree on waiting, diabetes in great control, then go back in. Youll have good tissue for 1ry closure and can do a lift if you are trained. Don, I enjoyed your course in Hattiesburg earlier this year. I need to get up there to your course in Arkansas and I will try to this year. Bill
I too had a pt dramatically loose a bone graft after later finding out the pt was just diagnosis with diabetes several months after the surgery was done. Does anyone think it prudent to simply check a patient’s sugar with one of the stick meters on the market now? I am thinking this might be a good idea. Any thoughts please?
Osteolysis of the facial bones is usually the result of a specific pathologic process, such as an infection, cyst, tumor, endocrine dysfunction, metabolic disorder, or immunologic abnormality. In most patients, massive osteolysis develops in early adulthood, although it has been described in patients ranging in age from 1 month to 75 years. There is no gender or racial predilection, and there is no associated endocrine, metabolic, or immunologic abnormality. These abnormalities also are observed in acro-osteolysis (Hajdu-Cheney) syndrome, but it needs to be confirmed by the presence of other signs such as the destruction of the distal phalanges and other skeletal defects which are characteristics of the syndrome. Papillon-Lefèvre syndrome also had to be considered in the differential diagnosis. This is an autosomal recessive trait characterized by palmo-plantar hyperkeratosis and premature exfoliation of the primary teeth, followed by loss of the succedaneous teeth in association with periodontal disease. Papillon-Lefèvre syndrome has also been reported in association with acro-osteolysis. Quantitative and qualitative defects in neutrophilic function result in recurrent bacterial and fungal infections. Moreover, severe neutrophilic functional defects are generally associated with both accelerated periodontal disease, often affecting the primary and secondary dentitions in both the maxilla and mandible, and a history of serious infections in the other sites of the body. However, a low incidence of marked periodontal disease has been previously reported in patients with neutrophilic chemotactic and phagocytic defects. The widespread loss of alveolar bone may be associated with Capnocytophaga, Actinobacillus actinomycetemcomitans, prevotella melaninogenica and of course, bacteroides species. Diabetes Mellitus can certainly impair the body’s defense system and cause a subsequent functional WBC defect that makes the alveolar bone more vulnerable to the above mentioned bacteria. Chronic granulomatous disease and focal osteolysis from actinomycotic osteomyelitis may also be considered in the differential diagnosis. Actinomycosis is characterized by a dense inflammatory infiltration with fibrosis. The use of haemostatic sponges with a collagenous base makes the area even more vulnerable to bacterial contamination/infection, because it works as a culture and growth environment, per se. I believe that this patient should also be checked out for any kind of those maladies that are categorized as Langerhans Cell Histiocytosis. In that case, do not hesitate to consult an oral and maxillofacial surgeon.
Anon, Puros is only HA, there is nothing in this material to make bone form. However, it does allow bone to form on the material. The material is only osteoconductive and NOT osteoinductive. Please, I am not saying the material is bad, it is only a filler. It should not be used for bone regeneration. There should be as much living bone as possible next to the implant not just a bunch of filler material.
Another point to question is the bone density of the patient. while all of those conditions are germain, the obvious reasons of this complete failure need to be ruled out first, in my view. I placed three implants in a senior patient last year, osteotome technique for the two laterals. One failed miserably and the other, solid as a rock. I couldnt even see it on the radiograph until it was uncovered. Ill post a pic if I can become momentarily computer literate. Anyway, the graft was placed as I would any graft, but it covered a much wider area than just covering the socket. I think the patient just couldnt repair the defect with what I did. I think that the whole buccal plate was a thin thread of bone and I did not flap it after the atraumatic exo. Implant failed and subsequent graft did as well, leaving the grand canyon for me to look at later. Fortunately this patient was very very gracious and understood the pitfalls. we elected to bridge the space, restore the other two implants and she is happy. My point is, things can go south on any clinician and any patient. When it does, assess what is most likely happening or has happened, and revise the approach. I had a buccal plate and it sounded firm but it was too thin and i didnt flap it prior to implantation. It wasnt a thick sure fire 1-2mm plate and with the patients biotype (thin), I missed taking that into account, so I think it was an early sx failure due to that oversight. The repair graft was due to the patients inbility to handle such a tremendous graft bed. If I had it to do it over, it would be a delayed placement. For what its worth. Bill
The following study is worth a mention. It concluded that diabtetes may lead to bone lose
2969 Glucose Intolerance and Alveolar Bone Loss in Japanese Men
T. MARUGAME1, H. HAYASAKI1, H. EGUCHI2, and S. MATSUMOTO2, 1Kyushu University, Fukuoka, Japan, 2Self Defense Forces Fukuoka Hospital, kasuga, Japan
Objectives: Type II diabetes mellitus is known to affect alveolar bone loss. However, epidemiologic findings are sparse concerning whether or not impaired glucose tolerance, an important precursor of type II diabetes mellitus, is associated with periodontal disease. The purpose of this study was to examine the relation between glucose tolerance status, especially focusing on impaired glucose tolerance, and alveolar bone loss. Methods: Study subjects were 698 men aged 46 to 57 years who received a preretirement health examination at the Self Defense Forces Fukuoka Hospital in Japan from August 1997 to January 2000. Glucose tolerance status was classified as: 1) normal, 2) impaired glucose tolerance, and 3) diabetic, based on the 75g oral glucose tolerance test. Alveolar bone status was measured from a panoramic radiograph and was classified into three categories: 1) good alveolar bone, 2) moderate alveolar bone loss, and 3) severe alveolar bone loss. Oral health behavior and other lifestyle characteristics were ascertained by use of a self-administered questionnaire. Odds ratios and 95% confidence intervals were obtained from logistic regression. Results: After adjustment for potential confounding factors, there was a significant, positive association between newly diagnosed type II diabetes mellitus and moderate or severe alveolar bone loss. However, impaired glucose tolerance status was not related to alveolar bone loss. Conclusion: Glucose tolerance status can have a significant impact on periodontal status, especially during the process of deterioration from impaired glucose tolerance to type II diabetes mellitus. The present findings imply that prevention of periodontal disease should be started early, before impaired glucose tolerance has progressed to type II diabetes mellitus.
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