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| CASE REPORT |
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| Year : 2020 | Volume
: 14
| Issue : 1 | Page : 43-45 |
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Clinical application of guided bone regeneration in a periodontally compromised implant-supported denture and flow cytometric analysis of the soft tissue growth
Manish Mukherjee1, Sanjay Manohar Londhe2, Subrata Roy3, JS Adhikary4
1 ADC (R & R), New Delhi, India
2 Dte Gen Dental Services, New Delhi, India
3 CMDC (CC), C/o 56 APO, New Delhi, India
4 Department of Radiation Biology, INMAS, New Delhi, India
| Date of Submission | 06-Jan-2020 |
| Date of Acceptance | 07-Jan-2020 |
| Date of Web Publication | 31-Jan-2020 |
Correspondence Address:
Manish Mukherjee
ADC (R & R), New Delhi - 110 010
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/JODD.JODD_2_20
A 69-year-old male, ex-serviceman from the defense research organization, reported to the dental outpatient department of a tertiary care center, with the chief complaint of inability in wearing of the lower dentures. General and systemic examinations were noncontributory. Intraoral examination revealed a firm, tender, pedunculated fibrotic growth measuring 3 cm × 2 cm located inferiorly and buccally to a titanium dental implant on the right aspect of the edentulous mandible, which was excised under local anesthesia, and guided bone regeneration was performed. The soft tissue overgrowth was subjected to flow cytometric analysis.
Keywords: Expanded poly tetra fluoro ethylene, flow cytometry, guided bone regeneration, p53 tumor suppressor protein, peri-implantitis
How to cite this article:
Mukherjee M, Londhe SM, Roy S, Adhikary J S. Clinical application of guided bone regeneration in a periodontally compromised implant-supported denture and flow cytometric analysis of the soft tissue growth. J Dent Def Sect. 2020;14:43-5 |
How to cite this URL:
Mukherjee M, Londhe SM, Roy S, Adhikary J S. Clinical application of guided bone regeneration in a periodontally compromised implant-supported denture and flow cytometric analysis of the soft tissue growth. J Dent Def Sect. [serial online] 2020 [cited 2023 Mar 27];14:43-5. Available from: http://www.journaldds.org/text.asp?2020/14/1/43/276405 |
| Introduction | |  |
Dental implantology has indeed come a long way. It is rather awe-inspiring to realize that it required a rather serendipitous incident in the 1950s to give birth to “osseointegration” Prof. Per-Ingvar Branemark, a Swedish orthopedic surgeon, while studying the healing aspects of bone annoyingly, found that he could not remove a titanium inspection chamber from a rabbit's tibia.[1] Although dental implants have metamorphosed the very face of oral health care delivery in the field of replacing missing teeth, poor home care leading to accumulation of dental plaque and trauma from occlusion has become one of the leading causes of implant failure [Figure 1]a. One of the management techniques involves guided bone regeneration (GBR). It is based on the same principles of guided tissue regeneration (GTR) derived from the classic studies of Gottlow et al.[2] | Figure 1: Peri-implantitis. (a) Soft tissue growth-preoperative. (b) Radiograph with bone density measurement-preoperative
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We present one such case report where the application of the principles of regenerative periodontics successfully restored the periodontium.
| Case Report | | |
A 69-year-old male, ex-serviceman from the defense research and development organization, reported to the dental outpatient department of a tertiary care center, with the chief complaint of inability in wearing of the lower dentures. History revealed that the patient was provided with an implant-supported complete denture 5 years ago. He was quite comfortable with the dentures until the last 6 months when he noticed a small soft growth on the labial aspect of the dental implant on the right side; the lesion reportedly grew in dimensions over the last 6 months, leading to a gradual inability in the wearing of the lower implant-supported denture.
General and systemic examinations were noncontributory. Intraoral examination revealed a firm, tender, pedunculated fibrotic growth measuring 3 cm × 2 cm located inferiorly and buccally to a titanium dental implant on the right aspect of the edentulous mandible [Figure 1]a. Right submandibular lymphadenopathy was also noticed on palpation. Radiographic examination and mineral density analysis revealed bone loss and reduction in bone mineral density [Figure 1]b. The patient was administered a course of amoxicillin and diclofenac potassium and was placed on 0.2% chlorhexidine rinse as part of periodontal health maintenance. Intensive oral hygiene instructions were given. It was decided to address the condition by excision of the growth and regeneration of the defect by applying the principles of GBR. His hemogram and other biochemical investigations, including blood sugar, were normal.
Under local anesthesia, the soft tissue growth was excised, granulation tissue was removed, and thorough debridement of the osseous defect was carried out [Figure 2]a. Osteoconductive bone graft (SynOss™) was placed on the defect and was covered with a nonresorbable expanded poly tetra fluoro ethylene (Cytoplast™) [Figure 2]b. A mucoperiosteal flap was mobilized and sutured back covering the sutured membrane. The overlying sutures were removed after 10 days and the membrane removed after 6 weeks. The patient was reviewed at 1½, 3, and 6 months postoperatively. Oral hygiene instructions were reinforced. There was marked improvement in periodontal health [Figure 3]a, and postoperative radiography with bone density analysis showed evidence of increased mineral density at 6 months [Figure 3]b. | Figure 2: Intraoperative. (a) Soft tissue growth excised and osseous debridement performed; (b) bone graft and expanded poly tetra fluoro ethylene membrane placed over the osseous defect
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 | Figure 3: Postoperative. (a) Clinical view after 6 months; (b) radiograph with bone density measurement at 6 months postoperative
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| Discussion | | |
Implant failure may be defined as the total failure of the implant to fulfill its purpose (functional, esthetic, or phonetic) because of mechanical or biological reasons.[3],[4] Authors have long identified the warning signs of implant failure, which may be enumerated as:[5]
- Connecting screw loosening
- Connecting screw fracture
- Gingival bleeding and enlargement
- Purulent exudates from large pockets
- Pain
- Fracture of the prosthetic component
- Angular bone loss noted radiographically [Figure 1]b
- Longstanding infection and soft tissue inflammation.
Oral status – Poor home care
A direct relationship between accumulation of dental plaque and the onset and progression of gingivitis has been established.[6] Subsequently, dental plaque and trauma from occlusion set up a vicious cycle, leading to implant failure [Figure 2]a. In addition, the nature of the implant surface seems to influence the microbial colonization.[7] Bacterial infection of the peri-implant tissues results in soft tissue inflammatory changes and rapid bone loss. This condition was termed peri-implantitis and was defined by Meffert as the progressive loss of peri-implant bone as well as soft tissue inflammatory changes. GBR is an accepted therapeutic modality in which the resident mesenchymal and osteoblastic cells are given an opportunity to repopulate the previously diseased implant surface by placing a membrane between the soft tissue/implant interfaces so as to prevent epithelial down-growth into the recipient bed. Since the objective of GBR is to regenerate a single tissue, namely bone, it is theoretically easier to accomplish than GTR, which strives to regenerate multiple tissues in a complex relationship. Histopathological examination of the excised tissue revealed chronic inflammatory infiltrate with overwhelming fibroplasia.
Flow cytometry
As the patient gave a history of marked growth of the soft tissue growth, a flow cytometric analysis was performed to understand its cellular dynamics. p53 is a tumor suppressor protein, also known as “Guardian of the Genome.” It plays an important role in cell cycle control and apoptosis. In normal cells, the p53 protein level is low. DNA damage and other stress signals may trigger the increase of p53 proteins, which have three major functions: growth arrest, DNA repair, and apoptosis (cell death). The growth arrest stops the progression of cell cycle, preventing replication of damaged DNA. During the growth arrest, p53 may activate the transcription of proteins involved in DNA repair. Apoptosis is the “last resort” to avoid proliferation of cells containing abnormal DNA.[8]
Cells were acquired in list mode of the software for their scatter plot forward scatter cells (FSCs) versus side scatter cells (SSCs) as well as histogram plots. The scatter gives us the idea of size (FSC) and the granularity (SSC) of the cells as shown in [Figure 4]a and [Figure 4]a1. The histograms display cells in the different phases of the cell cycle and the relative DNA content as shown in [Figure 4]b. | Figure 4: Flow cytometric analysis. (a and a1) Size and granularity of the cells; (b) histogram showing DNA content of different cell populations
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Analysis
After acquisition of these parameters, plots were analyzed with the help of FACSCalibur (Becton-Dickinson and Co., USA) flow cytometer, using the Cell Quest Software (v. 3.0.1; Becton Dickinson) for acquisition and ModFit LT software (v. 2.0; Verity Software House, Inc., USA) for cell cycle analysis. From the over lay histogram, plot transformed gingival (blue) cells showed greater hyperdiploidy than its normal (red) counterpart. A majority of the transformed cells showed apoptosis (all the cells left to the G1 population in blue color). This is also confirmed by the dot plot [most of the cells are of smaller size in [Figure 4]a1. This clearly showed that different subpopulations of cells exist in such fibrous growths, and probably, p53 is actively involved in preventing the growth of cells with damaged DNA.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | El Askary AS, Meffert RM, Griffin T. Why do dental implants fail? Part I. Implant Dent 1999;8:173-85.  |
| 2. | Gottlow J, Nyman S, Karring T, Lindhe J. New attachment formation as the result of controlled tissue regeneration. J Clin Periodontol 1984;11:494-503. |
| 3. | English CE. Biomechanical concerns with fixed partial dentures involving implants. Implant Dent 1993;2:221-42. |
| 4. | Cox JF, Zarb GA. The longitudinal clinical efficacy of osseointegrated dental implants: A 3-year report. Int J Oral Maxillofac Implants 1987;2:91-100. |
| 5. | Ten Bruggenkate CM, van der Kwast WA, Oosterbeek HS. Success criteria in oral implantology. A review of the literature. Int J Oral Implantol 1990;7:45-51. |
| 6. | Meffert RM. Treatment of failing dental implants. Curr Opin Dent 1992;2:109-14. |
| 7. | Smith DE, Zarb GA. Criteria for success of osseointegrated endosseous implants. J Prosthet Dent 1989;62:567-72. |
| 8. | Calonje E, Fletcher CD. Immunohistochemistry and DNA flow cytometry in soft-tissue sarcomas. Hematol Oncol Clin North Am 1995;9:657-75. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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