Pancreatic Cancer and Periodontal Disease

Pancreatic Cancer linked to Gum Disease?

Scientists have recently discovered what appears to be a definitive link between pancreatic cancer and periodontal (gum) disease. Pancreatic cancer is the fourth leading cause of cancer deaths in the U.S. because it is so difficult to treat. More than 300,000 Americans are expected to die from it this year.

The study found that men with periodontal disease have a 63% greater risk of developing deadly pancreatic cancer. The research studied 51,000 professional non-smoking males from 1986 to 2002. It may be that the chronic inflammation from periodontal disease is setting off an inflammatory response which is detrimental to overall health, or that the bacteria associated with periodontal diseases are the culprit. More research is needed to determine the actual action periodontal disease has in creating a higher risk of cancer.

At PerioPeak Innovations we are committed to addressing chronic periodontal disease and the inflammation associated with it proactively and definitively.  By using a synergistic approach, involving advanced miniature fiberoptic technology and host modulated therapy, the periodontal inflammation can very effectively be put into a remissive state for the long term…lowering the overall health risks associated with all stages of periodontitis, or gum disease.

Below are recent articles about the link between periodontal disease and pancreatic cancer:

http://abcnews.go.com/GMA/OnCall/story?id=2813658&CMP=OTC-RSSFeeds0312

http://www.medicalnewstoday.com/medicalnews.php?newsid=60977&nfid=rssfeeds

http://www.healthcentral.com/newsdetail/408/601047.html

How does Perioscopy Work?

How does Perioscopy, or periodontal endoscopy, technology work?

Periodontal endoscope technology, or Perioscopy, is an important part of the PerioPeak protocol, RPE℠ – Regenerative Periodontal Endoscopy℠.  It is a crucial component to achieving excellent overall results for many reasons.  Periodontal endoscopy is a non-invasive way to view and clean root surfaces microscopically in all depths of pockets, without performing surgery, using micro-ultrasonic technology simultaneously.

Important: We prefer the term “periodontal endoscopy” rather than the commercial trademark term “perioscopy”, which over the years has become a term associated with “removing calculus only”.  We view this narrowly focused use of the periodontal endsocope as antiquated use of the technology.

The dental endoscope, or periodontal endoscope, is a fiber optic is less than 1mm in diameter, it incorporates powerful illumination with 48X magnification.  It is essentially employing the use of a miniature microscope under the gums. The image is viewed live on a high resolution flat panel color monitor. It takes a great deal of  experience to perform periodontal endoscopy procedures (diagnosis and periodontal treatment) with proficiency.  PerioPeak Innovations has provided this treatment successfully for over a decade on hundreds of clients with advanced periodontal disease.

Below are four still endoscopic pictures viewing the area between the root and gums (deep gum pocket) during a periodontal endsocopy procedure.  Click on images to enlarge

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SCI 3:  Subgingival Calculus Index 3 is calculus that extends beyond the plane of the root, it can be felt and possibly seen in x-rays (radiographic calculus).

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SCI 2:  Subgingival Calculus Index 2 is calculus which cannot be felt with instruments (explorers) beneath the gum line…also known as burnished calculus (tartar).  This tartar left behind following traditional root planing because it is very smooth and can fill in the tooth depressions, furcations, and flutings in the roots.

Burnished tartar is typically left on the roots following traditional root planing. Burnished calculus cannot be seen or felt with traditional techniques beyond a depth of 4mm.   30-50% of the root may have residual calculus; infection and inflammation may persist.

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SCI 1:  Subgingival Calculus Index 1 is microscopic calculus which cannot be seen or felt, even with direct vision, as in surgery.  Commonly referred to as “glitter”, SCI 1 is found in all depths of pockets and even on exposed recessed root surfaces – inflammation may persist.

The presence of microscopic calculus can be identified and removed by experienced individuals using a periodontal endoscope. Surgical microscopes and loupes (magnified glasses) do not reveal this truth because they do not incorporate 48X magnification with tremendous illumination.  In addition, a surgical microscope cannot be placed beneath the gums.

Note: Only a scanning electron microscope on extracted teeth will reveal this detail.

click on image to enlarge

SCIO:  Sub-gingival Calculus Index Zero is what we refer to as “microscopically clean”.

The limitations of current traditional techniques, such as root planing, was unknown until the innovation of the periodontal endoscope. Using lasers beneath the gum blindly, root planing tactilely in deep pockets, or performing periodontal surgery without an endoscope, may allow toxic calculus to remain embedded in the roots, hence, periodontal inflammation and infection may continue.

Endoscope Assisted Bone Regeneration with Emdogain

Regenerative Periodontal Endoscopy℠  (RPE℠) – Periodontal endoscopy and Emdogain

Non-surgical periodontal bone fill is finally possible thanks to a new biological technology called Emdogain, by Straumann. But what is Emdogain and how does it work? The following post will help clarify what Emdogain is and also help the reader to understand the tremendous benefits of endoscope assisted regeneration using this natural protein.

IMPORTANT: Emdogain is used non surgically at PerioPeak Innovations with an innovative technique and protocol utilizing a periodontal endoscope, soft tissue laser,  micro-piezo ultrasonics, and enzyme inhibitors. Emdogain is typically used only during some type of flap periodontal surgery procedure.  However, a recent study demonstrates histological bone regeneration with Emdogain used in a non surgical periodontal therapy approach.

So what exactly is Emdogain?

Emdogain contains Enamel Matrix Protiens, or Bioactive Molecules, called amelogenin proteins, which are harvested from the developing teeth of pigs.  What are enamel matrix proteins and how do they help humans to regenerate periodontal tissues and bone? The answer is in the unique biology of tooth development. When teeth are still developing, we can extract these “bioactive molecules” and use them in humans for the stimulation of adult stem cells to promote regeneration in periodontal defects created by chronic or acute infections of the gums.  The body responds by growing new cementum, ligament, and bone (osteogenesis) in areas where periodontal disease has damaged these important supporting structures. The damage of periodontal disease can be repaired and reversed with Emdogain.

Read easy to understand information about Emdogain

The Mechanism of Emdogain:

Attachment – the mesenchymal cells attach to the root surface covered by Emdogain.

Proliferation and Growth -the cells start to produce cementum. Cementum is the key tissue in periodontal regeneration. The recreation of alveolar bone starts from the root cementum.

Alveolar Bone – the process of mineralization starts a certain distance from the root and alveolar bone (periodontal bone around the teeth) is formed.

Note:  Efficient piezo microscopic root debridement (proper root preparation) and laser soft tissue curettage are guided by the use of a periodontal endoscope with 48X magnification.    

View non-surgical bone restoration cases using endoscope assisted RPE℠ techniques instead of surgery.

The DV2 Dental Endoscope with 48X Magnification is used to definitively access and clean all root surfaces prior to the placement of Emdogain with this non surgical technique.

Summary of the Clinical Benefits of Emdogain:

Case Report

Clinical and Histologic Evaluation of Non-Surgical
Periodontal Therapy With Enamel Matrix
Derivative: A Report of Four Cases

James T. Mellonig,* Pilar Valderrama,* Holly J. Gregory,* and David L. Cochran*  (read entire paper)

EMD stimulates fibroblast proliferation, the growth of periodontal ligament (PDL) cells, osteogenesis, and the proliferation and differentiation of osteoblasts;  it also prolongs osteoblast growth and enhances trabecular bone regeneration, promotes osteoprotegerin production, and enhances osteopontin expression and transforming growth factor-beta1 production. EMD stimulates bone sialoprotein, signal transduction of bone morphogenetic protein, release of vascular endothelial growth factor, and angiogenesis. EMD also has anti-inflammatory properties. It limits the release of proinflammatory cytokines, modulates tumor necrosis factor-alpha and prostaglandin, and inhibits caspase activation. EMD has a negative effect on the growth of periodontal pathogens and might be useful as an antiadhesive agent for breast cancer cells.

The history of Emdogain:

– 1988 Biora founded by Professor Lars Hammerstrom, Stockholm Sweden.

– 1995 CE Certification

– 1996 FDA approval- 1997 introduction into the US market.

– Since 1989 produced in Malmo Sweden

– 2004 completion of integration by Straumann.

There are numerous studies involving the safety, efficacy, and statistical clinical significance with Emdogain.  Over one million people have been treated successfully with Emdogain.  Go to www.straumann.com for more information.

 

 

Genetic risk factor’s for Periodontal Disease

Could my periodontal disease be genetic?

One third of the population have a genetic tendency to develop periodontal disease.  One half of these individuals will develop the advanced stages of periodontal disease. Many people are born with a “sensitivity” to plaque bacteria – making their periodontal disease much worse due to a “hyper-inflammatory immune response”.  One could describe it as an “allergy” or even an “auto-immune response”.  The body goes into a very destructive chronic inflammatory response. For these individuals the presence of plaque bacteria (biofilm) causes inflammation on contact, triggering the immune system to go into hyper-drive, leading to periodontal destruction.  This hyper-inflammatory immune response creates an over-production of harmful enzymes, allowing chronic periodontal bone loss and tissue destruction to ensue.  It’s important to also realize that this genetic mutation will actually create periodontal destruction, even in the absence of, or in the presence of minimal amounts of periodontal pathogens. 

 

How can I find out if my periodontal disease is genetic (genetic polymorphism)?

A simple genetic test called a PST or Perio ID can be performed to determine genetic susceptibility.

Salivary DNA testing identifies patients genetically predisposed to severe periodontal disease. Early detection of patients at increased risk facilitates prevention/early intervention efforts. For those patients already affected with periodontal disease, the Oral DNA Perio ID test assists a clinician in creating a personalized treatment plan. The information gained from this test can be useful for all dental and medical professionals and their patients, leading to more targeted therapy.

The Oral DNA Perio ID test detects specific variations in the IL 6 gene. The presence of this variation (mutation or polymorphism) increases the risk for periodontal disease 3 to 7-fold and for tooth loss 3-fold. The combination of an IL 6 positive test result and smoking or other risk factors such as hyperglycemia or deficiencies leads to an even greater likelihood for severe periodontal disease and early tooth loss.

What it means to be IL6 positive (genotype G/G – high risk):

Significance: The prevalence of the G/G genotype is reported to be higher in individuals with
moderate to severe chronic periodontitis and aggressive periodontitis than in individuals with no periodontal disease. This finding was independent of other risk factors such as age, smoking,
ethnic origin. The G allele is associated with overproduction of interleukin-6 (IL-6) cytokine in the
presence of pathogenic periodontal bacteria.
Risk: Individuals carrying an IL6 G allele are associated with increased odds of the concomitant
detection of A. actinomycetemcomitans, P. gingivalis and T. forsynthensis.
Consider: IL-6 is a potent stimulator of osteoclast differentiation and bone resorption, is an
inhibitor of bone formation, and overproduction has been implicated in systemic diseases such
as juvenile chronic arthritis, rheumatoid arthritis, osteoporosis, Paget’s disease and Sjogren’s
syndrome. The MyPerioID test assesses one of several risk factors that should be included in an
overall evaluation of periodontal disease. Specific bacteria are associated with the initiation of
the periodontal disease. Additional risk factors including other genetic markers, smoking,
diabetes, and oral hygiene have an amplifying effect on disease progression and duration. The
incidence of IL6 genotypes is reported to vary by ethnicity.

 

Patients with positive PST results overproduce the 2 active forms of interleukin 1, IL-1α and IL-1β.  What does this mean?

According to Carranza in the 9th Edition of Clinical Periodontology, IL-1 is one of the pro-inflammatory cytokines that has a central role in tissue destruction.

IL-1 is typically produced by PMN’s (polymorphic neutrophils) in response to a bacterial challenge (periodontal pathogens).  However, in the absence of periodontal pathogens, the genetic situation of the patient causes the IL-1 production.  To make matters worse, IL-1 up-regulates its own production, resulting in even more production of the cytokine.

IL-1 stimulates endothelial cells to produce chemical mediators that recruit macrophages to the site.  The macrophages are then induced to produce prostaglandin E2 (PGE2), which causes periodontal bone loss.  IL-1 is also a potent stimulant of osteoclast proliferation, differentiation and activation.  As well as inducing periodontal bone loss, IL-1 also induces production of proteinases in mesenchymal cells, including MMP’s, which may contribute to connective tissue destruction.  Matrix metalloproteinases (MMP’s) degrade extracellular matrix molecules, such as collagen, gelatin, and elastin.

The bottom line here is that people with the genetic profile are predisposed to exhibit periodontal bone and tissue loss, even in the presence of few periodontal pathogens (regardless of virulence) and even if they have good home care.  Host response is a major risk factor for chronic inflammation and continued periodontal breakdown.

Go to www.oraldnalabs.com for more information on genetic testing, as well as the DNA pathogen testing we provide.

For more information on genetics and periodontal disease go to these sites:

www.perio.org
www.dentistry.com
www.umm.edu

What is the outlook for genetically inclined individuals?  

The good news is that advanced technologies (such as anti-inflammatory medications, periodontal endoscope treatment, and comprehensive integrative care) will now allow us to alter the predictably poor outcome of genetic periodontal disease.  These individuals are typically blamed for having poor home care, which is not always true.  Strong risk factors such as genetics must be addressed more definitively to effectively put periodontal disease into remission. No longer will only cutting the pockets out with gum surgery, or only doing blind or visual root planing, be the entire solution for these individuals.  A synergistic approach must be incorporated involving addressing the hyper-inflammatory response.  Utilizing a multifaceted approach is absolutely necessary for the successful long term management of the periodontal disease in these individuals.

Is genetic periodontal disease like an auto-immune disease?  YES

Individuals with a genetic predisposition must be identified before anything we do clinically will be successful long term. This type of disease is characterized by the over-production of destructive enzymes which causes severe destruction of the bone and gums supporting the teeth. The chronic and subtle nature of this type of disease can fool even the most astute clinician. Damage can occur quickly or slowly, therefore, preventative and more definitive care becomes crucial.  These individuals must be treated as if they have an auto-immune disease.

For more information about our non invasive periodontal protocol go to How RPE℠ works

Host Modulated Therapy

Host Modulated Therapy – Adjuntive use of Periosat (SDD)

Sub-antimicrobial dose doxycycline 20mg (SDD), also called PerioStat, is an effective way to therapeutically control, or “down-regulate”, exaggerated levels of harmful enzymes associated with chronic periodontal disease destruction (bone loss around the teeth).  This post will help clarify the adjunctive benefit of  Periostat (SDD – sub-antimicrobial dose doxycycline) as an important part of  the PerioPeak Innovations protocol called RPE℠, or Regenerative Periodontal Endoscopy℠.

Periodontal research has revealed that the body’s exaggerated and chronic inflammatory response is what causes periodontal destruction in many individuals.  While inflammation is a normal and healthy immune response, we now know that chronic inflammation can be very harmful and destructive – especially the chronic inflammation associated with periodontal disease. Periodontal research published on PerioStat demonstrates that it is an effective adjunct to periodontal therapy – reducing chronic inflammation, periodontal pockets, and arresting or slowing bone loss.  Periodontal inflammation can be well controlled with Periostat used adjunctively with professional care (periodontal therapy).  Meanwhile, all risk factors (host factors) contributing to the chronic inflammation can be revealed and defintively addressed (we recommend comprehensive medical labs and molecular testing on all of our clients to determine underlying cause beyond plaque and calculus).

Why is Periostat (host modulated therapy) such an integral part of the Regenerative Periodontal Endoscopy℠ protocol?

Down regulating chronic inflammation with host modulation (Periostat – SDD), starting one – two weeks before performing a microscope procedure called Regenerative Periodontal Endoscopy℠, reduces bleeding and inflammation significantly, allowing clear vision into all deep periodontal pockets with a periodontal endoscope – allowing for more definitive treatment overall.  Down-regulating the chronic inflammation immune response with host modulation prior to treatment  also firms all gum tissues, promoting more rapid healing (reattachment of gum pockets) following RPE℠.  But most importantly, Periostat reduces the levels of bone destroying (osteoclasts), while activating the bodies bone building cells (osteoblasts).

Host factors contributing to chronic periodontal inflammation may include presence of pathogenic bacteria, genetic predisposition (exaggerated host response), smoking, diabetes and prediabetes(elevated glucose levels), obesity, AIDS or other immune diseases,  neglect, inadequate professional cleanings, depression, certain medications, depleted or excess hormones including thyroid, poor diet, vitamin deficiencies (especially D), anemia, dry mouth (xerostomea), alcoholism, medications for high blood pressure (calcium channel blockers), and stress.

More about risk factors in periodontal disease:  www.umm.edu

Sub-antimicrobial dose doxycycline (Periostat) 20mg tablet, taken up to twice daily, slows the progression of periodontal disease by suppressing or down-regulating the “over-production” of a destructive enzyme called collagenase.   At only 20mg, this low dose of doxycycline puts the body back into balance by reducing inflammation and allowing periodontal health to be restored when combined with active periodontal therapy (professional care).  If  used with periodontal endoscopy and emdogain, Periostat can actually enhance and promote reattachment and regeneration – Regenerative Periodontal Endoscopy℠ -RPE℠.    

Important note about SDD (Periostat):  At this very low dose, 20mg doxycycline is sub-clinical (sub-antimicrobial dose), meaning it has no effect on the bacteria whatsoever. The therapeutic benefit of this medication has nothing to do with killing bacteria anywhere in the body.  In addition, research demonstrates that there has been no evidence of antibacterial resistance using SDD (Periostat), even long term (12 months).

Suggested important reading on SDD:  “Host reponse modulation in Periodontics” – by Philip Preshaw, DDS, MS, Periodontology 2000, Volume 48, 2008, 92-110.

-exerpts from the above paper below –

 Certain individuals appear to be more susceptible to periodontal disease, and this increased susceptibility is largely determined by the immune-inflammatory response that develops in the periodontal tissues following chronic exposure to bacterial plaque. Periodontal pathogenesis has been extensively reviewed by a number of authors (52, 54, 73) and it is not the purpose of this paper to cover this ground again. Suffice to say, the microbial challenge presented by subgingival plaque results in an upregulated host immune-inflammatory response in the periodontal tissues that is characterized by the excessive production of inflammatory cytokines (e.g. interleukins, tumor necrosis factor- (e.g. prostaglandin E matrix metalloproteinases (MMPs)]. These proinflammatory mediators are responsible for the majority of periodontal breakdown that occurs, leading to the clinical signs and symptoms of disease.

 Effects of low dose doxycycline (SDD)

• Direct inhibition of active MMPs by cation chelation (dependent on Ca2+- and Zn2+-binding properties)

• Inhibits oxidative activation of latent MMPs (independent of cation-binding properties)

• Downregulates expression of key inflammatory cytokines (interleukin-1, interleukin-6 and tumor

necrosis factor-a) and prostaglandin E2

• Scavenges and inhibits production of reactive oxygen species produced by neutrophils

• Inhibits MMPs and reactive oxygen species thereby protecting a1-proteinase inhibitor, and thus

indirectly reducing tissue proteinase activity 

 • Stimulates fibroblast collagen production (stimulates regeneration of collagen)

• Reduces osteoclast activity and bone resorption

• Inhibits osteoclast MMPs

Clearly, SDD has regenerative benefits as chronic inflammation subsides.  Thus, it is one of the most valuable tools available in the fight against periodontal disease, especially if there are systemic host factors which cannot be controlled such as a genetic hyper-inflammatory immune response. 

Published research also demonstrates that added benefits of taking SDD daily include lowering blood glucose levels,  lowering CRP (C-Reactive Protein) and other biomarkers for cardiovascular disease, and lowering cholesterol in patients with chronic periodontitis and cornonary artery disease.  This is profound, and it demonstrates well that SDD has a positive effect throughout the body.  SDD is also effective in the treatment of rosacea and rheumatoid arthritis.

Preventative periodontal care is about helping our patients to understand what is causing their disease, discussing options for treatment, and empowering them to move forward in health.  There are host factors (risk factors) which cannot be controlled with all the best intentions – such as genetic predisposition – without modifying the host response.  SDD is an excellent and effective adjunct to alter the course of periodontal disease safely and effectively.

Note:  SDD (Periostat) requires a prescription and is available in generic form to reduce the expense.  Generic sub-antimicrobial dose doxycycline 20mg is avialable in most drug stores.   The brand name of SDD is PerioStat.

Excerpts from the Journal of Clinical Periodontology 2004 Sept. re SDD:

Subantimicrobial dose doxycycline as adjunctive treatment for periodontitis. A review.

Preshaw PM, Hefti AF, Jepsen S, Etienne D, Walker C, Bradshaw MH.

School of Dental Sciences, University of Newcastle upon Tyne, UK.

Studies have shown that SDD, when prescribed as an adjunct to scaling and root planing (SRP), results in statistically and clinically significant gains in clinical attachment levels and reductions in probing depths over and above those that are achieved by SRP alone. SRP must be thorough and performed to the highest standard to maximise the benefits of adjunctive SDD.

SDD does not result in antibacterial effects, or lead to the development of resistant strains or the acquisition of multiantibiotic resistance. The frequency of adverse events is low, and does not differ significantly from placebo.

Articles about sub-antimicrobial dose doxycycline (SDD):

http://www.umm.edu/patiented/articles/how_antibiotics_being_used_long-term_prevention_of_periodontal_disease_000024_9.htm

http://ezinearticles.com/?Low-Dose-Doxycycline-Therapy&id=552971

What about published research with Peirostat (sub-antimicrobial dose doxycycline)?  There are numerous papers published on SDD demonstrating the therapeutic benefits in the treatment of periodontal disease.  Click on the links below and browse through additional links there.

http://www.ncbi.nlm.nih.gov/pubmed/15766366?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

http://periopeak.com/_media/pdf/HostedModularTherapy/subantimicrobial-dose-doxycycline-modulates-gingival-crevicular-fluid.pdf

http://periopeak.com/_media/pdf/Emdogain/Perio-2000-2008-Host-response-modulation.pdf