Group 7: Sophie
Erika, Steven & Mia

Periodontal Disease & Diabetes


1. Introduction

2. What is Periodontal Disease?

  • Signs and Symptoms of Gingivitis

  • Signs and Symptoms of Periodontitis

3. What is Diabetes?

  • Diabetes Type I

  • Diabetes Type II

  • The Hormonal Imbalance That Causes Diabetes

  • Characteristics of the Endocrine System

  • The Pancreas

  • Regulation of Glucagon and Insulin Secretion

4. The Relationship between Diabetes and Periodontal Disease

  • How Does Diabetes affect the Body and Oral Cavity?

  • How is Periodontal Disease and Diabetes Linked Immunologically?

  • How is Uncontrolled Diabetes Detected through the State of the Periodontal Tissues?

  • Effects of Increased Blood Glucose Levels on the Periodontium

5. Periodontal Treatment and Diabetes

  • Treatment Considerations

  • Treatment Modalities

  • Non-surgical Treatment

  • Periodontal Surgery

  • Laser Treatment

6. Conclusion

7. Reference List

1. Introduction

Periodontal disease is a multi-factorial disease, which in the past was known of bacterial origin, however due to vigorous studies it has been discovered that there are other factors involved (Wolf & Hassell, 2006). Periodontal Disease and Diabetes both separately affect individuals all over the world. Continual research has shown that there is quite a strong link between the two conditions (Nield-Gehrig, & Willmann, 2008) and this relationship goes both ways (American Journal of Periodontology, 2008).

2. What is Periodontal Disease?

Periodontal disease is a generic term which refers to a bacterial infection of the periodontium (Nield-Gehrig, & Willmann, 2008). It can affect gingival tissues, periodontal connective tissues, and/or alveolar bone. Periodontal disease can broadly be classified as gingivitis or periodontitis. Gingivitis is a bacterial infection which involves damage to the gingival tissues but is reversible. Periodontitis on the other hand is not reversible, and is a bacterial infection involving the destruction of all parts of the periodontium (gingiva, periodontal ligament, alveolar bone, and possibly cementum).

Figure 2.1: Cross section of healthy periodontium and unhealthy periodontium (AAP, 2009)

Figure 2.2: The Stages of Periodontal Disease (, 2009)

Figure 2.3: Etiology of Periodontitis - Interaction between Dental Plaque and the Host (Wolf & Hassell, 2006).

Signs and Symptoms of Gingivitis:

Gingivitis is essentially the mildest form of periodontal disease and has different levels of severity (AAP, 2009). When an individual has gingivitis their gingiva will become red, inflamed (swollen), and bleed easily (AAP, 2009). Gingivitis is most commonly a result of a person's poor oral hygiene practices (AAP, 2009).

Signs and Symptoms of Periodontitis:

If gingivitis is left untreated it may further progress to become periodontitis (AAP, 2009). Plaque now accumulates subgingivally (below the gum line) where by-products (toxins) produced by bacteria, retained in the plaque, irritate the gingival (gums) and periodontal tissues (periodontal ligament, alveolar bone) (AAP, 2009). The gingiva will slowly detach or separate from the tooth or teeth in the affected area(s) which then forms pockets that become more susceptible to infection (AAP, 2009). As periodontitis advances pocket depths increase and more periodontal tissues are destroyed (AAP, 2009). Eventually teeth may be lost due to lack of attachment of the supporting tissues if no periodontal treatment is undertaken (AAP, 2009). Unlike gingivitis, there is often little bleeding associated with periodontitis (AAP, 2009).

The following video shows some signs and symptoms of periodontal disease as well as a basic overview of its progression. Video 2.1: Gingivitis -

3. What is Diabetes?

Diabetes mellitus is the most common form of endocrine disorder in which the body is unable to produce or use insulin (Tortora & Derrickson, 2006). The body cannot use the hormone for transportation of glucose into cells, resulting in high blood glucose levels (Marieb & Hoehn, 2005). If the elevated blood glucose levels exceed the re-absorption capacity of the kidneys they will excrete glucose into the urine (Campbell, et al. 2006). Characteristics of Diabetes include excessive urine production, as the kidneys are unable to reabsorb water, excessive thirst and excessive eating (Marieb & Hoehn, 2005). There are two forms of Diabetes mellitus which are caused by a variety of genetic and environmental factors.

The following video shows insulin and glucose at work on a cellular level. Video 3.1: Diabetes, Type 1, Type 2, Insulin, Glucose -

Diabetes Type I

Type 1 diabetes or insulin-dependent diabetes mellitus (IDDM) is caused by damage to the pancreas and is diagnosed when a person has a low insulin level (Nield-Gehrig & Willmann, 2008). This occurs when the body's immune system destroys beta cells of the pancreas that produce insulin (Maireb & Hoehn, 2005).

Type 1 Diabetes can be fatal and insulin injections are required to prevent death (Tortora & Derrickson, 2006). Most patients develop the condition before 20 years of age, and symptoms are present when approximately 80-90% of the islet beta cells have been destroyed (Tortora & Derrickson, 2006).

As insulin is not present within the body to aid in the transportation and entry of glucose into cells, the body compensates by using fatty acids to produce energy (ATP) (Tortora & Derrickson, 2006). Stores of ATP in adipose tissue (fatty tissue) are broken down to access fatty acids and glycerol (Tortora & Derrickson, 2006). When this catabolism occurs by-products called ketones are produced and accumulate within the body causing a drop in blood pH level, a condition called Ketoacidosis resulting in death unless treated quickly (Tortora & Derrickson, 2006).

As lipids are transported to cells via the blood, lipid particles are deposited on the walls of blood vessels leading to Arteriosclerosis (hardening of the walls of arteries) and a variety of cardiovascular problems such as Ischemic Heart Disease, Peripheral Vascular Disease and Gangrene (Marieb & Hoehn, 2005).

Complications of diabetes include weight loss from triglyceride breakdown and loss of vision due to cataracts as the glucose attaches to lens proteins which damages the retina (Tortora & Derrickson, 2006). Severe kidney problems may also arise from resultant damage to renal blood vessels (Tortora & Derrickson, 2006).

People suffering from type 1 Diabetes must constantly monitor their blood glucose levels (up to 7 times a day) and eat regular meals containing 45-50% carbohydrates and less than 30% fat (Campbell, et al. 2006). Exercise, along with periodic insulin injections (up to 3 times per day) also aid in maintenance of this condition (Campbell, et al. 2006). Alternatively, pumps providing insulin to the body are also available instead of injections (Campbell, et al. 2006). However blood glucose levels must be monitored to determine when needed (Campbell, et al. 2006). Pancreas transplants are also an option, but immunosuppressant drugs must be taken for life (Campbell, et al. 2006).

Diabetes Type II

Type 2 Diabetes or non-insulin-dependent diabetes mellitus (NIDDM) is much more common than Type 1 Diabetes (Campbell, et al. 2006). Of all people suffering from diabetes, 90% are diagnosed with Type 2 (Campbell, et al. 2006). Type 2 Diabetes often occurs in obese people over the age of 35 (Campbell, et al. 2006). However with obesity increasing in the population, children and teenagers are also developing the condition (Campbell, et al. 2006).

People diagnosed with type 2 Diabetes either do not produce enough insulin or have become ‘insulin resistant’ (Campbell, et al. 2006). Usually the body is still producing insulin however the receptors on their target cells have become de-sensitized and less responsive (Campbell, et al. 2006). The high glucose levels in the blood can be controlled by diet, exercise and weight loss (Campbell, et al. 2006).

Figure 3.1: Regulation of blood glucose levels by insulin and glucagon: When blood glucose levels are high, the pancreas releases the hypoglycaemic hormone insulin, which stimulates glucose uptake by cells and glycogen formation in the liver, so that blood glucose levels are lowered. When blood glucose levels are low, the pancreas releases the hyperglycaemic hormone glucagon, which stimulates glycogen breakdown and thereby increases the amount of blood glucose (Marieb & Hoehn, 2005).

The endocrine system produces, releases and circulates hormones in the bloodstream which regulate the growth and activity of target cells, providing homeostasis within the body (Tortora & Derrickson, 2006).

  • Hormones delivered to tissues throughout the body by the blood (Tortora & Derrickson, 2006)
  • Mediator action occurs far from the site of release; binds to receptors on or in target cells, which are found throughout the body (Tortora & Derrickson, 2006)
  • Onset of action is seconds to hours or days (compared with nervous system which occurs in milliseconds) (Tortora & Derrickson, 2006)

The pancreas is both an exocrine and endocrine gland (Tortora & Derrickson, 2006). The exocrine portion makes up roughly 99% of the entire pancreas and consists of clusters of gland cells known as Pancreatic Acini, along with their associated ducts (Martini, 2006). These glands secrete large amounts of an alkaline, enzyme rich fluid (Martini, 2006). The exocrine portion of the pancreas contains clusters of cells known as Pancreatic Islets or Islets of Langerhans (Martini, 2006).
Figure 3.2: Structure of the enzyme-producing tissue of the pancreas. (a) One acinus (a secretory unit). The cell apices contain abundant zymogen (enzyme-containing) granules. (b) Photomicrograph of pancreatic acinar tissue (x200) (Marieb & Hoehn, 2005).

  • Alpha or A cells make up approximately 17% of pancreatic islet cells and secrete glucagon (Tortora & Derrickson, 2006). Glucagon is secreted when there is a decrease in the blood glucose levels, and their principal action is to raise blood glucose by accelerating the breakdown of glycogen into glucose (Tortora & Derrickson, 2006).
  • Beta cells or B cells make up 70% of pancreatic islet cells and secrete insulin (Tortora & Derrickson, 2006). Insulin is released when blood glucose levels are elevated and acts by accelerating transport of glucose into cells to lower blood glucose (Tortora & Derrickson, 2006).
  • Delta cells release a peptide hormone that is identical to growth hormone-inhibiting hormone (GH-IH). GI-IH prevents the release of glucagon and insulin by other islet cells and decreases the rate of food absorption and enzyme secretion along the digestive tract (Martini, 2006).

Figure 3.2: Islet of Langerhans (NIH & DHHS, 2009)

Figure 3.3: Photomicrograph of pancreatic tissue, differentially sustained: A pancreatic islet is surrounded by blue-gray acinar cells, which produce the exocrine product (enzyme-rich pancreatic juice). In this preparation, the beta cells of the islets that produce insulin are stained pale pink, abd tge alpha cells that produce glucagon are stained bright pink (x150) (Marieb & Hoehn, 2005).

The principal action of glucagon is to increase blood glucose levels when it drops below normal (Tortora & Derrickson, 2006). In comparison insulin helps lower blood glucose levels when it is too high (Tortora & Derrickson, 2006). The regulated secretion of insulin and glucagon are a negative feedback system (Tortora & Derrickson, 2006).

Figure 3.4: Effects of insulin on metabolism: When insulin concentrations are low (during the post absorptive period), these normal effects of insulin are inhibited and glycogenolysis and glyconeogenesis occur, that is, the insulin-mediated intracellular reactions are reversed (Note: Not all effects are shown in all cells) (Marieb & Hoehn, 2005).

Figure 3.5: Influence of glucagon on blood glucose levels: Negative feedback control exerted by rising plasma glucose levels on glucagon secretion is indicated by dashed arrows (Marieb & Hoehn, 2005).

4. The Relationship between Diabetes and Periodontal Disease

Studies have found that Diabetic patients were twice as likely to have periodontal attachment loss then lose without Diabetes (Matthews, 2002). However it has been found that Diabetic patients with good or moderate control of their Diabetes had similar levels of periodontal health as non-Diabetic patients (Matthews, 2002). Patients with poorly controlled or uncontrolled Diabetes have increased attachment loss and are more likely to exhibit recurrent Periodontal Disease (Matthews, 2002). Various researchers have concluded that "prevention and control of periodontal disease must be considered an integral part of diabetes control" (Matthews, 2002).

Well controlled Diabetes is defined by the fact that blood glucose levels, for an individual, are stable and within the recommended range (Nield-Gehrig, & Willmann, 2008). Severe Periodontal Disease has been found to increase an individual’s blood glucose levels (AAP, 2009).

How Does Diabetes Affect the Body and Oral Cavity?

  • Diabetic Retinopathy - proliferation of capillaries and haemorrhaging of the retina can lead to partial or complete blindness (Martini, 2006)
  • Cataracts - changes in the clarity of the eye lens (Martini, 2006)
  • Diabetic Nephropathy - small haemorrhages and inflammation of the kidney's which may cause kidney failure (Martini, 2006)
  • Neuropathy - variety of neural problems which are induced by disturbances in the blood supply to the neural tissues (Martini, 2006)
  • Cardiac circulation degeneration which may lead to a heart attack (Martini, 2006)
  • Reduction in blood flow to limbs may cause death, ulceration, infection or loss of that limb (Martini, 2006)

Oral Cavity:
  • Decreased saliva flow (Nield-Gehrig & Willmann, 2008)
  • Sensation of a burning tongue (Nield-Gehrig & Willmann, 2008)
  • Xerostomia (dry mouth) (Nield-Gehrig & Willmann, 2008)
  • Increased susceptibility to oral Candidiasis - bacterial, viral and fungal (Vernillo, 2003)
  • Taste impairment (Vernillo, 2003)
  • Lichen Planus (Vernillo, 2003)
  • Burning Mouth Syndrome (Vernillo, 2003)
  • Increased caries susceptibility (Vernillo, 2003)
  • Gingivitis - gingival inflammation after periodontal treatment (supragingival and subgingival scaling, oral hygiene instruction), severe gingival inflammation in response to plaque accumulation and proliferation of the gingival tissues along gingival margins (Vernillo, 2003 & Hirsch, 2004)
  • Periodontal Disease - alveolar bone loss, despite undergoing periodontal treatment (Vernillo, 2003 & Hirsch, 2004)
  • Deep periodontal pockets (Hirsch, 2004)
  • Tooth mobility and/or migration from normal place (Hirsch, 2004)
  • Over-erupting teeth (Hirsch, 2004)
  • Alveolar bone loss (Hirsch, 2004)
  • Several periodontal abscesses which may form simultaneously (Hirsch, 2004)

Figure 4.1: Symptomatic results of insulin deficit (diabetes mellitus) (Marieb & Hoehn, 2005).

Figure 4.2: Severe gingival inflammatory reaction to dental plaque. This 55 year old patient has just been diagnosed with Type II Diabetes. The gingival tissue is friable, oedematous and prone to bleeding on tooth brushing (Hirsch, 2004).

Figure 4.3: Alveolar Bone Loss. This orthopantomograph (OPG - full mouth x-ray) of a 54 year old patient with poorly controlled Diabetes shows extensive alveolar bone loss involving most teeth. The destruction of bone has been rapid even though the patient has been undergoing Periodontal Therapy (Hirsch, 2004).

Figure 4.4: Periodontal Abscess Formation. This 56 year old patient has poorly controlled Type II Diabetes. The lower left lateral incisor (*) is very mobile and has migrated from its usual location in the arch. The tooth has lost more than two-thirds of its supporting alveolar bone because of Periodontitis (Hirsch, 2004).

How is Periodontal Disease and Diabetes Linked Together Immunologically?

Patients with Diabetes mellitus have increased susceptibility to and severity of infections (Alba-Loureiro & Hirabara, 2006). Various studies have discovered that Diabetes alters the function of neutrophils, the primary defence cells of the body, thus contributing to the increased incidence or risk of infection (Alba-Loureiro & Hirabara, 2006). The alteration of neutrophils is due to the high levels of glucose and ketone bodies which influence neutrophil function via the production of polyols (Hirsch, 2004). The changes that have been observed in neutrophil functions include the alteration of the following: (Alba-Loureiro & Hirabara, 2006)
  • Adhesion to endothelium - a single layer of simple squamous cells, which line the walls of blood vessels, lymphatic vessels and the heart (Marieb & Hoehn, 2005)
  • Migration to the site of inflammation
  • Chemotaxis - movement of a cell toward or away from a chemical substance (Marieb & Hoehn, 2005)
  • Bactericidal activity
  • Phagocytosis - engulfing and breaking down of foreign substances by phagocytic cells (Marieb & Hoehn, 2005)
  • Production of reactive oxygen species
  • Release of lysosomal enzymes (Alba-Loureiro, Munhoz, Martins, Cerchiaro, Scavone, Curi, & Pannomiyo, 2007)

The energy required by neutrophils is produced by the metabolisation of glucose to lactate (Alba-Loureiro & Hirabara, 2006). Only 2-3% of glucose is oxidised through the Krebs cycle in neutrophils (Alba-Loureiro & Hirabara, 2006).

Video 4.1: A video on the Krebs cycle can be viewed here: Animation: How the Krebs Cycle Works (McGraw-Hill Higher Education, 2006)

The complications of diabetes are related to the elevation of blood glucose concentrations (hyperglycaemia) (Hirsch, 2004). Hyperglycaemia can cause the deposition of advanced glycation end products (AGEs) within tissues, which is a significant factor in the pathogenesis of complications such as Periodontitis (for individuals with Diabetes) (Ren, Fu, Deng, Qi, & Jin, 2009). Ren, et al. 2009 explains that AGEs 'are a heterogeneous group of irreversible products of non-enzymatic glycation, which accumulate in the plasma and tissues during aging and are known to be involved in the pathogenesis of diabetes.' AGEs alter the phenotype of macrophages and other cells through a specific cell-surface receptor (Hirsch, 2004). AGEs induce cells that produce inflammatory mediators (Matthews, 2002). Macrophages are one of the key cells in pathogenesis of periodontitis through the ability to produce large amounts of cytokines (Hirsch, 2004). Cytokines are chemical mediators which are involved in cellular immunity (Marieb & Hoehn, 2005). They are able to influence the inflammatory response system by metabolising fibroblasts, lymphocytes and stimulate bone resorption via prostaglandin E2 (Hirsch, 2004). Many researchers have noted that the AGEs transform macrophages into cells with a destructive phenotype, uncontrollably producing pro-inflammatory cytokines (Hirsch, 2004). Recent evidence shows that AGE-enriched gingival tissues have greater vascular permeability, experiencing greater breakdown of collagen fibres and show accelerated destruction of non mineralised connective tissue and bone (Matthews, 2002 & Ren, et al. 2009).

Hirsch, 2004 indicates that while Periodontal Disease is a result of uncontrolled Diabetes, it has been suggested that severe periodontitis may make the metabolic control of diabetes more difficult. This process may be mediated through the systemic release of inflammatory cytokines such as TNF - a form of periodontal lesions, and chronic, low-level systemic exposure to gram negative organisms (Hirsch, 2004).

How Can Diabetes Be Detected Through the State of the Periodontal Tissues?

Well controlled diabetes:
  • Healthy periodontium; minimal localized gingivitis (Matthews, 2002)
  • Healthy periodontium, generalized gingivitis (Matthews, 2002)

Uncontrolled diabetes:
  • Chronic, mild to moderate periodontal disease (Matthews, 2002)
  • Advanced attachment loss or aggressive (early onset) periodontal disease (Matthews, 2002)

Continual gingival inflammation after periodontal treatment (ie: supragingival and subgingival scaling, and oral hygiene instruction – OHI) (Hirsch, 2004)
  • Severe inflammation of the gingiva in response to plaque accumulation (Hirsch, 2004)
  • Alveolar bone destruction (loss) despite periodontal treatment (Hirsch, 2004)
  • Deep periodontal pockets (Hirsch, 2004)
  • Tooth mobility, migration and over-eruption (Hirsch, 2004)
  • Multiple periodontal abscesses (Hirsch, 2004)

Effects of Increased Blood Glucose Levels on the Periodontium:

A person with poorly controlled Diabetes is at an increased risk of suffering from periodontal abscesses, extensive attachment loss and progressive bone loss (Nield-Gehrig & Willmann, 2008). The increased blood glucose levels also affect the gingival crevicular fluid, as the bacteria found in the plaque colonies are able to easily metabolise the sugars in the crevicular fluid (Nield-Gehrig & Willmann, 2008).

5. Periodontal Treatment

Treatment Considerations:

Due to the link between Diabetes and Periodontal Disease, as previously mentioned, there are some important treatment considerations that need to be taken into account for a dental patient who has Diabetes and requires periodontal treatment
  1. The patient's General Practitioner needs to be contacted before the commencement of treatment to determine whether their patient will require antibiotic prophylaxis (cover) prior to the appointment (Nield-Gehrig, & Willmann, 2008).
  2. Any type of periodontal treatment should be postponed if a patient's Diabetes is not under control as the patient will be at a much higher risk of bacterial or fungal infections like gingivitis, periodontitis, and candidiasis (Nield-Gehrig, & Willmann, 2008).
  3. Periodontal Disease can be classified as an infection, so as Diabetes lowers an individual's immune response a patients healing time will be longer than it normally would be (Nield-Gehrig, & Willmann, 2008). This means that longer time is required between any consecutive appointments.
  4. On the day of the appointment the patient should be advised to bring their blood glucose meter along in order for the operator to check their blood glucose levels prior to treatment (Nield-Gehrig, & Willmann, 2008). The patient should also be advised to eat as per normal and take any medication required (Nield-Gehrig, & Willmann, 2008).
  5. After having periodontal treatment a patient may not be able to eat, which predisposes them to hypoglycaemia (Nield-Gehrig, & Willmann, 2008). Thus the dental operator needs to consult the patient's General Practitioner prior to the appointment for any recommendations for alternations in the patient's medication (Nield-Gehrig, & Willmann, 2008).

Treatment Modalities:

As the extent to which Periodontal Disease and Diabetes affects a patient varies from one individual to another, there are a number of different treatment options available depending on the severity of one or both conditions.

Non-surgical Treatment:

Healthy periodontium should be achieved through the least invasive and most cost-effective ways possible (AAP, 2008). This can often be done through the use of non-surgical treatment such as scaling and root planning (AAP, 2008). Root planning involves carefully removing plaque and calculus (tartar) from deep periodontal pockets (AAP, 2008) and thus removing bacterial toxins which contribute to the deterioration of the periodontium. Scaling and root planning can then be followed by local delivery of antimicrobials and host modulation as per each patient’s requirements (AAP, 2008). The majority of Periodontist’s have concluded that after scaling and root planning many patients will not required further invasive treatment like periodontal surgery (AAP, 2008). However, most patients do require a continual maintenance regime to sustain a health periodontal state (AAP, 2008). Non-surgical treatment is not 100% guaranteed to achieve periodontal health for every patient so surgery may be required in order to restore damaged periodontal tissues (AAP, 2008).

Periodontal Surgery:

  • Pocket Reduction Procedures: Pocket reduction involves folding back the gingival tissues and removing the disease-causing bacteria and smoothing of any damaged alveolar bone prior to firmly securing the gingival tissues in place in order to gain gingival reattachment to the alveolar bone (AAP, 2008).
  • Regenerative Procedures: Regenerative Procedures are similar to pocket reduction procedures. However after folding back the gingival tissues membranes, bone grafts or tissue-stimulating proteins are placed into the pocket to encourage the regrowth of periodontal tissues (AAP, 2009).
  • Soft Tissue Graft Procedures: Soft tissue grafts are used to cover the roots of teeth and to replace gingival tissue that has been lost due to severe gingival recession (AAP, 2009). Grafts are either taken directly from a patient's palate or from a donor (AAP, 2009).

Laser Treatment:

Little research has been done to prove the effectiveness of laser therapy in conjunction with scaling and root planning (AAP, 2008). However if lasers are used properly they can be useful in reducing bleeding, swelling and patient discomfort during periodontal treatment (AAP, 2008). Lasers are not are all identical and some can be multipurpose, so damage may ensue if the incorrect wavelength or power level is used (AAP, 2008).

6. Conclusion

Diabetes and Periodontal Disease, although often looked at separately, have quite a strong link with one another. Thus it is important for to have a good understanding of the two in order to able to assess, diagnose and treatment both conditions in conjunction with the other, if necessary. The affects of Diabetes, while not limited to the oral cavity, plays a significant role in the pathogenesis of Periodontal Disease (but not always the case) so knowledge of the immunology behind blood glucose levels of various cells of the body like leukocytes (ie: neutrophils and macrophages) along with AGEs will help with treatment planning and considerations that may be required for Diabetic patients, either type I or II.

7. Reference List:

Alba-Loureiro T, & Hirabara S, (2006), "Diabetes Causes Marked Changes in Function and Metabolism of Rat Neutrophils," Journal of Endocrinology, no. 188, pp. 295-303

Alba-Loureiro T.C, Munhoz C.D, Martins J.O, Cerchiaro G.A, Scavone C, Curi R, & Pannomiyo P, (2007) “Neutrophil function and metabolism in individuals with diabetes mellitus,” Brazilian Journal of Medical and Biological Research, vol. 40(8), pp. 1037-1044

American Journal of Periodontology (AAP), (2009), Gum Disease and Diabetes, viewed 18th September 2009,

Campbell N, Reece J, & Meyers N, (2006), Biology 7th Edition Australian Version, Pearson Education, New South Wales, Australia

Dentistalfredo, (2008) "Gingivitis," © YouTube, LLC,, (last checked 01/10/2009)

EnCognitive, (2008) "Diabetes, Type 1, Type 2, Glucose, Insulin," © YouTube, LLC,, (last checked 01/10/2009)

Hirsch R, (2004), "Diabetes and Periodontitis," Australian Prescriber, 27(2), pp. 36-38, (2009), 'The Stages of Periodontal Disease,' Google Images

Marieb E.N & Hoehn K, (2005), Human Anatomy & Physiology Seventh Edition, Pearson Benjamin Cummings, San Francisco, USA

Martini, F.H, (2006), Fundamentals of Anatomy & Physiology Seventh Edition, Pearson Benjamin Cummings, San Francisco, USA

Matthews D, (2002), "The Relationship Between Diabetes and Periodontal Disease," Journal of the Canadian Dental Association, 68(3), pp.161-164

McGraw-Hill Higher Educaion, (2006), Animation: How the Krebs Cycle Words (Quiz 1),, (last checked 01/10/2009)

National Institutes of Health (NIH), Department of Health and Human Services (DHHS), (2009), 7. Stem Cells and Diabetes

Nield-Gehrig J.S, & Willmann D.E, (2008), Foundations of Periodontics for the Dental Hygienist 2nd Edition, Philadelphia, USA

Ren L, Fu Y, Deng Y, Qi L, & Jin L, (2009), “Advanced Glycation End Products Inhibit the Expression of Collagens Type I and III by Human Gingival Fibroblasts,” Journal of Periodontology, vol. 80, no.7, pp. 1166-1173

Tortora G, & Derrickson B, (2006), Principles of Anatomy and Physiology 11th Edition, John Wiley & Sons Inc. MA** viewed 18th September 2009,

Vernillo A.T, (2003), “Dental considerations for the treatment of patients with diabetes mellitus,” Journal of American Dental Association, vol. 134, pp. 24S-33S

Wolf F, Hassell T, (2006), Color atlas of dental hygiene: Periodontology, Stuttgart, Thieme Publishing Group