Overview of Oral Inflammation

Overview of Oral Inflammation: The Oral-

Systemic Ramifications of Periodontal Disease

David J. Verbik DDS, PhD

Inflammation

• Is a protective attempt by the body to remove injurious stimuli (bacteria) and to initiate the healing process.

• It is part of a complex biological response involving the vascular tissues and the host immune system (vascular changes, complement cascade, bradykinin, fibrinolysis system, cellular component).

• Inflammation is the basis of gingivitis and periodontitis.

InflammationInflammation includes vasodilation and increased permeability of nearby blood vessels and the migration of white blood cells out of blood vessels into the surrounding tissue.

Swelling Redness Pain Heat Loss of function.

Inflammation If the injurious stimuli

(bacteria) are not removed, inflammation can lead to tissue destruction and can often lead to permanent tissue loss.

It is also believed that chronic oral inflammation can lead to chronic disease.

Periodontal Disease• Gingivitis: the inflammation of gingival tissue caused by the

accumulation of bacteria and other organic material on the tooth.

• Periodontitis: an inflammatory disease of the periodontium: gingival tissues, cementum, periodontal ligament, alveolar bone.

• As the disease progresses we find deepening of periodontal pockets, resorption of alveolar bone, loosening and loss of teeth.

***This disease process is believed to be episodic rather than continuous, with alternating periods of disease progression and remission.

Periodontal Disease

• Periodontal disease is one of the most prevalent diseases in man. It is typically a gram (-) anaerobic bacterial infection of the supportive structures of the teeth.

• In 2005, the American Association of Periodontists estimated that 5 to 20% of American adults have severe periodontitis while the majority of adults have moderate periodontitis.

• According to the U.S. Surgeon General’s 2000 report, periodontal disease has become a silent epidemic.

Periodontal Disease

• It is caused by bacteria that adhere to the tooth surface and aggregate to produce a dental biofilm.

• When pathogenic bacteria breakdown the host’s defense mechanism, this initiates an inflammatory response which ultimately contributes to tissue damage.

• Tissue damage can worsen as the inflammatory process extends to the periodontal ligament and surrounding alveolar bone.

Histopathogenesis of gingivitis and periodontitis

Periodontal Disease

• Approximately 700 bacterial species have been identified in the oral cavity and nearly 300 species have been cultured and found to contribute to the biofilm of the periodontal pocket.

• There is a much smaller number of species that have been shown to be more closely related to the initial incidence and continued persistence of periodontitis.

Periodontal Disease

• The risks of developing periodontal disease varies among patients and includes: age, smoking, family history, diabetes, oral hygiene practice and frequency of preventative dental appointments.

• Periodontal disease was once thought to be an inevitable consequence of aging. Today we know that periodontal disease can be prevented and successfully treated once it develops.

Relationship Between Oral and Systemic Health

• It has long been recognized that systemic disease can contribute to the development of periodontal disease.

• Today however, researchers have shifted their focus to periodontitis and periodontal pathogens and how they may impact systemic health.

• Results from several recent studies suggest a relationship between periodontal disease and the development of cardiovascular disease, respiratory disease, Alzheimer’s, diabetes.

Relationship Between Oral and Systemic Health

• Most of these studies have not “proven” a cause/effect relationship between periodontitis and systemic disease.

• However, the general mechanism is believed to involve a systemic inflammatory response to blood-born bacterial endotoxins (lipopolysaccharides) and/or oral bacteria including: Porphyromonas gingivalis and Treponema denticola

Oral Pathogens and Systemic Disease

• Atherosclerosis is recognized as an inflammatory disease and is one of the principle causes of death in the United States, Europe and around the world.

• It is characterized by the build-up of inflammatory plaques on the arterial wall caused largely impart form the accumulation of macrophages, cholesterol, fat and fibrous connective tissue.

• Similar to periodontitis, one of the hallmarks of early atherosclerotic lesions is the presence of neutrophils followed by monocytes and lymphocytes.

Oral Pathogens and Systemic Disease

• In 1989, researchers began to study the relationship between cardiovascular disease and periodontitis. They found that even after controlling for many factors, such as smoking, diabetes, and serum lipid concentrations, heart-attack patients still had significantly worse dental health than control subjects.

• Similar studies have also linked heart disease and periodontitis. For example, Beck and colleagues found that patients with severe periodontitis were twice as likely to have a fatal heart attack and three times as likely to have a stroke when compared to patients without periodontal disease (Beck et al. 1996 and Beck et al. 1998).

Oral Pathogens and Systemic Disease

• It was also discovered that patients suffering from cardiovascular disease have significantly elevated levels of acute-phase proteins in their blood (Emst, 1990 and Ridker et al. 1997).

• Acute-phase proteins are produced and secreted by the liver in response to inflammation in the body. This response is called the acute-phase reaction.

Oral Pathogens and Systemic Disease

• In response to noxious stimuli (bacteria) or tissue injury, local inflammatory cells secrete a number of cytokines (IL-1, IL-6, and IL-8) and other pro-inflammatory mediators (TNF-alpha).

• In response to bacterial products, gingival epithelium also secrete IL-1, TNF-alpha, and prostaglandins which also promotes the inflammatory process.

• These mediators stimulate the liver to release acute phase proteins including: C-reactive proteins (CRP), haptoglobin, alpha-1 antitrypsin and fibrinogen.

Oral Pathogens and Systemic Disease

• Noak et al. recently reported a positive correlation between increased levels of CRP and the presence of periodontal pathogens in the oral cavity (2001). Furthermore, the severity of periodontal disease correlated with increased levels of CRP.

• D’Ajuto et al. (2004) have shown when periodontal treatment is performed and clinical inflammation decreases, the serum levels of these inflammatory mediators including CRP.

Oral Pathogens and Systemic Disease

• Recent studies have shown the presence of periodontal pathogens (T. denticola and P. gingivalis) in aneurysmic aortic walls. (Haraszthy et. al. 2000, Cavrini et al. 2005)

• Li and colleagues have shown an increase in aortic lesion development in animals inoculated with P. gingivalis. In addition, they also found P. gingivalis in the aortas and hearts of the inoculated animals. (Li et al. 2002, Gibson et al 2004)

Oral Pathogens and Systemic Disease

• Martin and colleagues found identical bacterial species isolated from blood and plaque samples from the same patients. (Martin et. al 2004)

• Haraszthy et. al were able to detect P. gingivalis in human atheromatous tissue indicating that P. gingivalis gains access to the vasculature and localizes at sites of atheroma development.

Oral Pathogens and Systemic Disease

Results from these studies indicate:

• 1) Oral pathogens can enter the circulatory system.

• 2) Periodontal pathogens may increase the risk of developing atherosclerotic lesions.

• 3) There is a correlation between increased levels of CRP and the presence of periodontal pathogens in

the oral cavity.

Oral Pathogens and Systemic Disease

The long-term systemic complications of chronic adult periodontitis remains unknown.

It is believed that the circulating bacterial endotoxin(s) adversely affects the vascular endothelium by inducing a cytokine cascade which could account for the elevated acute phase protein levels (Engebretson et al. 1999).

Prevention and Treatment

I) Diagnosis: Disease Discovery – Evaluation and Assessment

• Medical and Dental history

• Clinical examinationPeriodontal AssessmentAppropriate radiographsIntra-oral pictures

• Inform Patient (Increase patient awareness of periodontal disease, Explain treatment goals, Explain risk factors, Informed consent)

Prevention and Treatment

II) Treatment Plan:

• Personal Periodontal Counseling (Effective home care program)

• Fabrication of Perio Trays (this allows placement of a 1.7% hydrogen peroxide gel deep into the sulcus/perio pocket)

• Scaling and Root Planing (removal of calculus and bacterial biofilm)

• Supportive Periodontal Maintenance Appointments

Wax Up on Models

Anterior view Right side

Wax Try-in appointment

Anterior view Right side

Wax try-in. Next step, placement of implants and deliver dentures

Anterior View Maxillary anterior overjet

Final Implant Impression

Impression posts in place

Final impression using the open tray technique

Seating custom abutments and frame-work try-in.

Anterior View Occlusal View

Framework try-in

Frame-work try-in Recording bite with frames in place

Try-in and delivery of implant-supported bridges

Porcelain bisque bake try-in

Final Delivery

Try-in and delivery of implant-supported bridges

Right side Left side

Partial frame with teeth set in wax on model

Bridge frame on model

Wax try-in for LRPD Frame try-in for implant- supported bridge

Frame try-in for implant- supported bridge

Wax try-in for LRPD