PERI-IMPLANTITIS AND ITS MANAGEMENT

October 26, 2011

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Review of the treatment protocols for peri-implantitis

Oct 12, 2011

By Scott Froum, DDS

Peri-implantitis is an inflammatory process affecting the soft and hard tissues surrounding an implant. This disease is associated with loss of supporting bone, bleeding on probing, and occasionally suppuration. The etiopathogenesis of peri-implantitis is complex and related to a variety of factors that affect the peri-implant environment. Peri-implantitis can be influenced by three factors:

  1. Patient-related factors including systemic diseases (e.g, diabetes, osteoporosis) and prior dental history (periodontitis)
  2. Social factors such as inadequate oral hygiene, smoking, and drug abuse
  3. Parafunctional habits (bruxism and malocclusion).

In addition to the above, iatrogenic factors such as faulty restorations, cement left following restoration delivery, and/or loose components can also play a significant role in the development of peri-implantitis.

Although restorations of endosseous implants have demonstrated a very high survival rate1, one study suggested that over a five-year period, 0 to 14.4% of dental implants demonstrated peri-implant inflammatory reactions associated with crestal bone loss.2

Many methods of treating peri-implantitis have been documented in the literature and most focus on removal of the contaminating agent from the implant surface. These treatments include:

  1. Administration of systemic antibiotics alone
  2. Mechanical debridement with or without systemic antibiotic treatment3
  3. Mechanical debridement with or without localized drug delivery and chlorhexidine oral rinses3a
  4. Mechanical debridement combined with LASER decontamination4
  5. Surgical debridement, and more recently …
  6. Surgical debridement with guided bone regeneration (GBR) for reparation of bony and soft-tissue defects.5

To date, GBR using a bone graft and membrane has had the best success as in demonstrating bone fill of the defects associated with peri-implantitis as described in the literature.6

Because there are biologic differences between teeth and implants, the progression of infection around implants is different than natural teeth. The inflammatory cell infiltrate around implants was reported to be larger and extend more apically when compared to a corresponding lesion in the gingival tissue around natural teeth. In addition, the tissues around implants are more susceptible to plaque-associated infections that spread into the alveolar bone.7

Implant surface bacterial decontamination is essential in treating peri-implantitis infections. Systemic administration of antibiotics has been used in the treatment of peri-implantitis, resulting in a reduction of inflammation. However, the efficacy of antibiotic therapy as a sole therapy has limited efficacy due to bacterial recolonization of the implant surface.8

Because nonsurgical treatment approaches failed to promote the reosseointegration of the exposed implant sites,9additional surgical interventions have been used in order to minimize the risk for a reinfection of the peri-implant pocket. Some of the treatment modalities suggested for peri-implantitis are:

  1. Mechanical/ultrasonic debridement with localized drug delivery; i.e., antimicrobial minocycline spheres (Arestin®)
  2. Laser treatment with and without flap access
  3. Open flap debridement
  4. Open flap debridement with guided bone regeneration

Renvert et al. (2006) compared the combination of mechanical debridement and topical application of minocycline microspheres to the combination of mechanical debridement and 1% chlorhexidine gel application in peri-implant lesions. The results obtained after a follow-up period of 12 months showed that with the chlorhexidine group, only a limited reduction in bleeding on probing was achieved and the mean peri-implant probing depth (PD) remained unchanged (3.9 mm). On the other hand, in the minocycline group, the reduction of bleeding on probing was greater and an improvement in mean peri-implant PD (from 3.9 mm to 3.6 mm) was seen. These results suggest that the topical application of chlorhexidine provides limited or no adjunctive clinical improvement when treating shallow peri-implant lesions as compared with using mechanical debridement alone.10

Schwarz et al. (2005, 2006a) compared the efficacy of the Er:YAG laser with that of the combination of mechanical debridement (using plastic curettes) and antiseptic (0.2% chlorhexidine digluconate) administration for the treatment of peri-implantitis. In both studies, the results obtained six months after therapy suggested that the treatment modalities were equally effective in improving peri-implant probing pocket depth (PPD) and clinical attachment level (CAL). However, at 12 months, the mean values for both groups of peri-implant PPD and CAL were not statistically significantly different from the corresponding values at baseline. Therefore, the results of the Er:YAG laser seem to be limited to a six-month period, particularly for advanced peri-implantitis lesions.

Leonhardt et al. evaluated the five-year outcome of a combined surgical (open flap) and antimicrobial treatment of peri-implantitis in humans. Leonhardt studied the effect of systemic antimicrobial therapy (amoxicillin and metronidazole) together with an open flap procedure and in conjunction with mechanical debridement of the implant surface for decontamination. The treatment was successful in 58% of the implants treated during follow-up for five years. Smoking was found to be a negative risk factor for treatment success.11

Schwarz et al. (2006b) evaluated and compared the efficacy of two bone regenerative procedures for the treatment of moderate intrabony peri-implantitis lesions that included a greater than 6 mm probing depth and an intrabony component of 3 mm as detected on radiographs. The defects were randomly treated either with a surgical debridement and filled with nanocrystalline hydroxyapatite, or surgical debridement and filled with bovine-derived xenograft (Bio-Oss®, Geistlich, Wolhusen, Switzerland) combined with a bioresorbable porcine-derived collagen membrane (Bio-Gide®, Geistlich, Wolhusen, Switzerland). After two years, the study showed that the combination of bovine bone mineral and the collagen membrane seemed to yield greater improvements in clinical parameters, showing 0.9 ± 0.2 mm more in PD reduction and 1.0 ± 0.3 more clinical attachment gain.12,13

Conclusion
The ideal management of peri-implant infections should focus both on infection control of the lesion, detoxification of the implant surface, and regeneration of lost support. Treatment options can be surgical or nonsurgical. To date, studies suggest that nonsurgical treatment of peri-implantitis is unpredictable, and the use of chemical agents such as chlorhexidine has only limited effects on clinical and microbiological parameters. Adjunctive local or systemic antibiotics have shown to reduce bleeding on probing and probing depths in combination with mechanical debridement. Beneficial effects of laser therapy on peri-implantitis have been shown, but this approach needs to be further evaluated. Implant surface bacterial decontamination is essential in treating peri-implantitis infections. Most studies suggest that establishing an adequate healthy peri-implant tissue environment proves to be difficult since inflammation is still present in a significant number of patients. New treatment modalities need to be evaluated using long-term randomized-controlled studies to identify predictable and successful treatment of peri-implantitis.

Author bio
Scott Froum, DDS, is a periodontist and co-editor of Surgical-Restorative Resource e-newsletter. He is a clinical associate professor at the New York University Dental School in the Department of Periodontology and Implantology. He is in private practice in New York City. You may contact him by email at drscottfroum@yahoo.com.

References
1. Albrektsson T et al. Osseointegrated oral implants — A Swedish multicenter study of 8139 consecutively inserted Nobelpharma implants. J Periodontol 1988;5 9:287-296.
2. Berglundh T et al. A systematic review of the incidence of biological and technical complications in implant dentistry reported in prospective longitudinal studies of at least 5 years. J Clin Periodontol 2002; 29:197-212.
3. Renvert S. (2008), Nonsurgical treatment of peri-implant mucositis and peri-implantitis: a literature review. J Clin Periodontol. Sept. 2008; 35(8 Suppl):305-315.
3a. Rosenberg ES et al. Microbial differences in two clinically distinct types of failures of osseointegrated implants. Clin Oral Implants Res 1991; 2:135-144.
4. Schwarz F et al. (2006a). Nonsurgical treatment of moderate and advanced peri-implantitis lesions: a controlled clinical study. Clinical Oral Investigations 10, 279–288.
5. Klinge B et al. A systematic review of the effect of anti-infective therapy in the treatment of peri-implantitis. J Clin Periodontol 2002; 29:213-220.
6. Grunder U et al. Treatment of ligature-induced peri-implantitis using guided tissue regeneration: a clinical and histologic study in the beagle dog. Int J Oral Maxillofac Implants 1993; 8:282-292.
7. Lindhe J et al. (1992). Experimental breakdown of peri-implant and periodontal tissues. Clin Oral Impalnts Res 1992; 3:9-16.
8. Mombelli A, Lang NP. Antimicrobial treatment of peri-implant infections. Clin Oral Implants Res 1992; 3:162-168.
9. Schwarz F et al. (2006). Influence of different treatment approaches on nonsubmerged and submerged healing of ligature-induced peri-implantitis lesions: an experimental study in dogs. Journal of Clinical Periodontology Aug. 2006; 33(8):584-595.
10. Renvert S. Topical minocycline microspheres versus topical chlorhexidine gel as an adjunct to mechanical debridement of incipient peri-implant infections: a randomized clinical trial. J Clin Periodontol. May 2006; 33 (5): 362-369.
11. Leonhardt A. (2003). Five-year clinical, microbiological, and radiological outcome following treatment of peri-pmplantitis in man. J Periodontol 2003; 74:1415-1422.
12. Schwarz F et al. (2006b). Healing of intrabony peri-implantitis defects following application of a nanocrystalline hydroxyapatite (Ostim®) or a bovine-derived xenograft (Bio-Oss) in combination with a collagen membrane (Bio-Gide). A case series. Journal of Clinical Periodontology 33; 491–499.
13. Schwarz F et al. (2008). Two-year clinical results following treatment of peri-implantitis lesions using a nanocrystalline hydroxyapatite or a natural bone mineral in combination with a collagen membrane. Journal of Clinical Periodontology 35; 80–87.

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New CT technology promises much loser radiation doses

September 24, 2011

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GE Healthcare has just introduced in Canada the Veo, a new low-dose CT image reconstruction technology. Veo uses a model of the scanning system itself to improve image quality. As was apparent during last year’s RSNA, CT radiation dose reduction while maintaining or improving image quality is a hot topic with CT manufacturers. For decades, the standard CT image reconstruction algorithm has been filtered back projection, which uses mathematical methods to reconstruct tomographic images from the projections that are obtained by the circling detectors. More recently, a new reconstruction algorithm, adaptive statistical iterative reconstruction (ASIR), has been introduced that performs modeling of the noise distribution, cutting radiation dose by up to 80% for many applications.
Model-based iterative reconstruction (MBIR), employed by Veo, goes a step further by incorporating a physical model of the CT system into the reconstruction process to characterize the data acquisition phase, including noise, beam hardening, and scatter. It has the potential to cut radiation doses even more but is computationally more demanding, leading to longer reconstruction times (which will gradually become less of a problem with ever increasing computing power). It may potentially deliver lower noise, increased resolution, improved low contrast detectability and fewer artifacts. Veo is available on the GE Discovery CT750 HD system, and is suitable for use throughout the body. Veo is already available in Europe and much of Asia, and is still awaiting FDA clearance.

Experts: Unhealthy gums can end in heart attacks

September 21, 2011

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More and more evidence of a definite link between periodontal disease and systemic disease is accumulating.  Here is the latest in a growing body of evidence.

You better start taking your oral health seriously because the trouble in your mouth could be a subtle indicator of something as grave as diabetes or even heart attack.
City doctors revealed many such facts on the occasion of World Oral Health Day on Monday. Other than diabetes and heart disorders, they said mouth-related diseases could also be symptoms of hypertension, breathing problems, weakening of bones and even hint at a probable miscarriage in pregnant women.
“Several studies have been done in the west in this regard. Women with poor gum hygiene are more likely to have miscarriages,” said Dr Achuth Baliga, head of the department of dental sciences in Manipal Hospital.
He said pregnant women with gum diseases are seven times more likely to have a baby that is born prematurely or underweight. He added that these women’s babies might be born with physical anomalies.
“The circulating bacteria from the mouth can harm the foetus,” he explained.
There is more that poor health of gums suggests. Dr CD Dwarakanath, director of postgraduate studies and head of the department of periodontics (a field of specialisation in dentistry) at Oxford Dental College and Hospital, said gum diseases might lead to heart attack.
He said in people suffering from periodontitis (a gum disease), the bacteria might enter the bloodstream while chewing or brushing and the bacteria could contribute to formation of clots in the arteries, thereby causing heart attack.
He said research had shown that people with gum diseases are almost twice as likely to suffer from coronary artery disease when compared with people with healthy gums.
Unhealthy gums have more warning about an unhealthy heart.
Dr Baliga said tooth decay and gum disease for a long time could lead to inflammation of the inner lining of the heart’s chambers and heart valves.
He said it could start with fever, anaemia and lead to formation of a blood clot.
Oral health has a connection with diabetes too. Dr Dwarakanath said gum disease is often considered the sixth complication of diabetes. Diabetics are prone to have periodontal disease if their condition is not under control, he added.
Osteoporosis—characterised by weak bones, decrease in the bone density—is another complication that is reflected in poor oral health.
Dr Dwarakanath said loose teeth, severe gum disease and even difficulty in eating and speaking could be a sign of decreasing bone density, an advanced stage of osteoporosis. Osteoporosis’s symptoms often go unnoticed until a major fracture occurs.
However, your dentist may be able to detect the early signs of osteoporosis during a regular dental exam.
Studies show that the top oral health complaints in India comprise tooth decay, gum problems and bad breath. The oral health experts say a lot of people suffer from such complaints without being aware of it, letting the complication affect their quality of life.

Published: Tuesday, Sep 13, 2011, 12:34 IST
By Soumita Majumdar | Place: Bangalore | Agency: DNA

Are antibiotics of any use in implant therapy?

August 28, 2011

Filed under: Uncategorized — admin @ 11:12 pm

Many times in implantology we perform procedures based on anecdotal evidence or on dogma.  One subject that often come up is whether or not to use antibiotics prophylactically either before or after surgery. This evidence based review seems to indicate that the administration of a single dose of amoxicilling prior to surgery may be of benefit.

Summary Review/Restorative Dentistry

Evidence-Based Dentistry (2008) 9, 109–110. doi:10.1038/sj.ebd.6400612

Do preoperative antibiotics prevent dental implant complications?

Does giving antibiotics at the time of dental implant placement prevent complications?
Address for correspondence: Luisa M Fernandez Mauleffinch, Cochrane Oral Health Group, MANDEC, School of Dentistry, University of Manchester, Higher Cambridge Street, Manchester M15 6FH, UK. E-mail: luisa.fernandez@manchester.ac.uk
Ben Balevi1
1Private practitioner, affiliated with Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
Esposito M, Grusovin MG, Talati M, Coulthard P, Oliver R, Worthington HV. Intervention for replacing missing teeth: antibiotics at dental implant placement to prevent complications. Cochrane Database Syst Rev 2008, issue 3
Top

Abstract

Data sources

 

The Cochrane Oral Health Group’s Trials Registry, the Cochrane Central Register of Controlled Trials, Medline and Embase were consulted to find relevant work. Searches were made by hand of numerous journals pertinent to oral implantology. There were no language restrictions.

Study selection

 

Randomised controlled clinical trials (RCT) with a followup of at least 3 months were chosen. Outcome measures were prosthesis failures, implant failures, postoperative infections and adverse events (gastrointestinal, hypersensitivity, etc.).

Data extraction and synthesis

 

Two reviewers independently assessed the quality and extracted relevant data from included studies. The estimated effect of the intervention was expressed as a risk ratio together with its 95% confidence interval (CI). Numbers-needed-to-treat (NNT) were calculated from numbers of patients affected by implant failures. Meta-analysis was done only if there were studies with similar comparisons that reported the same outcome measure. Significance of any discrepancies between studies was assessed by means of the Cochran’s test for heterogeneity and the I2 statistic.

Results

 

Only two RCT met the inclusion criteria. Meta-analysis of these two trials showed a statistically significantly higher number of patients experiencing implant failures in the group not receiving antibiotics (relative risk, 0.22; 95% CI, 0.06–0.86). The NNT to prevent one patient having an implant failure is 25 (95%CI, 13–100), based on a patient implant failure rate of 6% in people not receiving antibiotics. The following outcomes were not statistically significantly linked with implant failure: prosthesis failure, postoperative infection and adverse events (eg, gastrointestinal effects, hypersensitivity).

Conclusions

 

There is some evidence suggesting that 2 g of amoxicillin given orally 1 h preoperatively significantly reduces failures of dental implants placed in ordinary conditions. It remains unclear whether postoperative antibiotics are beneficial, and which is the most effective antibiotic. One dose of prophylactic antibiotics prior to dental implant placement might be recommended.

DO SHORT IMPLANTS WORK???

Filed under: Uncategorized — admin @ 11:01 pm

Much has been published about implants with a length 10mm or over enjoying greater success than their shorter counterparts.  However, Misch et al  have published in an evidence based manner to cast some doubt on this.  here is the abstract:

Carl E. Misch, Jennifer Steigenga, Eliane Barboza, Francine Misch-Dietsh, Louis J. Cianciola & Christopher Kazor

Background:
Implants <10 mm long in the posterior regions of partially edentulous patients have a higher failure rate in many clinical reports. The purpose of this case series study was to evaluate implant survival when a biomechanical approach was used to decrease stress to the bone-implant interface. Methods:
A retrospective evaluation of 273 consecutive posterior partially edentulous patients treated with 745 implants, 7 or 9 mm long, supporting 338 restorations over a 1- to 5-year period was reviewed from four private offices. Implant survival data were collected relative to stage I to stage II healing, stage II to prosthesis delivery, and prosthesis delivery to as long as 6 years follow-up.

A biomechanical approach to decrease stress to the posterior implants included splinting implants together with no cantilever load, restoring the patient with a mutually protected or canine guidance occlusion, and selecting an implant designed to increase bone-implant contact surface area.

Results: Of the 745 implants inserted, there were six surgical failures from stage I to stage II healing. All five failures were with a one-stage surgical approach (240 implants). There were two failures from stage II healing to prosthesis delivery. No implants failed after the 338 final implant prostheses were delivered. A 98.9% survival rate was obtained from stage I surgery to prosthetic follow-up.

Conclusions:
Short-length implants may predictably be used to support fixed restorations in the posterior partial edentulism. Methods to decrease biomechanical stress to the bone-implant interface appear appropriate for this treatment.

INCREASING IMPLANT SURFACE AREA AT NANO LEVEL SPEEDS HEALING

July 27, 2011

Filed under: Uncategorized — admin @ 9:25 am

Recent research out of the University of Gothenberg indicates that increasing surface roughness of implants at the nano level speeds the integration process.

Increasing the Active Surface of Dental Implants at Nano Level Quickens Healing

Published on June 15, 2011 at 7:35 AM
By Cameron Chai

Researchers at the University of Gothenburg have conducted studies on the surface arrangement of dental implants both at the micro and nano level to enable speedy healing of patients.

Johanna Löberg from the Department of Chemistry at the University of Gothenburg stated that by causing an increase of the active surface area at the nano scale and altering the implant’s conductivity, the biomechanics of the body is influenced in such a way as to avoid discomfort and to speed up the healing process.

Scanning electron microscope images taken on the titanium samples with (from left), turned, sanded and blasted surfaces treated with oxalic acid and dilute sulfuric acid

It was evident that the surface of dental implants is often associated with the level of roughness, from the superimposed nanostructures to the thread. When the implant is placed in the bone, the bone tissue experiences a mechanical force known as biomechanical stimulation, which leads to the formation of new bone. Although roughness is not the only factor that influences healing, it is crucial for new bone formation. It is also necessary to measure and illustrate the appearance of the surface in detail.
Johanna Löberg has formulated an approach that explains the topography of the implant from nanometre to micrometre scale. This approach enables theoretical estimation of placing the implant in the bone by diverse surface topographies. It can be used to develop new dental implants and to enable optimization of properties for quick healing and increased bone formation. The results demonstrate that a small increase in conductivity delivers improved cell response and quick deposition of minerals that are essential for bone formation. Surfaces with a clearly defined nanostructure feature a larger active area and react faster to the deposition of bone-forming minerals.
The project was performed by the University of Gothenburg in collaboration with the Astra Tech AB in Mölndal, and has scope for further study.
Source: http://www.science.gu.se/

AVASTIN- ANOTHER DRUG ASSOCIATED WITH ONJ

July 23, 2011

Filed under: Uncategorized — admin @ 10:35 am

As you know, intravenous bisphosphonates and to a lesser extent oral bisphosphonates like fosamax have been associated with an increased rick of osteonecrosis of the jaw (ONJ).  Recently, Dr. Richard Wynn at the University of Maryland published on a human monoclonal antibody, bevacizumab (Avastin), used in treating metastatic carcinoma, that also appears to be associated with an increased incidence of ONJ.

About the Author

Dr. Richard L. Wynn is Professor of Pharmacology at the University of Maryland Dental School. He holds a BS degree in Pharmacy and a PhD degree in Pharmacology. He chaired the Department of Pharmacology at the University of Maryland Dental School from 1980 to 1995. He is the lead author of the Drug Information Handbook for Dentistry, a co-author on many other dental drug publications, an author of over 300 refereed scientific journal articles, a consultant to the Academy of General Dentistry, a featured columnist, and a featured speaker presenting more than 500 courses in continuing dental education. One of his primary interests continues to be keeping dental professionals informed of all aspects of drug use in dental practice.

Bevacizumab (Avastin®): Another Drug Associated With Osteonecrosis of the Jaw

First it was the intravenous bisphosphonates, zoledronic acid (Zometa®) and palmidronate (Aredia®), then the oral bisphosphonates (the Fosamax® family of drugs), then the anti-RANKL drug, denosumab (Prolia®, Xgeva®). Now it’s a human monoclonal antibody known as bevacizumab (Avastin) that is associated with osteonecrosis of the jaw (ONJ) syndrome.
Bevacizumab (Avastin) belongs to a class of drugs known as antiangiogenic agents, used with increasing frequency in treating cancer. Bevacizumab is indicated for the treatment of metastatic colorectal cancer, and metastatic nonsquamous, nonsmall cell lung cancer. Angiogenesis in tumor cells involves the formation and growth of new blood vessels which help tumor growth. Bevacizumab acts to block angiogenesis through inhibition of cell proliferation and vessel sprouting, as well as by decreasing circulating vascular endothelial growth factor (VEGF) levels. This action is similar to the antiangiogenic action ascribed to the bisphosphonates. There are literature reports on patients receiving bevacizumab who developed ONJ. These reports are described in this month’s newsletter.
A case of ONJ associated with bevacizumab exposure was reported in a letter to the editor in 2008 (Greuter S, Schmid F, Ruhstaller T, et al, “Bevacizumab Associated Osteonecrosis of the Jaw,” Ann Oncol, 2008, 19(12):2091-2).
A 63-year old woman was treated for breast cancer. Bone scans were normal and she had never taken bisphosphonates. While being treated with liposomal doxorubicin and bevacizumab, the patient experienced left-sided maxillary pain after one-month therapy. A tooth infection was diagnosed and numbers 25 and 26 were extracted. One month later, a mouth-antrum fistula was surgically revised and occluded. Soon afterward, the patient suffered from a trigeminal neuralgia. Imaging showed maxillary sinusitis and signs of ONJ. The jaw lesion was extirpated and the sinus drained. Histology verified the clinical diagnosis of ONJ and an infiltration from the cancer was excluded. At 3 months of follow-up, the patient remained free of lesions and symptoms.
The authors commented that bevacizumab acts to block angiogensis through inhibition of cell proliferation and vessel sprouting, as well as by decreasing circulating vascular endothelial growth factor (VEGF) levels. This action is similar to the antiangiogenic action described for the bisphosphonates.
The authors stated that this was the third published case of ONJ associated with bevacizumab therapy. The doxorubicin the patient was taking is an anthracycline antineoplastic agent that has been on the market for many years and has never been known for causing ONJ. The authors suspected that bevacizumab, which hampers wound healing and possibly bone remodeling, was the causative agent in this case.
The other two published cases were included in a report by Estilo, et al (Estilo CL, Fornier M, Farooki A, et al, “Osteonecrosis of the Jaw Related to Bevacizumab,” J Clin Oncol, 2008, 26(24):4037-8).
A 51-year-old female with a history of infiltrating ductal carcinoma of the right breast was diagnosed in late 2001 and treated with mastectomy in 2002. She subsequently underwent treatment with chemotherapy, doxorubicin, cyclophosphamide, and letrozole for various cycles over a 3-year period. Since 2006, she underwent additional chemotherapy, capecitabine therapy, and radiation. In late December 2006, she was started on bevacizumab at a dose of 15 mg/kg every 3 weeks for a total of 8 doses, the last dose given in May 2007. Six weeks after the last dose, the patient presented with a 2-month history of complaints of lower jaw discomfort and protruding bone in the lower jaw. Examination revealed an area of bone exposure in the left posterior lingual mandible approximately 1 X 1 mm in diameter. The area appeared necrotic. The surrounding tissue had no evidence of infection. The exposed bone was smoothed with a bone file and the patient prescribed chlorhexidine 0.12% oral rinse. The bevacizumab and capecitabine were then discontinued. The area of exposed bone had resolved within a few weeks. The overlying mucosa appeared normal. At that time, a new area of exposed bone appeared in the right posterior lingual mandible of 1 X 1mm in area. Histology showed devitalized necrotic bone with a scalloped “moth eaten” appearance. Bacterial colonies occupied the demineralized areas.
The other case was a 33-year-old woman with a history of glioblastoma multiforme diagnosed in November 2006. She underwent surgery followed by radiation therapy and temozolomide from December 2006 through January 2007. The patient started bevacizumab therapy in Feb 2007 at a dose of 10 mg/kg every 2 weeks. Thirteen weeks later, she was referred to the dental clinic for evaluation of a 2-week history of spontaneous mucosal breakdown overlying her right mandible. The patient complained of gingival pain. On examination, there appeared a 1 X 2 cm dehiscence at the junction of the unattached/attached gingiva in the mucobuccal fold overlying the lower right first and second premolar and first molar teeth. There was exposed necrotic bone visible through the dehiscence extending inferiorly and posteriorly. There was no evidence of infection. Other than that, the oral mucosa appeared healthy with intact dentition. The patient continued on biweekly bevacizumab. In August 2007, she returned with a small mucosal defect posterior to the original lesion. There was soft tissue dehiscence with no evidence of exposed bone.
The authors commented that the clinical features of bone exposure in the two cases were compatible with ONJ in patients exposed to bisphosphonate therapy. The two patients had no history of bisphosphonate use. The authors suggested that bevacizumab contributed to the oral mucosal breakdown with exposed necrotic mandibular bone in the two patients. The antiangiogenic property of bevacizumab could compromise microvessel integrity in the jaw and lead to subclinical compromise of the osteonecrosis. Trauma from tooth brushing or chewing could also increase the demand on this compromised bone to repair itself and result in localized bone necrosis, periosteal death, and eventual exposed necrotic bone.
Estilo et al went on to explain that angiogenesis is a critical step in tumor growth, invasion, and metastasis. VEGF is a family of cytokines that exert important functions in tumor angiogenesis. VEGF is overexpressed in various human tumors and overexpression of VEGF is associated with tumor progression. VEGF is also essential for osteogenic differentiation and bone formation. Thus bevacizumab, used as a VEGF inhibitor to suppress tumor progression, could also suppress the osteogenic differentiation and bone formation. This could result in failure to repair bone trauma.
In the two patients described, additional factors possibly contributing to the development of ONJ were the advanced cancer and chemotherapy. The authors cautioned that clinicians involved in the care of patients treated with bevacizumab should be aware of the potential complication of ONJ.

Antiangiogenic Agents and the Risk of ONJ

Christodoulou et al reported that a combination of bisphosphonates and antiangiogenic factors induces ONJ more frequently than bisphosphonates alone (Christodoulou C, Pervena A, Klouvas G, et al, “Combination of Bisphosphonates and Antiangiogenic Factors Induces Osteonecrosis of the Jaw More Frequently Than Bisphosphonates Alone,” Oncology, 2009, 76(3):209-11). Their introduction in the report stated that antiangiogenic agents may add to the risk of ONJ, especially when used in combination with bisphosphonates. The purpose of the study was to do a back review of data of patients receiving bisphosphonates with or without antiangiogenic factors for osseous metastases from various tumors between June 2007 and June 2008.
Among 116 patients being treated for various malignancies, 25 received concurrent treatment with antiangiogenic agents at some point. Twenty-two were taking bevacizumab, two were taking a drug called sunitinib, and one was taking a drug called sorafenib. The median duration to exposure to bisphosphonates was 28.5 months for the 25 patients taking the antiangiogenic drugs and 24 months for those not taking any antiangiogenic drugs. There were no significant differences between the two groups regarding treatment duration with the bisphosphonate.
Of the 25 patients receiving concurrent treatment with bisphosphonates and the antiangiogenic drug, 4 developed ONJ (incidence of 16%). Of the 91 patients receiving bisphosphonates without antiangiogenic factors, 1 developed ONJ (incidence 1.1%). This difference was statistically significant.
In this study, the diagnosis of ONJ was according to the clinical diagnoses made by dentists specializing in treating cancer patients and consisted of pain in the jaw with exposed, necrotic bone, some with purulent discharge. The authors commented that bisphosphonates have also been reported to possess antiangiogenic activity, particularly zoledronic acid (Zometa®) — a widely popular bisphosphonate used as an adjunct agent in cancer treatment.
Greuter et al (above) summed it up best by stating “if more cases of bevacizumab-associated ONJ are reported, special dental management (jaw x-ray, optimal dental health, and good oral hygiene) should become standard before patients start bevacizumab.”

Dental Management to Reduce the Risk of ONJ

The importance of special dental management to reduce the risk of ONJ in patients taking bevacizumab was shown in a recent report (Francini F, Pascucci FF, Francini E, et al, “Osteonecrosis of the Jaw in Patients with Cancer Who Received Zoledronic Acid and Bevacizumab,” J Am Dent Assoc, 2011, 142(5):506-13). They looked at cancer patients on zoledronic acid and chemotherapy combined with bevacizumab who underwent a dental exam before starting treatment. They found that none of the patients developed ONJ.
The study included 59 patients with either breast cancer or nonsmall cell lung cancer who received 4 mg zoledronic acid I.V. every 4 weeks and 15 mg per kg bevacizumab every 3 weeks. The median time of receiving zoledronic acid was 18 months and the median time of receiving bevacizumab was 16 months. All subjects received a dental exam and panoramic x-rays before starting treatment and every three months thereafter until the patient died or was lost to follow-up. If needed, patients received periodontal disease treatment and underwent tooth extraction before they received any drug.
None of the patients required dentoalveolar surgery while undergoing cancer treatment. After a median follow up of 19.7 months, none of the participants developed ONJ. The conclusion was that a bisphosphonate combined with an antiangiogenic drug did not predispose to ONJ in participants with cancer that metastasized to the bone, who underwent a baseline dental examination and preventive dental measures.

Indications for Bevacizumab (Avastin®) Approved by FDA:

Treatment of metastatic colorectal cancer; treatment of unresectable, locally advanced, recurrent or metastatic nonsquamous, nonsmall cell lung cancer; treatment of metastatic HER-2 negative breast cancer (who have not received chemotherapy for metastatic disease); treatment of progressive glioblastoma; treatment of metastatic renal cell cancer (not an approved use in Canada).
Note: For the treatment of metastatic breast cancer, effectiveness is based on improvement in progression-free survival; not indicated for the treatment of breast cancer with metastatic disease that has progressed following anthracycline and taxane treatment. For the treatment of glioblastoma, effectiveness is based on improvement in objective response rate.

Unlabeled/Investigational Use:

Treatment of recurrent ovarian cancer; recurrent cervical cancer; soft tissue sarcomas (angiosarcoma or hemangiopericytoma/solitary fibrous tumor); age-related macular degeneration (AMD).


Drug information is constantly changing. Promote medication safety in your practice with Lexicomp Online for Dentistry.

EVER WONDER WHAT TO CHARGE FOR AN IMPLANT???

July 20, 2011

Filed under: Uncategorized — admin @ 10:11 am

A recent survey was done and asked this very question.  here are the results.


EVER WONDER WHAT TO CHARGE FOR AN IMPLANT???

Filed under: Uncategorized — admin @ 10:06 am

In our teaching courses, we are often asked by beginning implatologists what to charge for implant placement.  Here is a recent survey which asked that very question.


Philadelphia’s Implant Information Central!: STEM CELLS WHAT ARE THEY, AND HOW CAN THEY HELP?

July 19, 2011

Filed under: Uncategorized — admin @ 11:09 am

Philadelphia’s Implant Information Central!: STEM CELLS WHAT ARE THEY, AND HOW CAN THEY HELP?: “Dr. Bruce Freund recently wrote a brief summary about stem cells and what they can do for us in dentistry and in implantology. They certain…”

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