We were delighted when Marc Quirynen of the Catholic University in Leuven kindly let us share with you his very informative patient information leaflet on halitosis. It was in Dutch so we have translated it for you. Any mistakes in the adaptation are entirely ours….
Taking your last (bad) breath
February 13th, 2012Does flossing work?
July 21st, 2011The evidence shows (within the limits of systematic reviews) that:
1. Flossing by patients has no effect on plaque index or gingival index. Author conclusions were that there is a lack of evidence to support “routine recommendation of the use of dental floss” and that “the dental professional should determine on an individual basis whether high quality flossing is an achievable goal”.
2. Woodsticks have no effect on plaque or gingival index, only a beneficial effect on bleeding scores.
3. Interdental brushes remove more plaque than flossing does. Studies showed a positive significant difference using IDB with respect to the plaque scores, bleeding scores and probing pocket depth.
4. Oral irrigators may have some benefits in reducing inflammation (better than floss).
But what about interproximal caries? Philippe Hujoel reviewed the literature and found a limited number of studies with significant study to study differences and a moderate to large potential for bias. Read the abstract here .
Links to the systematic reviews are shown below….
Perio disease: It’s not your problem
July 14th, 2011Three-monthly hygiene appointments may help but they are not the answer. Don’t let your perio patient think they are. Patients who are susceptible to perio disease have to understand that the disease is theirs to deal with for the long term, not yours to fix on a 3 monthly basis.
As a starting point, they need to work with you to reduce the factors that put them at risk. From their perspective this might be immaculate OH, stopping smoking or improving diabetic control, and ultimately adherence to your recommendations. From yours it may be replacing faulty restorations which trap plaque or inhibit cleaning, non-surgical perio therapy or indeed 3 monthly hygiene appointments.
But at the end of the day, providing you are sure that your patient understands their personal risk and disease status, what they should do about it, and the potential consequences of inaction, if they choose not to follow your advice it is not your problem. There is a great article by Dental Protection on the subject here.
Periodontal disease nevertheless remains the fastest growing area of dental litigation. Make sure your patients have been told, and ensure they DO understand. http://previser.co.uk
Periodontology is changing
June 3rd, 2011Our understanding of the cause of periodontal disease has changed dramatically over recent years. From a starting point of perio as an infectious disease to our current understanding of the role of inflammation and the host response, this chart adapted from Philip Preshaw’s presentation at the BSP summarises just how fast our knowledge is changing. The next step is how we respond to the new challenges this knowledge presents. It is no longer enough to simply focus on the plaque.
| 1963 | Periodontal diseases are infectious diseases (Loe: exp ging) |
| 1965 | Non-specific plaque hypothesis (calculus as an irritant) |
| 1979 | Specific plaque hypothesis (Loesche) |
| 1985 | Concept of susceptible host (Socransky: specific bacteria are necessary, but not sufficient to cause disease) |
| 1991 | Environmental plaque hypothesis (Marsh: subgingival microbial environment is key) |
| 1995 | Inter-individual variations (Haffajee) |
| 1997 | Importance of host response (Page: tissue damage is due to host response) |
| 2000 | Inflammation determines composition of microflora (Serhan) |
| 2008 | Periodontitis is an inflammatory disease (AAP workshop) |
| 2010: AAP – Yesterday, scientists believed that periodontal disease resulted from the actions of bacteria in plaque. Today, scientists have determined that periodontal disease results from the inflammatory response to bacteria in plaque. |
| 2011: EFP - Current preventive and treatment approaches are only partially effective and this appears due to the therapeutic focus remaining primarily on biofilm management rather than embracing a role for inflammation as a driver of biofilm composition as well as tissue damage. |
PreViser starts by identifying the risk of the host. Go to www.previser.co.uk for more information.
Perio disease: modification of the biofilm and the host response
May 18th, 2011The Seventh European Workshop on Perio took place in 2010 gathering together 78 experts in Periodontology and implant dentistry from across Europe to reach consensus statements on the biology of periodontal and periimplant diseases.
The Results and Discussion of the consensus on Biological approaches to the development of novel periodontal therapies published in the Journal of Clinical Periodontology, was as follows:
“Current preventive and treatment approaches are only partially effective and this appears due to the therapeutic focus remaining primarily upon biofilm management rather than embracing a pivotal role for inflammation as a driver of biofilm composition as well as tissue damage. There is a need to develop new, more effective and efficient preventive treatment approaches for gingivitis and periodontitis which embrace recent advances in the understanding of host modulation as well as direct management of the microbiota”
Possible approaches for controlling inflammation were discussed in terms of modification of the biofilm and modification of the host response. The following categories were examined:
- Antimicrobial peptides
- Probiotics
- Pro-resolving lipid mediators
- Nutritional modulation
To VERY briefly summarise:
Antimicrobial peptides: Several AMPs are present in saliva and GCF. The major sources are in gingival epithelia, neutrophils and salivary glands. Evidence is emerging that deficiencies in AMPs could play a role in periodontal disease. AMPS could have potential for the prevention and treatment of periodontal disease in their antibacterial, anti-inflammatory and/or immune modulatory actions. Approaches that stimulate or restore the natural expression patterns of AMPS might be the most successful.
Probiotics: So far there is only limited data from pilot studies, but these suggest that probiotics have the potential, at least in the short term, to modify the oral microbiota either directly or through the host’s immunological response. Clinical benefits have not yet been demonstrated. It is currently unclear whether it is the antimicrobial or anti-inflammatory effects of such agents which might be important.
Pro-resolving lipid mediators: In the past it was thought that aggressive periodontitis was due to deficiencies or defects in the innate immune response. It is now recognised that it stems from the chronic priming of inflammatory cells which result in increased release of tissue destructive enzymes and reactive oxygen species. It is doubtful that an inflammation-modulating agent will ever completely replace some form of mechanical control of the biofilm, but they may provide an interesting preventive approach against the acquisition or overgrowth of pathogenic bacteria. Pro-resolution lipid mediators are early in development and not yet available for human use. It is possible that dietary micronutrient sources of such mediators (eg omega-3 PUFAs) could be a viable alternative.
Nutritional modulation: There is evidence that diet causes inflammation: directly through post prandial oxidative stress and indirectly through visceral fat accumulation. Conversely restriction of caloric intake reduces clinical and biological measures of inflammation. Increased central adiposity is associated with increased periodontitis prevalence. Association studies have demonstrated an inverse relationship between periodontitis prevalence and intake of fibre, antioxidant micronutrients and PUFAs, and plasma levels of Vitamins D and C, magnesium and combined small molecule antioxidants. At present there is some evidence that suggests that perio outcomes may be improved by Vitamin D supplements in deficient patients and by using phytonutritional interventions. Further studies are however needed. Evidence is emerging that a diet high in fibre, fish oils, fruits vegetables and berries and reduction in intake of refined sugars is of benefit to periodontal as well as overall health.
Periodontal disease susceptibility is more about the host than the biofilm. To find out how you identify your patients’ susceptibility and monitor and manage their outcomes, take a look at our risk assessment tool at www.previser.co.uk
Periodontitis: a chronic inflammatory disease
March 28th, 2011Periodontal disease is a chronic inflammatory disease. What does this mean?
Inflammation is your body’s response to cell injury, protecting it from certain stressors and promoting repair. Some cell injuries are caused by infection or invading organisms such as bacteria, while other cell injuries can be attributed to trauma without invasion of microorganisms: for example, hitting your thumb with a hammer can cause cell injury. Inflammation, your body’s reaction to the cell injury, causes the swelling, redness, tenderness and heat to occur.
The human body can’t sustain itself for long without a defence and repair response. When cells are damaged, they release chemical signals that summon the body’s immune system to send help to the infected site. Potent biochemical signals trigger blood vessels to enlarge and become more porous. The enlarged blood vessels leak fluid into the tissue surrounding the infection or damage. This process enables the white blood cells (defence cells) to set up a perimeter defence against bacterial invasion and clean up damaged cells.
In the past it was thought that acute inflammation simply faded passively over time. What is now known is that the active processes (“switches”), triggered by the chemicals causing the inflammation, resolve it. If the resolution “switch” in the body is defective, then the inflammation becomes chronic, low-grade and unresolved. In chronic inflammation situations, the damaged cells continue to send signals downstream where they trigger inflammatory events in remote areas away from the site of the injury/infection.
Periodontal disease is one such remote trigger point which adds to the inflammatory burden of the body and is thought to contribute to the development of other chronic inflammatory diseases such as cardiovascular disease, stroke, diabetes, certain cancers and rheumatoid arthritis.
Periodontitis and Cardiovascular Disease: implications for dental professionals
March 22nd, 2011Over the past two decades, research has shown a linkage between cardiovascular disease and periodontal disease (gum disease).
Inflammation, the human body’s repair and defence mechanism against cellular injury or bacterial invasion, seems to be the common thread between the two diseases. In patients who have a high susceptibility to gum disease, their immune response fails to “resolve” the gum inflammation, which then becomes chronic in nature. The defending white blood cells produce small quantities of potent bio-active chemicals that flow away from the local site of the infection (the mouth) increasing inflammation throughout the body. This residual inflammation is believed to contribute to various side effects at remote sites from the mouth, including changes in the blood vessels that can lead to atherosclerosis and fatty arterial build up increasing a person’s risk for heart attack and/or stroke.
Although researchers have not yet identified a precise cause and effect relationship between periodontal disease and cardiovascular disease, the association between the two diseases is too strong to be ignored. Cardiologists and Periodontists have joined forces to produce a consensus paper summarizing the scientific evidence that links periodontal disease and cardiovascular disease.
The consensus paper recommends that periodontists not only inform their patients of the increased risk of cardiovascular disease associated with periodontal disease, but also assess their risk for future cardiovascular disease and guide them to be evaluated for the major risk factors. The paper also recommends that physicians managing patients with cardiovascular disease evaluate the mouth for the basic signs of periodontal disease such as significant tooth loss, visual signs of oral inflammation, and receding gums. Read a summary here: Healthy Gums and a Healthy Heart: The Perio-Cardio Connection
PreViser’s myDentalScore is the starting point to inform your patients about their oral risk and disease status and to encourage them to come and talk to you. Our Oral Health Library, which comes as part of your personalised myDentalScore, helps to educate them about the broader implications of their oral health. This will be added to over time and updated as the evidence evolves. Find out more and subscribe on-line at www.previser.co.uk/products/mydentalscore.html
Dentinal Tubules #tubulitebadge
March 18th, 2011Check out www.dentinaltubules.com, Dhru’s amazing dental website. Everything he does….
Do dentists agree with each other?
January 18th, 2011How good would you say dentists are at assessing a patient’s risk of periodontal disease? If you were to give a group of 50 dentists the same records from 100 patients and ask them to assign each patient into a risk group from 1-5, would they be broadly of one mind? This research has been done, and the findings compared to PreViser (which has been scientifically demonstrated to provide an accurate assessment of risk). The results are shown on the graph below. The y axis shows the proportion of patients assigned to each category.
Click on the image to enlarge it.
The results showed a very wide range of variability between the clinicians in each of the evaluator groups. Conclusion: “the assessment of risk by subjective judgement appears too variable and inaccurate to be useful in clinical decision making.” Persson et al., Assessing Periodontal Risk, J Am Dent Assoc 2003.
Clearly, where risk underpins your preventive periodontal treatment plan, then this under or over assessment is likely to translate into under or over treatment.
Find out more about the simple solution for consistently and objectively assessing periodontal risk www.previser.co.uk
