SmokingNCT01663298
Gene Expression Variation and Implant Wound Healing Among Smokers and Diabetics
An observational study of Smoking and Diabetes, run by University of North Carolina, Chapel Hill at 1 site in United States.
Trial summary
Periodontal wound healing is a complex multifactorial process that involves interactions among various cells, growth factors, hormones and extracellular matrices. Although still poorly understood, these interactions trigger a series of events that lead to new tissue formation. Read more about this study
- Who is it for?
- Ages 18 to 70 yearsHealthy volunteers can take part
- What is being tested?
- Dental implant surgery
- Type of treatment
- Surgery or procedure
- How many people
- 44 participants
- Where
- 1 siteUnited States
- Study dates
- Aug 2010to 23 Feb 2016
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Patients in the graduate periodontal clinic in the school of dentistry at the University of North Carolina
Who may be able to join
- Adult males or females between the age of 18 and 70 years (inclusive)
- Able and willing to follow study procedures and instructions
- Have read, understood and signed an informed consent form
- In good general health
- Have one or more implant placements as their future treatment needs. The implant placement can be either as one-stage or two-stage, and can be either in an edentulous ridge or an extraction socket
- Qualify for enrollment into one of the three study groups
- Have probing depth ≤ 4 mm for all teeth at the same quadrant of implant placement. Sites with probing depth 5 mm will also be included if bleeding on probing in these sites are absent.
Who cannot join
- Have a chronic disease with oral manifestations
- Exhibit gross oral pathology
- Use of either antibiotics or NSAIDs within 1 month prior to screening examination
- Chronic treatment (i.e. two weeks or more) with any medication known to affect periodontal status (e.g. phenytoin, calcium, antagonists, cyclosporin, Coumadin) within 1 month prior to screening examination
- Systemic conditions, except smoking and diabetes, that are known to affect the periodontal status
- With active infectious diseases such as hepatitis, HIV or tuberculosis
- Known to be pregnant or breastfeeding
Trial locations and contacts
1 site in 1 country.
United States1 site
Department of Periodontology, UNC School of Dentistry
Chapel Hill, North Carolina, 27514
About this study
Official title: FGF2 Promoter Hypermethylation and Implant Wound Healing Among Smokers and Diabetics
Periodontal wound healing is a complex multifactorial process that involves interactions among various cells, growth factors, hormones and extracellular matrices. Although still poorly understood, these interactions trigger a series of events that lead to new tissue formation. One growth factor that plays an important role in wound healing is fibroblast growth factor 2 (FGF2). Many animal and human studies have shown this protein is effective in periodontal regeneration. Recently, epigenetic modifications, such as DNA methylation, have been associated with changes in patterns of gene expression. Preliminary data suggests that FGF2 gene may be differentially methylated in periodontal tissues. Aberrant gene promoter methylation in smokers and diabetics has also been reported in many studies. However, the role of DNA methylation in wound healing has not yet been investigated.
The investigators hypothesize that the methylation status of FGF2 gene can affect the levels of FGF2 secreted during wound healing phase after dental implant surgery. The investigators also hypothesize there exists a difference in methylation levels of FGF2 gene in healthy, smoking and diabetic patients that can interfere with wound healing. The investigators seek to determine whether DNA methylation plays a role in wound healing and whether the methylation level of FGF2 gene varies among healthy, smoking and diabetic patients.
Read the detailed description
Periodontal wound healing is a complex multifactorial process that involves interactions among various cells, growth factors, hormones and extracellular matrices. Although still poorly understood, these interactions trigger a series of events that lead to new tissue formation. One growth factor that plays an important role in wound healing is fibroblast growth factor 2 (FGF2). FGF2 is a member of the heparin-binding growth factor family, secreted by macrophages and endothelial cells. During the proliferative healing phase, it stimulates fibroblast proliferation \& ECM synthesis, and increases chemotaxis, proliferation and differentiation of endothelial cells. During the bone remodeling phase, FGF2 also stimulates mesenchymal progenitor cell migration. Many animal and human studies have shown FGF2 are effective in periodontal regeneration. In 1999, Murakami showed surgically treated 3-wall intrabony defect in dogs grafted with FGF2 was able to demonstrate significantly greater cementum and bone formation. Four years later, his group again found that topical application of rhbFGF in surgically treated class 2 furcation defects in dogs also showed increase in formation of PDL, cementum and bone. In 2008, Kitamura performed a randomized controlled study in humans with 2- or 3-wall intrabony periodontal defects and found that rhbFGF was able to stimulate alveolar bone growth and PDL regeneration.
Recently, epigenetic modifications, such as DNA methylation, have been associated with changes in patterns of gene expression that do not involve changes in DNA sequence. DNA methylation is characterized by the addition of the methyl group onto cytokines within CpG regions. Methylated CpG regions interfere with the access of transcription factors to the promoter region, thereby silencing the gene. This DNA methylation phenomenon has important regulatory functions in normal and pathological cellular processes. It was recognized that alteration in the methylation states at the promoter regions of tumor suppressor genes are implicated with cancer. A persistent inflammation was also observed to cause DNA methylation, which inactivates suppressors of cytokine signaling and results in exaggerated cytokine production. This makes an individual susceptible to periodontal disease. In our laboratory, the investigators have discovered that periodontal disease is associated with increased DNA methylation of the COX-2 promotor, especially the locus immediately adjacent to the NF-kB in the promoter region. Preliminary data (not shown) suggests that FGF2 may be differentially methylated in periodontal tissues. Aberrant gene promoter methylation in smokers and diabetics has also been reported in many studies. However, the role of DNA methylation in wound healing has not yet been investigated.
We hypothesize that the methylation status of FGF2 can affect the levels of FGF2 secreted during wound healing phase after dental implant surgery. We also hypothesize there exists a difference in methylation levels of FGF2 in healthy, smoking and diabetic patients that can interfere with wound healing. We seek to determine whether DNA methylation plays a role in wound healing and whether the methylation level of FGF2 varies among healthy, smoking and diabetic patients.
- Being tested
- Dental implant surgery
- Keywords
- DNA methylation, FGF2, Wound healing, Smoking, Diabetes, Implant
- Medical subject headings
- Smoking, Diabetes Mellitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Dental implant surgeryProcedure or surgery
Surgery involving placement of one dental implant, of either Astra Tech or Straumann system, is performed in all subjects within 2 weeks of screening examination. Implant placement is 1-stage, but can be either on edentulous ridges or in extraction sockets.This is not a randomized treatment arm/group design. The study is observational with regards to the analysis of tissue samples that are collected prior to the routine placement of implants. The implant choice is based upon patient needs and is not related to any outcome.
| Study group | Role | What they receive |
|---|---|---|
| Control group | Subjects must have never smoked and must be non-diabetic. Receives: Procedure: Dental implant surgery | |
| Smoking group | Subjects must have had at least 5 pack-years of self-reported smoking history, must be currently smoking and must be non-diabetic. Receives: Procedure: Dental implant surgery | |
| Diabetic group | Subjects must have type 2 diabetes. The condition must be diagnosed subjects must be treated by medications and/or insulin. A HbA1C test result either within past 3 months or performed in the first visit must be available. They must have never smoked. Receives: Procedure: Dental implant surgery |
What is being measured
The primary outcome is the main question the study is designed to answer.
FGF2 methylation level
Genomic DNA is isolated from the collected gingival tissue samples. Methylation alterations in FGF2 are detected through differential methylation hybridization using the EpiTect® Methyl qPCR single assay.
Measured: On the day of implant surgery
Secondary outcomes (4)
FGF2 mRNA expression level
RNA is isolated from the collected gingival tissue samples and is then processed for gene expression analysis by quantitative real-time PCR.
Measured: On the day of implant surgery (DAY 0)
FGF2 protein level
Gingival crevicular fluid, obtained from the two adjacent sites closest to the implant location, is used to quantify specific FGF2 protein levels by ELISA.
Measured: On the day of implant surgery (DAY 0) and 2, 4 and 6 weeks following implant surgery
Implant stability quotient (ISQ)
The degree of implant stability at various time points following the surgery is measured using an Osstell ISQ instrument. An ISQ value, ranged between 1 and 100, is generated for each sample at each time point.
Measured: 4 and 6 weeks following implant surgery
Wound healing indices (WHI)
The degree of soft tissue healing at various time points following surgery is monitored by WHI.
Measured: 2, 4 and 6 weeks following implant surgery
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Aug 2012 (estimated)
- Study startAug 2010
- Primary completion12 Jan 2016
- Study completion23 Feb 2016
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for SmokingStudies of the same condition, open and under way.
- More trials run by University of North Carolina, Chapel HillThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 44 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of North Carolina, Chapel Hill
- Sponsor type
- University, hospital or other
- Collaborators
- National Institute of Dental and Craniofacial Research (NIDCR), National Center for Research Resources (NCRR)
- Responsible party
- Sponsor
- Investigators
- Silvana Barros, DDS, PhD, MS, Principal investigator, UNC Chapel Hill School of Dentistry
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01663298
- Sponsor's protocol ID
- 10-1184
- Other IDs
- 1R01DE021052-01, 1UL1RR025747, AWU
- Status last verified
- Feb 2019
- First submitted
- 1 Aug 2012
- Last updated
- 12 Feb 2020
- Results posted
- No
- Data monitoring committee
- No
Publications
Kaigler D, Cirelli JA, Giannobile WV. Growth factor delivery for oral and periodontal tissue engineering. Expert Opin Drug Deliv. 2006 Sep;3(5):647-62. doi: 10.1517/17425247.3.5.647.
PubMed 16948560Murakami S, Takayama S, Ikezawa K, Shimabukuro Y, Kitamura M, Nozaki T, Terashima A, Asano T, Okada H. Regeneration of periodontal tissues by basic fibroblast growth factor. J Periodontal Res. 1999 Oct;34(7):425-30. doi: 10.1111/j.1600-0765.1999.tb02277.x.
PubMed 10685372Murakami S, Takayama S, Kitamura M, Shimabukuro Y, Yanagi K, Ikezawa K, Saho T, Nozaki T, Okada H. Recombinant human basic fibroblast growth factor (bFGF) stimulates periodontal regeneration in class II furcation defects created in beagle dogs. J Periodontal Res. 2003 Feb;38(1):97-103. doi: 10.1034/j.1600-0765.2003.00640.x.
PubMed 12558943Kitamura M, Nakashima K, Kowashi Y, Fujii T, Shimauchi H, Sasano T, Furuuchi T, Fukuda M, Noguchi T, Shibutani T, Iwayama Y, Takashiba S, Kurihara H, Ninomiya M, Kido J, Nagata T, Hamachi T, Maeda K, Hara Y, Izumi Y, Hirofuji T, Imai E, Omae M, Watanuki M, Murakami S. Periodontal tissue regeneration using fibroblast growth factor-2: randomized controlled phase II clinical trial. PLoS One. 2008 Jul 2;3(7):e2611. doi: 10.1371/journal.pone.0002611.
PubMed 18596969Barros SP, Offenbacher S. Epigenetics: connecting environment and genotype to phenotype and disease. J Dent Res. 2009 May;88(5):400-8. doi: 10.1177/0022034509335868.
PubMed 19493882Gomez RS, Dutra WO, Moreira PR. Epigenetics and periodontal disease: future perspectives. Inflamm Res. 2009 Oct;58(10):625-9. doi: 10.1007/s00011-009-0041-7. Epub 2009 May 8.
PubMed 19440658Wilson AG. Epigenetic regulation of gene expression in the inflammatory response and relevance to common diseases. J Periodontol. 2008 Aug;79(8 Suppl):1514-9. doi: 10.1902/jop.2008.080172.
PubMed 18673005Ling C, Groop L. Epigenetics: a molecular link between environmental factors and type 2 diabetes. Diabetes. 2009 Dec;58(12):2718-25. doi: 10.2337/db09-1003. No abstract available.
PubMed 19940235Krupanidhi S, Sedimbi SK, Vaishnav G, Madhukar SS, Sanjeevi CB. Diabetes--role of epigenetics, genetics, and physiological factors. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009 Sep;34(9):837-45.
PubMed 19779253Simmons RA. Developmental origins of diabetes: the role of epigenetic mechanisms. Curr Opin Endocrinol Diabetes Obes. 2007 Feb;14(1):13-6. doi: 10.1097/MED.0b013e328013da5b.
PubMed 17940413Kuroda A, Rauch TA, Todorov I, Ku HT, Al-Abdullah IH, Kandeel F, Mullen Y, Pfeifer GP, Ferreri K. Insulin gene expression is regulated by DNA methylation. PLoS One. 2009 Sep 9;4(9):e6953. doi: 10.1371/journal.pone.0006953.
PubMed 19742322Han W, Wang T, Reilly AA, Keller SM, Spivack SD. Gene promoter methylation assayed in exhaled breath, with differences in smokers and lung cancer patients. Respir Res. 2009 Sep 25;10(1):86. doi: 10.1186/1465-9921-10-86.
PubMed 19781081Belinsky SA, Palmisano WA, Gilliland FD, Crooks LA, Divine KK, Winters SA, Grimes MJ, Harms HJ, Tellez CS, Smith TM, Moots PP, Lechner JF, Stidley CA, Crowell RE. Aberrant promoter methylation in bronchial epithelium and sputum from current and former smokers. Cancer Res. 2002 Apr 15;62(8):2370-7.
PubMed 11956099
Study at a glance
From the registry record, last updated by the sponsor on 12 Feb 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- FGF2 Promoter Hypermethylation and Implant Wound Healing Among Smokers and Diabetics
- ClinicalTrials.gov ID
- NCT01663298
- Acronym / sponsor ID
- 10-1184
- Keywords
- DNA methylation, FGF2, Wound healing, Smoking, Diabetes, Implant
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 44 participants (estimated)
- Lead sponsor
- University of North Carolina, Chapel HillUniversity, hospital or other
- Collaborators
- National Institute of Dental and Craniofacial Research (NIDCR), National Center for Research Resources (NCRR)
- Study start
- Aug 2010
- Primary completion
- 12 Jan 2016 (actual)
- Study completion
- 23 Feb 2016 (actual)
- First posted
- 13 Aug 2012 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Periodontal wound healing is a complex multifactorial process that involves interactions among various cells, growth factors, hormones and extracellular matrices. Although still poorly understood, these interactions trigger a series of events that lead to new tissue formation. One growth factor that plays an important role in wound healing is fibroblast growth factor 2 (FGF2). Many animal and human studies have shown this protein is effective in periodontal regeneration. Recently, epigenetic modifications, such as DNA methylation, have been associated with changes in patterns of gene expression. Preliminary data suggests that FGF2 gene may be differentially methylated in periodontal tissues. Aberrant gene promoter methylation in smokers and diabetics has also been reported in many studies. However, the role of DNA methylation in wound healing has not yet been investigated.
The investigators hypothesize that the methylation status of FGF2 gene can affect the levels of FGF2 secreted during wound healing phase after dental implant surgery. The investigators also hypothesize there exists a difference in methylation levels of FGF2 gene in healthy, smoking and diabetic patients that can interfere with wound healing. The investigators seek to determine whether DNA methylation plays a role in wound healing and whether the methylation level of FGF2 gene varies among healthy, smoking and diabetic patients.
Detailed description
Periodontal wound healing is a complex multifactorial process that involves interactions among various cells, growth factors, hormones and extracellular matrices. Although still poorly understood, these interactions trigger a series of events that lead to new tissue formation. One growth factor that plays an important role in wound healing is fibroblast growth factor 2 (FGF2). FGF2 is a member of the heparin-binding growth factor family, secreted by macrophages and endothelial cells. During the proliferative healing phase, it stimulates fibroblast proliferation \& ECM synthesis, and increases chemotaxis, proliferation and differentiation of endothelial cells. During the bone remodeling phase, FGF2 also stimulates mesenchymal progenitor cell migration. Many animal and human studies have shown FGF2 are effective in periodontal regeneration. In 1999, Murakami showed surgically treated 3-wall intrabony defect in dogs grafted with FGF2 was able to demonstrate significantly greater cementum and bone formation. Four years later, his group again found that topical application of rhbFGF in surgically treated class 2 furcation defects in dogs also showed increase in formation of PDL, cementum and bone. In 2008, Kitamura performed a randomized controlled study in humans with 2- or 3-wall intrabony periodontal defects and found that rhbFGF was able to stimulate alveolar bone growth and PDL regeneration.
Recently, epigenetic modifications, such as DNA methylation, have been associated with changes in patterns of gene expression that do not involve changes in DNA sequence. DNA methylation is characterized by the addition of the methyl group onto cytokines within CpG regions. Methylated CpG regions interfere with the access of transcription factors to the promoter region, thereby silencing the gene. This DNA methylation phenomenon has important regulatory functions in normal and pathological cellular processes. It was recognized that alteration in the methylation states at the promoter regions of tumor suppressor genes are implicated with cancer. A persistent inflammation was also observed to cause DNA methylation, which inactivates suppressors of cytokine signaling and results in exaggerated cytokine production. This makes an individual susceptible to periodontal disease. In our laboratory, the investigators have discovered that periodontal disease is associated with increased DNA methylation of the COX-2 promotor, especially the locus immediately adjacent to the NF-kB in the promoter region. Preliminary data (not shown) suggests that FGF2 may be differentially methylated in periodontal tissues. Aberrant gene promoter methylation in smokers and diabetics has also been reported in many studies. However, the role of DNA methylation in wound healing has not yet been investigated.
We hypothesize that the methylation status of FGF2 can affect the levels of FGF2 secreted during wound healing phase after dental implant surgery. We also hypothesize there exists a difference in methylation levels of FGF2 in healthy, smoking and diabetic patients that can interfere with wound healing. We seek to determine whether DNA methylation plays a role in wound healing and whether the methylation level of FGF2 varies among healthy, smoking and diabetic patients.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Control group | – | Procedure: Dental implant surgerySubjects must have never smoked and must be non-diabetic. |
| Smoking group | – | Procedure: Dental implant surgerySubjects must have had at least 5 pack-years of self-reported smoking history, must be currently smoking and must be non-diabetic. |
| Diabetic group | – | Procedure: Dental implant surgerySubjects must have type 2 diabetes. The condition must be diagnosed subjects must be treated by medications and/or insulin. A HbA1C test result either within past 3 months or performed in the first visit must be available. They must have never smoked. |
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Patients in the graduate periodontal clinic in the school of dentistry at the University of North Carolina
Key inclusion criteria (7 listed)
- Adult males or females between the age of 18 and 70 years (inclusive)
- Able and willing to follow study procedures and instructions
- Have read, understood and signed an informed consent form
- In good general health
- Have one or more implant placements as their future treatment needs. The implant placement can be either as one-stage or two-stage, and can be either in an edentulous ridge or an extraction socket
Key exclusion criteria (7 listed)
- Have a chronic disease with oral manifestations
- Exhibit gross oral pathology
- Use of either antibiotics or NSAIDs within 1 month prior to screening examination
- Chronic treatment (i.e. two weeks or more) with any medication known to affect periodontal status (e.g. phenytoin, calcium, antagonists, cyclosporin, Coumadin) within 1 month prior to screening examination
- Systemic conditions, except smoking and diabetes, that are known to affect the periodontal status
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Dental implant surgerySurgery involving placement of one dental implant, of either Astra Tech or Straumann system, is performed in all subjects within 2 weeks of screening examination. Implant placement is 1-stage, but can be either on edentulous ridges or in extraction sockets.This is not a randomized treatment arm/group design. The study is observational with regards to the analysis of tissue samples that are collected prior to the routine placement of implants. The implant choice is based upon patient needs and is not related to any outcome. | Procedure or surgery | Control group, Diabetic group, Smoking group |
Primary outcome
FGF2 methylation level
Time frame: On the day of implant surgery
Genomic DNA is isolated from the collected gingival tissue samples. Methylation alterations in FGF2 are detected through differential methylation hybridization using the EpiTect® Methyl qPCR single assay.
4 secondary outcomes
FGF2 mRNA expression level
Time frame: On the day of implant surgery (DAY 0)
FGF2 protein level
Time frame: On the day of implant surgery (DAY 0) and 2, 4 and 6 weeks following implant surgery
Implant stability quotient (ISQ)
Time frame: 4 and 6 weeks following implant surgery
Wound healing indices (WHI)
Time frame: 2, 4 and 6 weeks following implant surgery
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Feb 2020.
- Background: PubMed 16948560Kaigler D, Cirelli JA, Giannobile WV. Growth factor delivery for oral and periodontal tissue engineering. Expert Opin Drug Deliv. 2006 Sep;3(5):647-62. doi: 10.1517/17425247.3.5.647.
- Background: PubMed 10685372Murakami S, Takayama S, Ikezawa K, Shimabukuro Y, Kitamura M, Nozaki T, Terashima A, Asano T, Okada H. Regeneration of periodontal tissues by basic fibroblast growth factor. J Periodontal Res. 1999 Oct;34(7):425-30. doi: 10.1111/j.1600-0765.1999.tb02277.x.
- Background: PubMed 12558943Murakami S, Takayama S, Kitamura M, Shimabukuro Y, Yanagi K, Ikezawa K, Saho T, Nozaki T, Okada H. Recombinant human basic fibroblast growth factor (bFGF) stimulates periodontal regeneration in class II furcation defects created in beagle dogs. J Periodontal Res. 2003 Feb;38(1):97-103. doi: 10.1034/j.1600-0765.2003.00640.x.
- Background: PubMed 18596969Kitamura M, Nakashima K, Kowashi Y, Fujii T, Shimauchi H, Sasano T, Furuuchi T, Fukuda M, Noguchi T, Shibutani T, Iwayama Y, Takashiba S, Kurihara H, Ninomiya M, Kido J, Nagata T, Hamachi T, Maeda K, Hara Y, Izumi Y, Hirofuji T, Imai E, Omae M, Watanuki M, Murakami S. Periodontal tissue regeneration using fibroblast growth factor-2: randomized controlled phase II clinical trial. PLoS One. 2008 Jul 2;3(7):e2611. doi: 10.1371/journal.pone.0002611.
- Background: PubMed 19493882Barros SP, Offenbacher S. Epigenetics: connecting environment and genotype to phenotype and disease. J Dent Res. 2009 May;88(5):400-8. doi: 10.1177/0022034509335868.
- Background: PubMed 19440658Gomez RS, Dutra WO, Moreira PR. Epigenetics and periodontal disease: future perspectives. Inflamm Res. 2009 Oct;58(10):625-9. doi: 10.1007/s00011-009-0041-7. Epub 2009 May 8.
- Background: PubMed 18673005Wilson AG. Epigenetic regulation of gene expression in the inflammatory response and relevance to common diseases. J Periodontol. 2008 Aug;79(8 Suppl):1514-9. doi: 10.1902/jop.2008.080172.
- Background: PubMed 19940235Ling C, Groop L. Epigenetics: a molecular link between environmental factors and type 2 diabetes. Diabetes. 2009 Dec;58(12):2718-25. doi: 10.2337/db09-1003. No abstract available.
- Background: PubMed 19779253Krupanidhi S, Sedimbi SK, Vaishnav G, Madhukar SS, Sanjeevi CB. Diabetes--role of epigenetics, genetics, and physiological factors. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009 Sep;34(9):837-45.
- Background: PubMed 17940413Simmons RA. Developmental origins of diabetes: the role of epigenetic mechanisms. Curr Opin Endocrinol Diabetes Obes. 2007 Feb;14(1):13-6. doi: 10.1097/MED.0b013e328013da5b.
- Background: PubMed 19742322Kuroda A, Rauch TA, Todorov I, Ku HT, Al-Abdullah IH, Kandeel F, Mullen Y, Pfeifer GP, Ferreri K. Insulin gene expression is regulated by DNA methylation. PLoS One. 2009 Sep 9;4(9):e6953. doi: 10.1371/journal.pone.0006953.
- Background: PubMed 19781081Han W, Wang T, Reilly AA, Keller SM, Spivack SD. Gene promoter methylation assayed in exhaled breath, with differences in smokers and lung cancer patients. Respir Res. 2009 Sep 25;10(1):86. doi: 10.1186/1465-9921-10-86.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Silvana Barros, DDS, PhD, MS principal investigator
UNC Chapel Hill School of Dentistry
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Smoking and Diabetes, run by University of North Carolina, Chapel Hill at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 7 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Feb 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
FGF2 methylation level (time frame: On the day of implant surgery). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01663298, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Feb 2020.