Science topic

Periodontics and Oral Pathology - Science topic

Oral pathology, Oral medicine, Dentistry, Periodontology
Questions related to Periodontics and Oral Pathology
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The systemic antioxidant therapy is one of the therapeutic options for oral mucosal lesions. In Localized delivery of antioxidant molecules to the oral mucosal lesion, will the oral mucosal cells uptake/absorb the antioxidant molecules? Will the antioxidant molecules perform their action when delivered locally? Which route of delivery (systemic/local) of antioxidant molecules can have better activity?
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Antioxidants can be used topically on oral mucosal tissues, as many antioxidant agents are composed of some materials that aid in upcoming of the components by oral mucosal parts. For example, Aloe vera is an active antioxidant in which Lignin is used to be absorbed into deeper tissues of oral mucosa.
In addition, to prevent chemotherapy induced oral mucositis from taking place, topical use of some agents are studied. My last research wss about topical application of olive oil in order to prevent chemotherapy induced oral mucositis. Antioxidant proerties was one of the most important justifications of olive oil effectiveness as it was effective in prevention.
This is the url of that article
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I have noticed gingival and periodontal ligament fibroblasts have differing morphologies when cultured with MTA.
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Maybe MTA only caused periodontal ligaments with mild inflammation of osteofibrosis, without bony lesion formation.
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On the web: Dental caries food for thought
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Hi John,
See our recently published paper:
"Human neutrophils degrade methacrylate resin composites and tooth dentin."
This could help answer your question.
-Russel
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I am interested about the biology of the alveolar bone during the interdisciplinary orthodontic treatment of adult patients
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Biology of the alveolar bone during orthodontic treatment
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The apical coronal or coronal apico is known, the decision depends on the presence of necrosis or irreversible pulpitis or acute periapical abscess.
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Thank you very much for your contributions.
Recently I read a book where the author refers to what they are saying. He mentions the techniques of pulpectomy for primary teeth: with pulpal vitality (irreversible pulpitis), with pulpal necrosis without radiographic evidence of periapical lesion and necrosis with radiographic evidence of periapical lesion.
Also, the author suggests compensatory wear to facilitate cleaning and filling of the root canals.
For example, for vital teeth, it recommends the stepped technique with progressive anatomical recoil to clean the canal, give it a conical shape and facilitate sealing. The technique divides it into apical preparation and staggered preparation.
Thanks for your attention.
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Antibiotic resistant endodontic infection is a common finding in failed root canal treated tooth with history of long term medication. 
As a part of a research proposal to the Indo-Norwegian collaborative research, we would like to have a norwegian team to do a part of this project.
Interested Norwegian researchers kindly contact. 
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this absolutely right I would say
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I'm especially interested in relatively unworn adult dentition. Thanks in advance!
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Predrag:
Have a look at this link:
Best
Syed
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biological rationale for plaque  not  getting mineralized to calculus in aggressive periodontitis?
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As a clinician, to have an active periodontal condition with out calculus formation  is a bad sign. Also a good sign is to start having calculus formation as the biofilm of the pocket returns to a healthy flora with treatment. Calculus formation is a defence mechanism against periodontal pathogens. Calcified bacterial plaque never hurt anyone. The niches  its presence creates for unhealthy bio-film to establish itself  is the problem.
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We are aware of the discoloration of teeth by tetracycline administered during pregnancy and in young children. My question is, does tetracycline/doxycycline mouthrinse cause tooth discoloration?Any scientific studies/evidence on this please???
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Hello Sir,
I haven't yet seen an article addressing this topic, I could help you with articles on tetracycline antibiotics and its effect on teeth, anyway I will keep an eye out and post any favorable results I encounter regarding tetracycline mouthwash.
Regards
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Just got a question concerning the total aplasia (primary + permanent) in the 4th quadrant of a 4-y-old boy. No more info available at the moment.
Don't know what to recommend.
1. Transplantation: seems from the radiograph that there is no bone as alveolar process. Would mean lateralisation of nerve. Never heared of such surgery in such a young patient. Any information???
2. Tx 2: Never done such surgery in that age. Earliest tx was a primary canine in a 6-y-old to replace a lost incisor, earliest tx of a pm to replace an aplastic pm was at about 11y.
3. Tx 3: Never done that in cases like this: Will there be the development of an alveolar process or will it stay as lower-jaw basis? I guess it should develop, at least in parts, but I don't know for sure...
4. Indication to treat: Definitely yes, I have the impression of muscular hypertrophy on the left. But when? Still some time, or tomorrow?
5. Indication 2: Any other treatment? Temporary? Definitive?
Thx.
Yango
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Hi, Hayfaa,
(sry for using first name, could imagine that Hayfaa is female, but don't know for sure, thus trying to avoid Mr. or Mrs. + I prefer first name)
thanks again for your valuable comments.
Yes, maybe there is no permanent canine, the germ looks inddeed like an incisor. Since I don't want to judge from a radiograph, especially in the aplasia cases where there sometimes also the teeth show irregular appearance, I avoided to name the tooth. Nevertheless, I had a closer look onto the radiograph, and I think the primary canine 83 is also not what I thought (and or sure) but looks like an atypical primary incisor with some developmental coronal irregularities.
But - what would be the consequence for the treatment? Maybe, it is decisive in the long run, but I think these cases are much to rare to have any information whether there are better or worse results with a permanent canine. It is in my opninion most important to have as many natural teeth as possible.
That said, I think, I will propose the transplantation of the primary incisors to the 4th quadrant... Again, thank you for forcing me to rethink...
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Harmonal changes, Gingivitis,gingival enlargement, bleeding, epulis, periodontitis, tooth mobility, dental erosion, caries
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Pregnancy makes oral tissues more fragile and with tendency to inflammation and bleeding. The gravid granuloma erroneously called pyogenic granuloma is one of the most frequent situations. Minor trauma can trigger important inflammatory reactions. It is important to emphasize the role of strict hygiene due to gingival swelling due to hormonal stimulation
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Dear ResearchGate Community,
I'm currently working on the implementation of the Ligature-Induced model of Periodontitis in Rats (Winstar - Sprague Dawley). Yesterday I had my first try... however I discovered rat molars are very distal and difficult to access. I tried to use a 4-0 silk suture (3/8 circle) but found it impossible to access! 
Does someone has experience on this model? I need advice or guidance on how to reach the molars.
With best of Regards,
Constanza.
Ps. Sorry for my english, sadly I am not a native speaker.
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Hi, Constanza, try using the 3-0 silk (despite the greater thickness, the insertion is easier, without fraying it). The second maxillary molars and the first mandible molars are, according to our group experience, the ideal ones for beginning the process. Use two needle-holders (small ones) and insert the silk first in the distal interproximal space. The insertion movement must be firm and precise, from top to bottom, and not from one side to the other, because that usually frays the thread. The next insertion can be done in the mesial interproximal space. 
Good luck! 
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The current imaging method of choice is conventional dental radiography. Needed information regarding impacted teeth cannot be obtained adequately by lower dose conventional (traditional) radiography. Should the indication to use cbct be emphasized?
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If 3D information is needed for the management of the impacted tooth CBCT is indicated (This conclusion can be drawn on conventional X-ray imaging and clinical examination (palpation)).
If a 4cmx4cm volume is made with 90kV, low tubecurrent (2 to 3 mA) and limited arch rotation (180 degrees 9 seconds) this exposure can be made safely in children (dose aruond 10 micro Sievert).
This volume will not be crisp and sharp but it will give you the information at the lowest dose (ALADA as low as diagnostically acceptable).
If on the other hand the exposure is made with a large volume and custom parameters the dose can be 10 to 40 times higher.
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There are various methods for the dental age assessment like the Nolla's, Demirjian's, Willem's etc. Nolla's method seems to be an easy method to assess the dental age of any given population. What are the merits and demerits of using Nolla's method for dental age assessment?
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Ans: The Nolla’s method allows the classification of dental development from stage one (1 - no sign of calcification with the presence of crept), to stage ten (10 - apical end completed). In this method of age estimation, the Intra oral Periapical radiograph of each tooth is assessed individually and compared with the stage of the Nolla table. The dental age calculated corresponds to the sum of the Nolla scores. This method has been found to be more precise in boys  and more accurate than the Demirjian method in early and late childhood for both sexes. But this method could predict chronological age in adults. For girls, the Nolla method is significant up to late childhood.
A very few studies have investigated use of the Nolla’s method in different populations for age estimation and have concluded that the Nolla’s  method is more accurate than Havikko and Demirjian methods and  Nolla’s method constitutes a useful instrument for diagnosis and treatment planning.
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Is there any published literature which gives clear guidelines on when resective or regenerative periodontal surgery should be done ?
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Dear Ramachandra SS 
pls check the link.
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Cases of aggressive periodontitis are not plenty in number.
How to carry out a reliability study for an index on aggressive periodontitis?
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Dear Ramachandra SS 
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Does Space analysis of TMJ by CBCT is an accurate method for discrimination between patients with clicking and normal patients?
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A large body of literature has been published in recent times due to the fact that CBCT has inspired research in TMJ imaging. An important advantage of CBCT imaging of TMJ is that it allows accurate measurements of the volume and surface of the condyle. These measurements are extremely advantageous in clinical practice when treating patients with TMJ dysfunctions.
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Genetic susceptibility for the development of certain oral diseases
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 Thank you. 
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Please suggest what must be done to ensure our progress towards painless dentistry. Where are our research and clinical evidence? Needed more progress. (Not just the claim of pharma companies and sponsored research)
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From a practical point of view psychology surely plays an important role. A good way to approach that and the technical side has been shown above. However, we also know that there is a wide range of factors that govern pain sensitivity such as (but by far not limited to) sex, beliefs and values, and emotional and psychological state. Pain is ultimately an output of the brain. And how the brain works is largely still a mystery, just like the concept of consciousness, which we aim to turn off during general anesthesia. The complexity of this matter is extremely high and we have to acknowledge that without answering these questions first, we will not be able to exercise full pain control.
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 I  would   like  to  know  if   any  on e  knows  if  there  is   anything   out   there   in   the   market   place   that   will  help  a   dentist   with  this   problem  when   using   an  air  abrasion   unit   in   clinical    practice.  
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Dear Dr. John Bembenek,
                                               I would definitely like to learn more about your invention. This appears to be a promising solution.
With regards,
Alok Misra
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1.Root planning/Curettage/Flap surgey
2.Root conditioning/Local irrigation?
3. RCT
4. Crown
5. Extraction of hopeless tooth
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Hello there Alok, hope you are well. This question has a lot of divisions and we could see a long debate. lets hope the followers give their valuable comments and share their knowledge.
In my personal experience and as far as my knowledge is concerned regarding the subject, endo-perio or perio-endo whichever the case, we must perform endodontic therapy of a tooth. Curretage or root surface debridement is for sure recommended in case there is severe periodontal condition. Local irrigation would be a part of our overall treatment planning and maybe done. As far as crown fabrication is concerned, that would depend on the size of the access we make for endodontic therapy. and well extraction would be of course the BEST option for a tooth which is hopeless. 
I am attaching a link for you to have a look. Its an old article in dental update but quite sound and simple. Please share if you have something new,
Best wishes !
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Does it aid the speed of recovery? Long-term vs short-term benefits?
Is it as effective in extraction socket as using of particulate graft material in socket preservation?
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Dear Haroon sir, i did not find any description of L-PRF in the above link. IT just showed that there was no statistically significant difference in PRF treated and untreated extraction socket.
After centrifugation, L-PRF clot is separated from the portion of red blood cells (red thrombus), obtaining a fibrin clot with a red small portion in order to include the “buffy” coat richer in large leucocytes.
May be following link will be helpful:
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Itchy gums and periodontitis? What is the pathogenesis of the itchiness of the gums that periodontal patients sometimes complain about?
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Also amibae larva running aroud gum line! Patients feel it... Not surprising
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I am particularly concerned with the chance of brittle enamel getting chipped off while doing US scaling. 
Also, noticed excessive sensitivity to cold water and air in these patients. How to overcome the stated problems.
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Fluorosed enamel is often harder and more brittle than normal. Careful SRP is not only indicated but mandatory to keep these teeth healthy. Ultrasonics, on the other hand, may tend to fracture the brittle enamel crystals.
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What are the most recent host modulation therapies indicated in treatment of aggressive periodontitis? I am working on the anti-oxidant role of host modulation therapy.
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I would say that if you can convert the bacteria in the pocket from an unhealthy bacterial mix to a healthy bacterial mix, the inflammatory reaction will take care of itself.
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¿what type of bacteria are there in periimplantitis?
are they the same as periodontitis?
is there any protocol with antibitiotics?
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Dear Dr Garcia
The protocol I use is in coincidence with my research which is under review in one journal. Thus, I give you my results and protocol in treatment of periimplantitis after review process will be done.
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A 31-year-old male patient with exophytic mass growing out from his left buccal mucosa, measured 3X2 cm. Incisional biopsy was taken from periphery and it was proved as SCC. After the incisional biopsy (after 14 days) the patient came with progressively enlarged tumor mass from the biopsy site. 
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The healing of biopsy site involves upregulation of growth factors, that given the upregulation of receptors on tumor cells.  Cases of rapid growth of lesion at biopsy site and extraction sites are seen clinically in cancer patients, supporting this potential.  
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Evidence based dentistry started 20 years ago (1). Most Cochrane Systematic Reviews still end with the conclusion that recommendations for clinical practice cannot be made based only on the results of these trials and that more randomised controlled trials are needed to elucidate the interventions for treating a certain kind of malocclusion. Turning the Cochrane reviews into a tool that is more relevant in clinical practice will require implementation of a methodology allowing inclusion of non-RCTs while controlling for possible bias.(2)
1.. Richards D, Lawrence A. Evidence based dentistry. Br Dent J. 1995;179(7):270–3.
2. Teich ST, Lang LA, Demko CA. Characteristics of the Cochrane Oral Health Gro up Systematic Reviews. J Dent Eduacation. 2015;79(1):5–15.
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Do you agree with Meikle`s statement that If one asks whether RCTs have achieved their objective, or provided knowledge not previously available from retrospective studies or animal experimentation, then the answer would have to be no; it is also hard to justify the cost. What is particularly interesting is that knowledge based on years of clinical experience has been disregarded and then announced as if it was something completely new?
1. Meikle MC. What do prospective randomized clinical trials tell us about the treatment of class II malocclusions? A personal viewpoint. Eur J Orthod. 2005;27(2005):105–14.
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Dear colleagues,
I look for any kind of academic institution worldwide to collaborate in dental/periodontal research or lecturing/teaching.
Topics: periodontology / implantology / halitosis / lasers in dentistry.
Please contact me
Curd
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Yes, please contact me directly,  or through  The POSEIDO Academy (Periodontology, Oral Surgery, Esthetic & Implant Dentistry Open Academy) is an international on-line learning platform dedicated to the diffusion of clinical teaching, user-friendly scientific knowledge and global community information. The POSEIDO Academy is managed directly by the SIREN Professors, an international network of renowned clinicians and researchers members of the POSEIDO SIREN (Scientific International Research & Education Network). As convenors of this Academy, their duty is to diffuse their clinical and scientific knowledge and experience, to organize the themes of discussions, and to promote exchanges and debates through our Community, in the respect of the POSEIDO Academy Charter of Ethics. The Charter mostly implies for all SIREN Professors to remain independent from commercial considerations and advertisement in their teachings and comments, even if they can present freely their works with the implants or materials they are using in their daily practice. http://www.poseido.net/network/poseido-academy.html
Best Regards 
Nelson
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A patient presented to us with multiple keratocysts. Work-up did not show features of Gorlin-Goltz syndrome. Before being diagnosed as nonsyndromic or Gorlin-Goltz with partial expression, I need to rule out other possible syndromes. Do you know such? or an article listing them. I couldn't find in PubMed.
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Dear Omayma,
I have published an article regarding Conservative Management of Multiple Odontogentic Keratocyst in a Young Patient with 2 Years Follow Up - A case report
follow the citation: Nirmala SVSG,Sandeep C, Sindhuri V,Vimala Devi P. Conservative Management of Multiple Odontogentic Keratocyst in a Young Patient with 2 Years Follow Up. J Dent App. 2015;2(2): 149-152.
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Are there any dental consultations required before commencing chemo? 
Any fluoride treatment during the course of chemo and later? 
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Xerostomia is a permanent sequela of mouth cancer, without therapy.We can try the protection of salivary glands  with administration  of protective solutions,advertizing the patients for the limitations of these procedures
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As invasive as it is, this technique, with its variants, seems interesting and promising. I would much appreciate learning from your critical opinions and experience.
I attach one article and list here others, equally easily available on the net.
Periodontal Accelerated Osteogenic
Orthodontics: A Description of the
Surgical Technique
Kevin G. Murphy, DDS, MS,* M. Thomas Wilcko, DMD,†
William M. Wilcko, DMD, MS,‡ and
Donald J. Ferguson, DMD, MSD§
An Evidence-Based Analysis of Periodontally
Accelerated Orthodontic and Osteogenic
Techniques: A Synthesis of Scientific
Perspectives
M. Thomas Wilcko, William M. Wilcko, and Nabil F. Bissada
PERIODONTALLY ACCELERATED OSTEOGENIC ORTHODONTICS: A REVIEW OF THE LITERATURE
Yener ÖZAT1 Ruhi NALÇACI2
One-stage Surgical Alveolar Augmentation (PAOO)
For Rapid Orthodontic Movement. A Case Report.
1 Ashish Jain, M.D.S
2 Tarun Das, M.D.S
3 Rashi Chaturvedi, M.D.S, D.N.B
Piezocision Assisted Orthodontics: A new approach to
accelerated orthodontic tooth movement
Mittal S.K. 1, Sharma R.2, Singla A.3
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Periodontally accelerated orthodontic and osteogenic techniqueswill speed up tooth movement but will always remain additional invasive techniques. Treatment time can be much faster when you are able to avoid round tripping in using sound biomechanics and in improving time schedules.
1. Beckwith FR, Ackerman RJ, Cobb CM, Tira DE. An evaluation of factors affecting duration of orthodontic treatment. Am J Orthod Dentofac Orthop. 1999;115(4):439–47.
2. Sanon M, Taylor DC a, Parthan A, Coombs J, Paolantonio M, Sasane M. Effectiveness and duration of orthodontic treatment in adults and adolescents. J Med Econ. 2012 Jul 4;383–6.
3. Skidmore KJ, Brook KJ, Thomson WM, Harding WJ. Factors influencing treatment time in orthodontic patients. Am J Orthod Dentofacial Orthop. 2006 Mar;129(2):230–8.
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Aggressive periodontitis attacks people at early age of life and causes extensive bone loss which might lead to early loss of dentition, early detection of patients at high risk to be attacked by this type of periodontitis will help them a lot to be involved in a strict professional and personal preventive program thus minimize the periodontal damage to a large extent .I wonder if any one has ideas about any chairside methods  for early  detection of risk factors and  those who are at a high risk for developing this kind of periodontitis?
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I do agree with Martin and African Americans are more prone for this and risk may vary from individual to individual.
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Looking for association of DAS 21 and periodontal status, also looking in to role of stress in Hbac1c levels, DAS 21 and periodontal status
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I do agree with explanation given by HAMID RAKHSHAN
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I am conducting a research about Oral health related quality of life by using OHIP-14. One of my variable for conceptual framework is Knowledge,attitude and practice. I am having trouble with the literature part to support which model do I base on for the KAP part. Is there any model that support KAP and oral health related quality of life? I need to put something to support my variable for my literature review part. If anyone can help, please do. Thank you
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I wonder if OHQoL and KAP are so conceptually different that it would be unlikely to find a model that links them.   
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Is there any scientific data or published article to show that cases of aggressive periodontal disease with positive family history have or are at more risk for increased periodontal breakdown?
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1- Periodontal status among relatives of aggressive periodontitis patients and reliability of family history report  -M. A. Llorente andG. S. Griffiths
2- Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis
Ayala Stabholz, W. Aubrey Soskolne andLior Shapira
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An 11- year- old boy presented to the dental clinic with his father, complaining of poor esthetics and delaying of eruption of teeth. Examination revealed a suspicion of amelogenesis imperfecta ( clinically & radiographically). Teeth present: 11, 21, 31, 16, 26, 36, 46, all primary molars and canines and partially erupted 12,22, 42. Patient  has also angle, class III. Outline the treatment plan for such a case.
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hi
can you please upload panoramic radiography and photographies?
I think the first step is to know the exact type of amelogenesis imperfecta ,if accompanied by anterior openbite it seems that the case is of hypocalcified type.
these patients report tooth sensitivity too.If dental age of the patient is late(It takes some time for the primary molars to shed),SSC seems a good choice and if needed pulp therapies must be done.for anterior teeth,composite veneers can be used until reaching full growth when they can be replaced with crowns,if needed.for first permanent molars,permanent SSC are available if they are too hypoplastic.otherwise, more conservative approaches must be used.
Most importantly,I think it will be useful to begin the patient care with preventive approaches including fluoride therapy,sealants,diet consultation and etc.
For skeletal problems as you mentioned,consult with an orthodontist, although bonding procedures is some how difficult in these patients.
these are the plans I had, and wait for hearing more extensive treatment plans.
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In the treatment of gingival recession around lower incisors by applying free connective tissue graft along the area of recession, how it is possible to pull the alveolar mucosal flap from the vestibule and inner mucosa of lower lip with the purpose of covering the connective tissue graft over the gingival recession?
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Beautiful suggestions! From my experience, your dilemma seems to have arisen from insufficient keratinized gingiva. In such instances, I have found a two- stage procedure useful. Stage 1 will be to increase the zone of keratinized gingiva achievable with a free gingival graft. Allow a few weeks to heal then proceed to stage two. Harvest your CTG and suture to the prepared recipient site.Complete the process with an immediate coronally-advanced flap. Alternatively, place the CTG using the tunnelling technique. Cheers!
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Endemic fluorosis
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Hi in answer to your questions:
What about the people with high ground water fluoride levels with no provision for defluoridated drinking water ? Will it add to the detrimental systemic effects of excess fluoride? 
answer:  I am afraid that the end result will be very toxic  especially in high level of fluorides  here is a paper published to show that  levels higher than over 2.0 mg/L  can lead to liver damages
Dose–effect relationship between drinking water fluoride levels and damage to liver and kidney functions in children
Original Research Article
Environmental Research, Volume 103, Issue 1, January 2007, Pages 112-116
XianZhi Xiong, JunLing Liu, WeiHong He, Tao Xia, Ping He, XueMin Chen, KeDi Yang, AiGuo Wang
Abstract
Therefore, our results suggest that drinking water fluoride levels over 2.0 mg/L can cause damage to liver and kidney functions in children and that the dental fluorosis was independent of damage to the liver but not the kidney. Further studies on the mechanisms and significance underlying damage to the liver without dental fluorosis in the exposed children are warranted.
cheers
prof galil
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I have been using 910nm diode laser for treating the rct failure cases with periapical abscess forming a sinus tract into the sulcus, and I am seeing a very good prognosis.
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Have you got equally good results after ReRCT only (without laser). May be only retreatment is showing the magic and laser may actually not have any role.
I myself have done in vitro study (not published yet). And i found sodium hypochlorite irrigation was the best, followed by CHX irrigation and least effective was diode laser in reducing E.fecalis on culture plates.
Am personally not a believer of endo-sterilization using diode.
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The American dental Association has provided a statement on the use of lasers and dentistry. If you go to ADA.org and then search this topic you will find a pretty well thought out response.
Here is the section related to the LANAP protocol:
Laser-Assisted New Attachment Procedure
A 2007 publication compared the probing depth, attachment gain, and type of attachment from traditional mechanical therapy of advanced chronic periodontitis vs. traditional mechanical therapy that included two intrasulcular applications of Nd: YAG; one aimed at removing the sulcular epithelium and another said to “seal” the pocket.2 In this study, histology was performed on 6 pairs of single-rooted teeth at 3 months. Laser-treated pockets tended to show greater probing depth reductions and clinical attachment gains than non-lased pockets. Based on measurements from notches placed in periodontally involved root surfaces before treatment, lased teeth showed evidence of new cementum while 5 of the 6 control teeth showed a long junctional epithelial attachment. This study concluded that the Laser Assisted New Attachment ProcedureTM (LANAP) can be associated with cementum-mediated new connective-tissue attachment and apparent periodontal regeneration of diseased root surfaces in humans.
Although the Council is optimistic regarding the potential for lasers to enhance effectiveness in treating periodontitis, dentists should note that this study provides no more than pilot validation for this treatment concept. The study was not blinded, and the sample size was small thereby limiting extrapolation of the results to the general population. Further, pre-treatment notches in the teeth were difficult to place, hard to know exactly where they were placed and are difficult to clearly detect on histological specimens. Moreover, the advanced periodontal destruction initially present in these 6 test teeth make it difficult to extrapolate these results to cases of early and moderate chronic periodontitis, where the anatomic environment, laser energy distribution and clinical outcome may differ substantially. It is also unclear what laser-based “sealing” of a treated periodontal sulcus is and, if real, what benefits it might provide. Additional clinical data from properly designed clinical trials with adequate sample sizes are still required before it can be known to what extent LANAP is safe and effective across the spectrum of patients with chronic periodontitis. The Council therefore cautions clinicians to weigh the available evidence for LANAP when considering the options available for treatment of the periodontal diseases.
So my interpretation, using this statement from the American dental Association is that this procedure may have some potential but there is certainly no definitive hard scientific evidence to show that it is anything more than another way to address a problem.
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Identification of this problem as early as possible is very important in management. How do I do it?
There are many new antihypertensive drugs being used. Some of these might have a similar effect? Are there any research papers?
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You will find a number of research papers on drug induced gingival enlargement. Antihypertensive drugs, the calcium channel blockers, namely nifedipine and amlodipine to name a few can cause dose related gingival enlargement. If u get a patient with gingival enlargement with no history except that the patient is on calcium channel blockers, rest assured that it is a case of Drug induced gingival enlargement. You need to first perform a thorough oral prophylaxis and refer the patient to his or her physician for possible substitution of the drug. Then u put the patient on a maintenance program, u can wait upto 6-12 months, if the enlargement still does not subside, u can go for surgical periodontal therapy. If no of teeth involved are less than 6, go for gingivectomy and if it is more than 6, go for flap surgery.
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Does anyone have some experience in staining macrophage in periodontal tissue, especially in periodontally-infected (i.e., periodontitis) tissue in mice? Growing attention is paying on macrophage in periodontitis. However, it seems too few macrophages exist in periodontitis, let alone in the tiny gingiva in mice. If I hope to immunostain macrophages in paraffin-embedding jaw from mice, what are the notes during decalcification, tissue processing and immunohistochemistry?
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Dear Antonius Bronckers, Thank you for your so kind advice in detail ! I'm itching to try the classical TRAP staining method in periodontal tissue. Could you give me a TRAP protocol for parraffin-embedding jaw from mice, since very few articles have descripted this condition in detail? Your suggestions on distinguishing macrophage from osteoclast in periodontal tissue is noticeable and very useful. But I wonder if the TRAP kit will stain any cells other than macrophage and osteoclast, e.g., if any, mast cell or plasma cell? As you said, osteoclast is multicleated (>3 nuleus could be seen as a threshold ) which might be excluded to count macrophage in periodontal tissue? Strictly speaking, there are no specific but more representative markers for macrophage, such as F4/80 and CD68, with which I would try. According to your experience, how many macrophages-like cells could be stained in subepithelial connective tissue?
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I'm writing a review and I just want to test the opinion of the network.
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Yes platelet rich fibrin and platelet rich plasma have been extensively used in periodontal regeneration and excellent results have been achieved.The newer of the two, that is PRF has tremendous potential as it harbours lot of growth factors and are used even by oral surgeons in dental defects.Hence it makes a lot of sense to use them in regeneration procedures n dentistry.
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In a number of articles, diode laser is used along with scaling and root planing in moderate periodontitis cases. After the first diode laser application, it is used in intervals- on the 4th,7th,9th and 11th day (a total of 4 or 5 applications of diode laser in Periodontal pockets). Is there any standard criteria for using diode laser in intervals with multiple doses of laser?
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Because of the variation of dental diode laser parameters, it is difficult to standardize the laser dose. Some lesions subsided after the first laser irradiation, while most of advanced conditions need multisessions to cure. However, diode laser is one of the best treatments in periodontal conditions.
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I am using 2% curcumin gel to treat experimental periodontitis. I wanted to assess the acute toxicity and chronic toxicity of this gel used to apply subgingivally in rat model. Please let me know the answer.
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Thank you Mr. Gulam Husain. I am doing the study following OECD guidelines now.
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Odontogenic Cysts/Cancer
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According to recent scientific literature, it seems that the occurence of a primary intra-osseous squamous cell carcinoma arising from degenerated odontogenic cysts is around 0.3 to 3% of cases. (Jain et al. 2013)
This malignant degeneration seems to occur more frequently in large old cysts, which have gone untreated for several years.
It seems that the only way to ensure proper diagnosis is through systematic histopathological analysis of "suspect" cysts. On that matter, follow up is paramount.
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I am working on the effect of topical curcumin on ligature induced periodontitis in wistar albino rats. We have used a gel base which delivers curcumin for 24-48 hours. We confirmed the duration of activity using paw edema method, but the drug release rate is only 60% when the gel is applied and inflammation is induced using 0.1% carrageenan. We have treated 1 group with the same gel.
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If you are planning to use it for regeneration in bony defect you can try using it with B- TCP as curcumin extract (liquid form) gets absorbed in B- TCP granules, Susequenltly the graft can be delivered in a PMMA gel for delayed release. Slow exposure of the granules and subsequent release of curcumin following bio-absorption will prolong the availability of curcumin extract.
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Recently, I have observed in my clinical practice a re-swelling of infected canal after antiseptic dressing. Sometime the tooth become mobile and extruded. Please suggest the possible solution.
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Dear colleagues,
Based on the most current evidence-based literature published in peer-reviewed journals, canals should NOT be left "open to drain"! SC
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This is used to stimulate saliva secretion.
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Dear Naveena, you can try this: chewing paraffin wax (Ivoclar Vivadent AG, Schaan, Liechtenstein).
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Between fibroma, lipoma, hemangioma, and lymphangioma.
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My master Ruth Tramontani always said to us: "Watch from WHAT tissue the lesion came and it will be more simple to diagnose it." So, in oral cavity, we mostly have epitelium and conective tissue... following this line, most of the lesions in oral cavity arise from epitelium or conective tissue (wich includes dense conective tissue lesions, like Fibroma) According to Neville, Regezi, Boraks, and my clinical experience the most common is Fibroma. Thanks for asking, the most simple questions are the more Important!
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Is it safe to be ingested? And how can I get rid of the stain? Is Lawsonia inermis toxic and should not be used in vivo? And can I separate the stain from the component that cause therapeutic effects?
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Lawsonia inermis is used in vivo as dye or tattooing agent. though it is approved as hair dye by FDA, it's use as tattooing agent is contraindicated in america. yet, most of the countries in asia and africa use it for tattoing agent and consider it safer than artificial dyes. stain of Lawsonia inermis is because of Lawsone molecule which is released from leaves of Lawsonia inermis and is activated in acidic media hence lemon, tea leaves etc are used to increase it's efficacy. it's action is reduced in alkaline media hence any mild alkaline agent can be used to get rid of the stains. it is propagated to have many therapeutic action like anti-inflammatory, analgesic, and antipyretic effects and on application as hair dye, it is proposed to potentiate pentobarbitone-induced sleeping time. Lawsone can be extracted from Lawsonia inermis by liquid-liquid extraction procedure.
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I’m aware that a higher risk is observed in patients receiving bisphosphonates by IV (Gen Dent. 2010 Nov-Dec;58(6):484-92), but am curious to know specifically if recent studies have demonstrated a relationship between oral bisphosphonates, implants and osteonecrosis of the jaw. Is there a risk/relationship? And should implant patients taking oral BPs be informed of this possible additional risk?
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Guidelines for treatment of dental patients receiving intravenous bisphosphonate treatments should be different than for patients taking the oral formulations of these medications. In this study, oral bisphosphonate therapy did not appear to significantly affect implant success. Implant surgery on patients receiving bisphosphonate therapy did not result in bisphosphonate-associated osteonecrosis of the jaw. Nevertheless, sufficient evidence exists to suggest that all patients undergoing implant placement should be questioned about bisphosphonate therapy including the drug taken, the dosage, and length of treatment prior to surgery. For patients having a history of oral bisphosphonate treatment exceeding 3 years and those having concomitant treatment with prednisone, additional testing and alternate treatment options should be considered.
From:
J Oral Maxillofac Surg. 2008 Feb;66(2):223-30. doi: 10.1016/j.joms.2007.09.019.
Outcomes of placing dental implants in patients taking oral bisphosphonates: a review of 115 cases.
Grant BT, Amenedo C, Freeman K, Kraut RA.
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First solution is parental help but she wants to do it independently.
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Yes David, the brushes seem rather effective, maybe more than the floss. I am still working on making an opinion upon these instruments and the best ways they can be used (I am still a student...), but I wanted to acknowledge and thank you for your indication. I also attach a link with an article discussing effectiveness of brushes in orthodontic patients.
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What can make failure in heart disease treatment with a patient presenting tooth decay and periodontal disease?
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Sir i wanna research for any mining engineering topic and any guys suggest any intresting topic for me.
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Discussion is welcome keeping in mind the pros and cons of these mouthwashes. If we recommend it, do we monitor the patient compliance regarding its usage.
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Amit Sir, do you prescribe the alcohol-based m/w in your practice or verbally support the use of these by patients. Bcoz in both the cases the usage has to be discontinuous and periodic due to the ill effects of alcohol on the oral mucosa however minimal depending on the usage.
One more thing to notice here is that most of the patients use mouthwashes to mask the halitosis which may be due to local factors or systemic. One common local factor may be the use of tobacco or alcohol in their habits which gives added cytological stress to the oral mucosa.
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Treacher Collins syndrome (TCS), also known as Treacher Collins–Franceschetti syndrome, or mandibulofacial dysostosis is a rare autosomal dominant congenital disorder characterized by craniofacial deformities, such as absent cheekbones. Treacher Collins syndrome is found in about 1 in 50,000 births. The typical physical features include downward slanting eyes, micrognathia (a small lower jaw), conductive hearing loss, underdeveloped zygoma, drooping part of the lateral lower eyelids, and malformed or absent ears.
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Not at all, u r welcome.
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I am examining the differences in oral hygiene behaviours between compliant and non compliant periodontal patients.
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You may have a look at my article Koyio - Journal of Public Health Research
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It is related to some C-substance but still what does C stand for is not yet clear.
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Tatini Claudia's reference is correct but Fraction C was later identified as Capsular-polysaccharide. I attach an excerpt from my recent book that explains what C-polysaccharide is and its relevance to inflammation. The reference and URL of the book are: M. Levine, Periodontal disease: Section 13.3.1: Long-term Effects of Persistent PAMP Stimulation, In: Topics in Dental Biochemistry, Chapter 13. Published Online by Springer, 2011. See:http://www.springer.com/medicine/dentistry/book/978-3-540-88115-5)
EXCERPT: Activated leukocytes induce the synthesis and secretion from the liver of an unrelated set of proteins called acute-phase proteins. One such protein, C-reactive protein (CRP) was originally identified as binding to the phosphocholine attachment site of capsular polysaccharide (C-polysaccharide) from Streptococcus pneumoniae. CRP in blood has a half life of less than a day, compared with 4 days for fibrinogen. A continuously elevated CRP content indicates a persistent proinflammatory stimulus in the body. CRP binds to host or bacterial phosphocholine, and the complex activates a group of plasma proteins called complement (Sect. 3.3.2). The complement system resembles the blood clotting system, except that proteolytic cleavage of its components results in peptide fragments that to attract and enhance the phagocytosis (opsonization) of CRP- or antibody-bound material by macrophages (like IL-1 or IL-8). CRP is part of the innate immune response, and the antibody response is part of the acquired immune response (Sect. 12.1.4). For further details see also J Immunol. 1984 Sep;133(3):1424-30. PMID: 6747291
NOTE: PAMPs in the Chapter sub-heading are “Pathogen-Associated Molecular Patterns” whose nature and role in activating inflammation is described in section 13.2.1 and section 13.2.2 of the book.
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What do you think the prognosis will be in case of endo ttt with custom made post & crown later (note the age of the patient)?
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Famous author like Zehnder M (Zehnder M. Root canal irrigants. J Endod 2006;32:389–98) suggested 1% NaOCl could be sufficient. However 0.5 % (Dakin) hos not enough solving ability on organic soft tissue even if the antibacterial properties are interesting. Having said that, i agree with claudia and 2.6 % seems to be the best compromise. Finally, even if the NaOCl concentration is a matter of debate and has a clinical relevance, this later should be chosen according to other factors (type of root canal preparation, volume of irrigant, temperature of irrigant, viscosity and surface tension, agitation technique...). Moreover, fresh hypochlorite is used continuously that likely decrease the impact of the concentration. You can find the publication i mentioned in the attachment file.
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Can anyone advise on how to prepare 0.01mm of rhodamine dye from the powder form of the dye? What method of preparation do you use? What is the water:powder ratio?
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Dear Adit Bharat Mehta,
don't know whether there you got an answer to your question or not.
This your question should have been presented in Topic STAINING rather than this one (Periodontics and Oral Pathology), I guess.
Just to be short here: the requested water:powder ratio will depend on the mol-weight of the dye you use.... so you should at least define here (to the forum) which dye you intend(ed>) to use ;-): There are several forms of the dye (and therefore also different Mol-weights = g/mol) e.g. Rhodamine B (MW 442, water solubility: 2%; 1,8% in ethanol), Rhodamine 6G (MW= g/mol 479.02, water solubility: 20 g/l (25 °C) ), Sigma-Rhodamine 123 (MW 380.82, water solubility: at least 0.1 % (25 °C)), NHS-Rhodamine (W: 528)…(sources: Techn. Data Sheets, MSDS, and partially also CONN’s Biol.Stains,10th Ed, Handbook of Dyes, Stains and Fluorochromes for Use in Biology & Medicine (Horobin RW & Kiernan JA,,Eds) BIOS Scientifuic Publishers,Oxford UK, 2002,ISBN 1 85996 099 5).
I assume you can calculate 0.01mM of Rhodamine in g/L for your purposes. In water there should be sufficient solubility. If you have problems with dissolution, try ultrasonic treatment or heat water to 50-60°C, stir thoroughly(at least 3-4 hrs). Best regards and good luck, Wolfgang MUSS, SALZBURG, AUSTRIA
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I'd like to know the experience of the researchers about the use, efficacy, safety and side effects of this therapy for large CGCG.
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Thanks for contributions. This article published by Pogrel is really very good and will help us, so thank you Dr Bharkava. When I was in my post-graduate I followed one case reported in this attached paper and the results using calcitonin spray was very good in a growing child and really costed much time like said Dr Varol. Now I´m treating an adult woman with a large CGCG intra-osseous.
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What is the role of the host in dental Caries development?
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More favourite and friendly the host there is likelihood of more vigorous and prolonged stay of the guest depleting all resources and assets of the host. Thus micro environment of the host contributes significantly in caries development.
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I've read several periodontal articles written in the '90s that mention pulpal and gingival periodontitis. Are these titles alternative terms for the pathological types referred to as periapical and planar (AC) periodontitis in more recent work? Thanks!
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There is a lot of newer work that has explored the bacterial etiology of periodontitis using open-ended molecular approaches. I think it is important to understand the 70% of oral bacteria are presently uncultivated, and therefore, the findings of these sequencing based publications are important. A PubMed search using keywords uncultivated, 16S, sequencing, periodontal will pull up several recent publications
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Please provide any related citations
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Thanks Noel Claffey and Sameer Zope
My proposed research design is as follows
A total of 60 subjects of both the genders, above the age of 18 years and fulfilling the inclusion and exclusion criteria will be selected.
Inclusion Criteria:
1. Healthy subjects aged between 18 – 50 years
2. Availability for the entire duration of the study
3. Should have a minimum of 20 sound natural teeth
4. A gingivitis score of more than 1 & periodontal score with 3 and 4
Exclusion Criteria:
1. Subjects having systemic diseases such as Diabetes, Sjogren’s syndrome, Recent Myocardial Infarction( less than 6 months), Terminal neuropathy, Liver Pathology, Blood Cancers
2. Pregnant and Lactating Mothers
3. Subjects who have undergone Radiotherapy, Antibiotic therapy
4. Subjects receiving Orthodontic treatment
5. Subjects with history of smoking
Subjects will be divided into three groups i.e., Healthy group, Gingivitis group and Periodontitis group based on the CPITN Index scoring.
Gingival status will be assessed using Gingival Index given by Loe and Silness (1963). Periodontal status will assessed by using Community Periodontal Index given by WHO.
Healthy group subjects will be selected based on the following criteria: gingival score less than 1 and gingival group with gingival scores more than 1 and periodontal group with periodontitis scores with 3 and 4.
All the subjects will be asked to continue their normal oral hygiene practices during the study period.
Subjects will be clinically examined for their Gingival and Periodontal status at baseline and 6 months later. Stimulated saliva sample will be collected to check the Salivary LDH isoenzyme levels by Electrophoresis on both occasions. Subjects will be then subjected to Clinical examination and Oral Prophylaxis and the Salivary LDH isoenzyme levels will be checked again month after the second sample collection.
Please comment on the design.
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Please share if you have a case/article for an odontogenic keratocyst converting to unicystic ameloblastoma.
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The nearest I could get to your request is our publication on Onontogenic Keratocystic tumor. Solid keratocystic odontocystic tumor – report of a non aggressive case.
Shuster A , Shlomi B , Reiser V , Kaplan I
J Oral Maxillofacial Surg. 2011 ( Accepted )
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A simple device to quantitatively measure the stresses induced during polymerization of composite resins.
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ok thanks, Leontine. will check the article.
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Studies for forensic identification
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Dear Ma'am,
As Anirudha has rightly pointed out, drug concentration is one important area. I am attaching a relevant article here. I will also try to email a few others soon. Could I have your email address, or you may send a blank email to me at ashithacharya@hotmail.com, and will attach the articles.
Best wishes,
Ashith Acharya
Head of Forensic Odontology
SDM Dental College
Dharwad
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That resist traditional treatment
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There is no such term (resistant oral ulcer). If the ulcer is not traumatic, then it could be due to more systemic cause or infection. Treatment of the cause would resolve the ulcer.
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Is anyone working on periodontal microbiology?
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Dear Aluru,
You can find answer of your question in two articles in Journal of Research in Dental Sciences www.jrds.ir Vol7,No3,Autumn 2010.P:3and vol7,No:2,Summer2010
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Gingival prosthesis is seen as an alternative to expensive perio surgery. How is it performed and Is it worth it to try? What are its indications?
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It is an alternative, but usually a rather poor one, and only used in extreme cases where regenerative procedures have bad predictibility (such us large ridge defects) or when the patient is not willing to have a surgery. Whatever the case, is a last resort (and not a very good one). I hope it helps,
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I am interested in a link between the two pathologies. Does anybody have any experience on this topic which they could share?
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A moderately strong correlation was first noticed between periodontitis and pancreatic cancer via a large population study in 2007. The increase in risk is about 1.6X, compared to an increased risk of 2X with a family history of pancreatic cancer, or 1.8X with a smoking habit. This connection (perio/pancreatic ca) may be because of an underlying, and unidentified, immune or hormone problem, or common dietary habit, but all we know so far is that there is a correlation. Sorry I couldn’t be more helpful. I’ve included below summary papers for perio/pancreas and family history/pancreatic ca comparisons, if you want more detail:
Bouquot comment: Periodontitis and pancreatic cancer review, conclusion: persons with periodontitis have a 1.6X increased pancreatic cancer risk.
Michaud DS, Liu Y, Meyer M, Giovannucci E, Joshipura K.
Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study. Lancet Oncol. 2008 Jun;9(6):550-8.
Dr. Michaud works at Department of Epidemiology and Public Health, Imperial College London, London, UK. d.michaud@imperial.ac.uk
Abstract
BACKGROUND: Studies suggest that tooth loss and periodontal disease might increase the risk of developing various cancers; however, smoking might have confounded the reported associations. We aimed to assess whether periodontal disease or tooth loss is associated with cancer risk.
METHODS: The analysis was done in a prospective study (the Health Professionals Follow-Up Study [HPFS]), which was initiated in 1986 when US male health professionals aged 40-75 years responded to questionnaires posted by the Department of Nutrition, Harvard University School of Public Health, Boston, MA, USA. In addition to the baseline questionnaires, follow-up questionnaires were posted to all living participants every 2 years and dietary questionnaires every 4 years. At baseline, participants were asked whether they had a history of periodontal disease with bone loss. Participants also reported number of natural teeth at baseline and any tooth loss during the previous 2 years was reported on the follow-up questionnaires. Smoking status and history of smoking were obtained at baseline and in all subsequent questionnaires. Additionally at baseline, participants reported their mean frequency of food intake over the previous year on a 131-item semiquantitative food-frequency questionnaire. Participants reported any new cancer diagnosis on the follow-up questionnaires. Endpoints for this study were risk of total cancer and individual cancers with more than 100 cases. Multivariate hazard ratios (HRs) and 95% CIs were calculated by use of Cox proportional hazard models according to periodontal disease status and number of teeth at baseline.
FINDINGS: In the main analyses, 48 375 men with median follow-up of 17.7 years (1986 to Jan 31, 2004) were eligible after excluding participants diagnosed with cancer before 1986 (other than non-melanoma skin cancer, n=2076) and those with missing data on periodontal disease (n=1078). 5720 incident cancer cases were documented (excluding non-melanoma skin cancer and non-aggressive prostate cancer). The five most common cancers were colorectal (n=1043), melanoma of the skin (n=698), lung (n=678), bladder (n=543), and advanced prostate (n=541). After adjusting for known risk factors, including detailed smoking history and dietary factors, participants with a history of periodontal disease had an increased risk of total cancer (HR 1.14 [95% CI 1.07-1.22]) compared with those with no history of periodontal disease. By cancer site, significant associations for those with a history of periodontal disease were noted for lung (1.36 [1.15-1.60]), kidney (1.49 [1.12-1.97]), pancreas (1.54 [1.16-2.04]; findings previously published), and haematological cancers (1.30 [1.11-1.53]). Fewer teeth at baseline (0-16) was associated with an increase in risk of lung cancer (1.70 [1.37-2.11]) for those with 0-16 teeth versus those with 25-32 teeth. In never-smokers, periodontal disease was associated with significant increases in total (1.21 [1.06-1.39]) and haematological cancers (1.35 [1.01-1.81]). By contrast, no association was noted for lung cancer (0.96 [0.46-1.98]).
INTERPRETATION:
Periodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.
Bouquot comment: Pancreatic cancer and family history, conclusion: there seems to be a 2X increased risk of pancreatic cancer if there is a family history of pancreatic cancer.
Permuth-Wey J, Egan KM. Family history is a significant risk factor for pancreatic cancer: results from a systematic review and meta-analysis. Department of Cancer Epidemiology and Genetics, Fam Cancer. 2009;8(2):109-17.
Dr. Wey works at H Lee Moffitt Cancer Center and Research Institute, (MRC CAN-CONT), Tampa, FL 33612, USA. jenny.wey@moffitt.org
Abstract
Epidemiologic evidence suggests a family history of pancreatic cancer (PC) is a risk factor for the disease, yet the magnitude of risk varies between studies. We performed a systematic review of studies that quantified familial risks of PC, and through a meta-analysis, obtained more precise estimates of familial risk. A MEDLINE search identified published studies that reported relative risks (RR) of PC associated with a family history of the disease. A random effects model was used to summarize study-specific RRs and 95% confidence intervals (CI). Sensitivity and sub-group analyzes were performed. Seven case-control and two cohort studies involving 6,568 PC cases were identified. There was no evidence of statistical heterogeneity between studies (I(2) = 0%; P = 0.483). Results from case-control (RR = 2.82; 95% CI: 1.99-3.66) and cohort (RR = 1.62; 95% CI: 1.28-1.97) studies showed a significant increase in PC risk associated with having an affected relative, with an overall summary RR = 1.80 (95% CI: 1.48-2.12). Similar RR were observed for early (RR = 2.69; 95% CI: 0.56-4.82) and later (RR = 3.41; 95% CI: 0.79-6.03) onset disease in the index case. Data was too sparse to generate an overall summary RR based on the number or type of affected relatives. Individuals with a family history of PC have nearly a two-fold increased risk for developing PC compared to those without such a history. Families with two or more PC cases may benefit from comprehensive risk assessment that involves collection of detailed family history information and data regarding various risk factors for PC, especially smoking history. Those at highest risk may be referred to screening programs and studies; these are important steps toward early detection and greater odds of surviving this disease.
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I need to conduct mutagenicity tests in exfoliated buccal mucosa cells, except MN, and would like some procedural advice.
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oi Pam... vc já viu trabalhos que utilizam o teste cometa? aki no lab que estou o pessoal estuda mutagenecidade e faz muito o teste de MN e esse teste cometa. Se precisar de algo mais específico, posso ver com o pessoal aki. Bjinhos...
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Anyone interested in periodontal epidemiology and with experience in observational methods. would like to share my work.
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Hi sir i m intrested in priodontal epidemology