Periodontal Disease
Causes
Periodontal disease occurs as a result of untreated gingivitis. Infection and inflammation spread from the gums to the ligaments and bone supporting the teeth. Due to the loss of support, the teeth start to become loose and it is possible that they may peel. Periodontal disease is the leading cause of tooth loss in adults. This condition is not common in young children, but the risk of developing it increases during adolescence.
Plaque and tartar build up at the base of the teeth. The inflammation generated by these deposits causes a ‘pocket’ or space to form between the loose, attached gums and the tooth. Later, this space fills with plaque which calcifies, forming tartar. Inflammation of the soft tissue retains plaque in the space formed. Failure to treat the inflammation leads to damage to the epithelial tissue and bone surrounding the tooth. Because dental plaque contains bacteria, an acute infection is likely to occur, accompanied by the formation of a periodontal abscess that can include a healthy tooth. These abscesses also increase the possibility of bone mass destruction.
The reason for these problems is related to your genes and their molecular biology. In some patients, the immune system releases messenger proteins in response to oral bacteria, and these turn into T and B lymphocytes. Inflammation and loss of bone mass supporting the teeth can occur.
Bone formation is controlled by the OPG system RANK RANKL*
RANKL* = ligand RANK
The discovery of the OPG/RANK/RANKL system in the mid-1990s for managing bone resorption led to a deeper understanding of how bone shaping and remodelling are managed. Many years before this discovery it was already known that stromal cells managed osteoclast formation, but it was not anticipated that they would do so by expressing members of the TNF (tumor necrosis factor) superfamily: receptor activator of NF-IB ligand (RANKL) and osteoprotegerin (OPG) or that cytokine and NF-IB ligand receptor activator (RANK) signaling would have extensive functions beyond managing bone remodeling.
- RANKL/RANK signaling regulates osteoclast formation
- OPG protects bone from excessive resorption by binding to RANKL and preventing its binding to RANK (competitive inhibition).
- OPG inhibits bone formation by eating cells called osteoclasts.
- If OPG is blocked, osteoclasts form in an uncontrolled manner and destroy bone.RANKL/RANK signaling regulates osteoclast formation
The RANK, RANKL, OPG system is a major determinant of bone mass and strength.
If OPG is blocked, osteoclasts form in an uncontrollable manner and destroy the bone.
This happens in periodontal disease. The determining factor seems to be oral bacteria and poor oral hygiene.
Role of the RANK RANKL OPG system in periodontal disease
Periodontal disease and general health
There is a correlation between periodontal disease and general health:
- Cardiovascular disease
- Myocardial infarction
- Stroke
- Poor circulation at the extremities
- Diabetes
- Increased incidence of breast cancer
- Pregnancy with complications (Pre-term birth)
- Alzheimer’s disease
- Erectile dysfunction
There are 2 mechanisms known to be important:
1. Periodontal bacteria manage to enter the bloodstream via fragile blood vessels
Bacteria are the cause of the formation of branched proteins in the walls of blood vessels, which will form atheromatous plaque.
This results in narrowing of the blood vessels and ischemia of the tissue.
2. Chronic systemic inflammation
Any chronic inflammation anywhere in the body (including the periodontium) causes the liver to produce a substance called C-reactive protein.
When the C-reactive protein value is higher than > 3 mg/liter of blood, the patient has an increased risk of developing cardiovascular disease.
C-reactive protein causes blood clot formation and fatty plaque instability that can rupture and move to the heart or brain, where it deposits and can cause a heart attack. In the heart, it can cause a myocardial infarction and in the brain a stroke.
Diabetes and smoking also have a major effect on blood vessel disease. If combined with periodontal disease, the risk of serious complications increases significantly.
Medical implications of periodontal disease:
- A PCR analysis should be performed if:
- Family history contains:
- Cardiovascular disease
- Stroke
- Hypertension
- Hyperlipidaemia
- Kidney failure
- Obesity
- Diabetes
- Smoker
- Family history contains:
Those patients who have CRP (C-Reactive Protein) levels greater than 3 mg/l require referral to a general practitioner for further evaluation of cardiovascular status and risk.
Symptom
Symptoms of periodontal disease include:
- Halitoza
- Gum staining – bright red or red-violet
- Glossy gingham
- Bleeding gums – even with gentle brushing of teeth
- Gum sensitivity
- Swollen gums
- Dental mobility
- Radiographic – loss of supporting bone and subgingival tartar
Treatment
The aims of the treatment are:
- reduction of inflammation
- removal of periodontal pockets
- treatment of all underlying causes of periodontal disease (e.g. poorly fitting restorations)
- Good oral hygiene is the key to success
- Laser treatment
The PerioLase MVP-7 is a 6-watt Nd:YAG variable pulsed dental laser with digital technology and 7 pulse durations – the most available on the market – providing the power and versatility to perform a wide range of laser procedures.
FDA approval for True Regeneration procedure – new cement, new periodontal ligament and new alveolar bone.
LANAP bone augmentation using PerioLase MVP-7 has the power to stop periodontal disease with a simple, sutureless procedure.
The PerioLase MVP-7, an optimized Nd:YAG laser, is specifically designed to perform ROI LANAP and LAPIP procedures, the treatment protocols in periodontal disease and peri-implantitis.
The laser emits a specific wavelength that targets and destroys P. gingivalis bacteria and other periodontal pathogens.
The operation may be required for:
- Opening and cleaning deep periodontal pockets
- Construction of the mobile tooth support
- Making grafts for infrabony pockets
- Guided bone regeneration
- Strategic tooth extraction
- Periodontal plastic surgery to improve aesthetics
Outlook (Prognostic)
Prognosis should be considered in relation to local conditions and systemic control of periodontal disease.
- Varies according to genotype, phenotype and systemic conditions
- Varies according to oral hygiene measures
- Varies according to the patient’s compliance with the indications
Possible complications
These complications can occur:
- Soft tissue infections or abscesses
- Infections of the jaw bones
- Recurrent periodontitis
- Periodontal abscess
- Tooth loss
- Change in the position of the teeth – anterior teeth proclination
- Acute ulcero-necrotic gingivitis
When to contact a healthcare professional
Serology PCR > 3 mg/litre
Preventie
Good oral hygiene is the best way to prevent periodontal disease. This includes brushing your teeth and flossing, as well as regular professional cleaning by your dentist. Preventing and treating gingivitis reduces the risk of periodontal disease.
Bibliography
Periodontal disease and cardiovascular disease
James Beck,* Raul Garcia, Gerardo Heiss, Pantel S. Vokonas and Steven Offenbacher
*Department of Dental Ecology, University of North Carolina, Chapel Hill, NC.
U.S. Department of Veterans Affairs Outpatient Clinic, Boston, MA and Department of Oral Pathology and Medicine, Tufts University School of Dental Medicine, Boston, MA.
Department of Epidemiology, University of North Carolina, Chapel Hill, NC.
U.S. Department of Veterans Affairs Outpatient Clinic, Boston, MA, and Section of Preventive Medicine and Epidemiology and Evans Memorial Clinical Research Department, Department of Medicine, Boston University School of Medicine, Boston, MA.
Department of Periodontics and Center for Dental Research, University of North Carolina, Chapel Hill, NC.
It is our central hypothesis that periodontal diseases, which are chronic Gram-negative infections, are a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between the severity of periodontal disease and the risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait that puts an individual at high risk of developing both periodontal disease and atherosclerosis. In addition, we suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (particularly TxA2, IL-1, PGE2, and TNF) that serve to initiate and exacerbate atherogenesis and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the US Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured in 1147 men between 1968 and 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD and 40 had strokes. Adjusted incidence rates for established cardiovascular risk factors were 1.5, 1.9 and 2.8 for total CHD, fatal CHD and stroke, respectively. Bone loss levels and cumulative incidence of total CHD and fatal CHD indicated a biological gradient between exposure severity and disease occurrence. J Periodontol 1996;67:1123 1137.