# Diabetes and Periodontal Diseases Dr Leticia A Miranda & Dr. Pradeep Koppolu  Diabetes and Periodontal Diseases Dr Leticia A Miranda & Dr. Pradeep Koppolu A word cloud visualization centered on the topic of diabetes. The largest and most prominent words are 'diabetes', 'type', 'risk', 'glucose', 'insulin', 'pancreas', 'body', 'cells', 'blood', 'prevention', and 'factors'. Other smaller terms include 'symptoms', 'age', 'history', 'diet', 'weight', 'gestational', 'complications', 'management', and 'treatment', arranged to form a cohesive visual representation of key concepts related to diabetes. # Reading Resources - **Clinical Periodontology and Implant Dentistry**, 2 Volume Set by Niklaus P. Lang, Jan Lindhe, and Niklaus P Lang **PUBLISHER** John Wiley & Sons, Incorporated **DATE** 2015-03-25 ## SECTION V: CONDITIONS AFFECTING THE PERIODONTAL PATIENT **CHAPTER 25** ### Influence of Systemic Conditions on the Periodontium *Perry R. Klokkevold | Brian L. Mealey | Yvonne L. Hernandez-Kapila* For expanded discussions on female sex hormones, genetic disorders, and nutritional influences on periodontal disease as well as online-only content on hyperparathyroidism, anemia, thrombocytopenia, antibody deficiency disorders, and other systemic conditions, please visit the companion website at eBooks.Health.Elsevier.com. --- **JDR Centennial Series** ### Periodontal Medicine: 100 Years of Progress J.D. Beck<sup>1</sup> ID, P.N. Papapanou<sup>2</sup>, K.H. Philips<sup>3</sup>, and S. Offenbacher<sup>4</sup> Journal of Dental Research 2019, Vol. 98(10) 1053–1062 © International & American Associations for Dental Research 2019 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/0022034519846113 journals.sagepub.com/home/jdr    - **Clinical Periodontology and Implant Dentistry**, 2 Volume Set by Niklaus P. Lang, Jan Lindhe, and Niklaus P Lang - **PUBLISHER**: John Wiley & Sons, Incorporated - **DATE**: 2015-03-25 #### SECTION V: CONDITIONS AFFECTING THE PERIODONTAL PATIENT **CHAPTER 25** ##### Influence of Systemic Conditions on the Periodontium *Perry R. Klokkevold | Brian L. Mealey | Yvonne L. Hernandez-Kapila* For expanded discussions on female sex hormones, genetic disorders, and nutritional influences on periodontal disease as well as online-only content on hyperparathyroidism, anemia, thrombocytopenia, antibody deficiency disorders, and other systemic conditions, please visit the companion website at eBooks.Health.Elsevier.com. --- **JDR Centennial Series** ##### Periodontal Medicine: 100 Years of Progress J.D. Beck, P.N. Papapanou, K.H. Philips, and S. Offenbacher Journal of Dental Research 2019, Vol. 98(10) 1053–1062 © International & American Associations for Dental Research 2019 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/0022034519846113 journals.sagepub.com/home/jdr Book cover image and metadata block for 'Clinical Periodontology and Implant Dentistry, 2 Volume Set'. The visual includes the book cover on the left showing a dental professional in a purple coat, alongside details: authors (Niklaus P. Lang, Jan Lindhe), publisher (John Wiley & Sons, Incorporated), and date (2015-03-25). Chapter header graphic for 'Influence of Systemic Conditions on the Periodontium' from Section V. The visual features a red banner with 'SECTION V', a beige strip with 'CHAPTER 25', the chapter title, author names (Perry R. Klokkevold et al.), and a note box directing readers to eBooks.Health.Elsevier.com for expanded discussions. Journal header graphic for 'Periodontal Medicine: 100 Years of Progress' from JDR Centennial Series. Includes the JDR logo with a '100 YEARS' badge, article citation details (Vol. 98(10) 1053–1062), DOI, and a circular podcast icon labeled 'PODCAST'. ```mermaid graph TD subgraph Clinical_Health [Clinical Health] CH1[Health Promoting biofilm = Symbiosis] CH2[Low biomass] CH3[Proportionate Host response] CH4[Acute Resolution of inflammation] CH1 -- "Complement / PMNs" --> CH3 CH2 -- "Antigens / Bact'l DNA / fMLP" --> CH4 end subgraph Gingivitis [Gingivitis] G1["Incipient Dysbiosis (Quorum Sensing Bacteria)"] G2[High biomass] G3[Proportionate Host response] G4[Chronic Resolution of inflammation] G1 -- "Antibody / PMNs ++ / T & B cells" --> G3 G2 -- "Antigens / Virulence Factors / LPS" --> G4 end subgraph Periodontitis [Periodontitis] P1["Frank Dysbiosis (Pathogenic Biofilm)"] P2[High biomass] P3["Disproportionate Host response (hyper-inflammatory)"] P4[Failed Resolution of inflammation] P5["Connective Tissue & Bone Damage"] P6[Chronic non-Resolving inflammation] P1 -- "Antibody / PMNs +++ / Plasma cells" --> P3 P2 -- "Antigens / Gingipains / LPS" --> P4 P3 -- "DAMPs / Haem / GCF ↑" --> P5 P4 -- "Cytokines / Prostanoids / MMPs / Oxidative Stress" --> P6 end %% Risk Factors Arrows RF1[Behavioural risk factors absent] -->|Behavioural risk factors present| RF2[ ] RF3[Environmental risk factors absent] -->|Environmental risk factors evident| RF4[ ] RF5[Genetic risk factors absent] -->|Genetic risk factors present| RF6[ ] RF7[Epigenetic effects not evident] -->|Epigenetic effects evident| RF8[ ] ```  ```mermaid graph TD subgraph Clinical_Health [Clinical Health] CH1[Health Promoting biofilm = Symbiosis] CH2[Low biomass] CH3[Proportionate Host response] CH4[Acute Resolution of inflammation] CH1 -- "Complement / PMNs" --> CH3 CH2 -- "Antigens / Bact'l DNA / fMLP" --> CH4 end subgraph Gingivitis [Gingivitis] G1["Incipient Dysbiosis (Quorum Sensing Bacteria)"] G2[High biomass] G3[Proportionate Host response] G4[Chronic Resolution of inflammation] G1 -- "Antibody / PMNs ++ / T & B cells" --> G3 G2 -- "Antigens / Virulence Factors / LPS" --> G4 end subgraph Periodontitis [Periodontitis] P1["Frank Dysbiosis (Pathogenic Biofilm)"] P2[High biomass] P3["Disproportionate Host response (hyper-inflammatory)"] P4[Failed Resolution of inflammation] P5["Connective Tissue & Bone Damage"] P6[Chronic non-Resolving inflammation] P1 -- "Antibody / PMNs +++ / Plasma cells" --> P3 P2 -- "Antigens / Gingipains / LPS" --> P4 P3 -- "DAMPs / Haem / GCF ↑" --> P5 P4 -- "Cytokines / Prostanoids / MMPs / Oxidative Stress" --> P6 end %% Risk Factors Arrows RF1[Behavioural risk factors absent] -->|Behavioural risk factors present| RF2[ ] RF3[Environmental risk factors absent] -->|Environmental risk factors evident| RF4[ ] RF5[Genetic risk factors absent] -->|Genetic risk factors present| RF6[ ] RF7[Epigenetic effects not evident] -->|Epigenetic effects evident| RF8[ ] ``` A complex medical flowchart diagram illustrating the progression of oral health conditions from Clinical Health to Periodontitis. The diagram is organized into three main vertical columns: 'Clinical Health' (green), 'Gingivitis' (orange), and 'Periodontitis' (red). Each column details a specific stage: 1. Clinical Health: Shows 'Health Promoting biofilm = Symbiosis' and 'Low biomass'. It indicates a 'Proportionate Host response' leading to 'Acute Resolution of inflammation'. 2. Gingivitis: Shows 'Incipient Dysbiosis (Quorum Sensing Bacteria)' and 'High biomass'. It indicates a 'Proportionate Host response' but leads to 'Chronic Resolution of inflammation'. 3. Periodontitis: Shows 'Frank Dysbiosis (Pathogenic Biofilm)', 'High biomass', and 'Dis-proportionate Host response (hyper-inflammatory)'. This leads to 'Failed Resolution of inflammation', 'Connective Tissue & Bone Damage', and 'Chronic non-Resolving inflammation'. The diagram includes arrows indicating interactions between bacterial factors (Antigens, Virulence Factors, LPS, etc.) and host responses (Complement, PMNs, Antibody, Cytokines, etc.). Risk factors are noted at the top and bottom as absent or present for each condition. **The UNIVERSITY OF** **WESTERN** **AUSTRALIA** Although dental plaque accumulation is a cause of periodontal disease, it **may not be a sufficient** cause since some individuals have large accumulations of dental plaque and suffer little periodontal disease, while others have very little plaque accumulation and suffer severe periodontal disease. It appears then that **risk factors are important** in periodontal disease; determining **who develops the disease, the severity of the disease the individual develops, which sites in the dentition are affected, the rate of progression of the disease, the response to therapy, and the recurrence rate.** In assessing risk, the probability that a disease outcome will occur following a particular exposure is estimated (Last, 2001). Risk factors (behavioural, environmental and genetic), have the potential to **modify** patient's response to the presence of dental biofilm. This is important because periodontal tissue destruction in periodontitis fundamentally results from the body's response to plaque rather that the plaque itself (Page and Schroeder, 1976). Although dental plaque accumulation is a cause of periodontal disease, it **may not be a sufficient** cause since some individuals have large accumulations of dental plaque and suffer little periodontal disease, while others have very little plaque accumulation and suffer severe periodontal disease. It appears then that **risk factors are important** in periodontal disease; determining **who develops the disease, the severity of the disease the individual develops, which sites in the dentition are affected, the rate of progression of the disease, the response to therapy, and the recurrence rate.** In assessing risk, the probability that a disease outcome will occur following a particular exposure is estimated (Last, 2001). Risk factors (behavioural, environmental and genetic), have the potential to **modify** patient's response to the presence of dental biofilm. This is important because periodontal tissue destruction in periodontitis fundamentally results from the body's response to plaque rather than the plaque itself (Page and Schroeder, 1976). University of Western Australia institutional logo located in the top right corner. It features a blue shield with a white swan and three books above it, accompanied by the text 'THE UNIVERSITY OF WESTERN AUSTRALIA'. The University of Western Australia **What is a risk factor?** A risk factor can be an aspect of personal behaviour or life style, an environmental exposure, or an inborn or inherited characteristic that changes the susceptibility to periodontal disease. It can also be a local factor which increases the infection of a site. **Types of risk factors for periodontal disease** There are two major classes of risk factors for periodontal disease. 1. **Local factors** such as overhanging restorations and root caries that tend to allow for plaque accumulation and hence result in more periodontal disease. Other local risk factors for periodontal disease include pocket depth, intrabony pockets especially involving furcations, and root canal infections. 2. **Systemic factors** that affect the entire body, such as cigarette smoking, diabetes mellitus and genetic factors (Table 10.2). #### What is a risk factor? A risk factor can be an aspect of personal behaviour or life style, an environmental exposure, or an inborn or inherited characteristic that changes the susceptibility to periodontal disease. It can also be a local factor which increases the infection of a site. #### Types of risk factors for periodontal disease There are two major classes of risk factors for periodontal disease. 1. **Local factors** such as overhanging restorations and root caries that tend to allow for plaque accumulation and hence result in more periodontal disease. Other local risk factors for periodontal disease include pocket depth, intrabony pockets especially involving furcations, and root canal infections. 2. **Systemic factors** that affect the entire body, such as cigarette smoking, diabetes mellitus and genetic factors (Table 10.2). University logo featuring a shield with a swan and books, alongside the text 'THE UNIVERSITY OF WESTERN AUSTRALIA'. # Other used terms ## Predisposing Factors Predisposing factors might increase the probability of disease occurrence and usually have localised effects. These factors include anything, which retains or **hinders** the removal of dental plaque: - dental calculus - overhangs restorations, - subgingival restorations, - subgingival restoration margins, - open contact points, - partial dentures, - tilted/rotated/crowded teeth, - bulbous crowns, - grooves on teeth and more. ## Modifying Factors Modifying factors tend to act in a systemic fashion, which will alter the nature of a disease. A modifying factor can alter the nature or course of the inflammatory response to the plaque by modifying: - The susceptibility of disease, - Plaque microbiota, - Clinical presentation of periodontal disease, - Disease progression and - Response to treatment #### Predisposing Factors Predisposing factors might increase the probability of disease occurrence and usually have localised effects. These factors include anything which retains or **hinders** the removal of dental plaque: - dental calculus - overhangs restorations - subgingival restorations - subgingival restoration margins - open contact points - partial dentures - tilted/rotated/crowded teeth - bulbous crowns - grooves on teeth and more. #### Modifying Factors Modifying factors tend to act in a systemic fashion, which will alter the nature of a disease. A modifying factor can alter the nature or course of the inflammatory response to the plaque by modifying: - The susceptibility of disease - Plaque microbiota - Clinical presentation of periodontal disease - Disease progression - Response to treatment University logo for The University of Western Australia featuring a shield with a swan and books. # SYSTEMIC MODIFYING FACTORS FOR PERIODONTAL DISEASE **Diabetes** **Smoking** **Puberty** **Menopause** **Pregnancy** ### EFFECTS ON * Physiological response * Vascular system * Inflammatory response * Immune system * Tissue repair * Microbiota?     #### Systemic Modifying Factors for Periodontal Disease - Diabetes - Smoking - Puberty - Menopause - Pregnancy #### Effects on - Physiological response - Vascular system - Inflammatory response - Immune system - Tissue repair - Microbiota? Anatomical diagram of a heart showing internal chambers and valves. The image is illustrative in nature. Illustration of a coronary artery with a stent inserted. The caption explains that the CYPHER™ stent releases Sirolimus to prevent reblockage. Diagram depicting immune cell activity. A large green cell (likely a macrophage) contains a grey 'Infected Cell' and is interacting with other cellular elements, illustrating the inflammatory or immune response context. Comparative illustration of two feet labeled 'Normal' and 'Diabetic risk'. The diabetic foot shows visible vascular damage and tissue loss, demonstrating the systemic effects mentioned in the text. **The University of Western Australia** **Periodontal Medicine** **Definition of periodontal medicine** We view the term periodontal medicine, as first suggested by Offenbacher (7), to be a broad term that defines a rapidly emerging branch of periodontology focusing on the wealth of new data establishing a Willians & Offenbacher 2000 strong relationship between periodontal health or disease and systemic health or disease. This means a two-way relationship in which periodontal disease in an individual may be a powerful influence on an individual's systemic health or disease as well as the more customarily understood role that systemic disease may have in influencing an individual's periodontal health or disease. Logically included in this definition would be new diagnostic and treatment strategies that recognize the relationship between periodontal disease and systemic disease.   #### Definition of periodontal medicine We view the term periodontal medicine, as first suggested by Offenbacher (7), to be a broad term that defines a rapidly emerging branch of periodontology focusing on the wealth of new data establishing a strong relationship between periodontal health or disease and systemic health or disease. This means a two-way relationship in which periodontal disease in an individual may be a powerful influence on an individual's systemic health or disease as well as the more customarily understood role that systemic disease may have in influencing an individual's periodontal health or disease. Logically included in this definition would be new diagnostic and treatment strategies that recognize the relationship between periodontal disease and systemic disease. *Willians & Offenbacher 2000* Clinical photo of a chattering teeth toy used to demonstrate periodontal disease (gum inflammation and tooth mobility). Figure showing five anatomical models of the human body illustrating different systems: respiratory, skeletal, muscular, digestive, and circulatory. This visual supports the concept of systemic health relationships mentioned in the text. **Periodontal Medicine** SYSTEMIC DISEASES → PERIODONTITIS More than a 100 systemic diseases/conditions and 500 medications have oral manifestations. Kane, 2017 SYSTEMIC DISEASES ← PERIODONTITIS **EFP** European Federation of Periodontology DOSSIER ON PERIODONTAL DISEASE Periodontal Health for a Better Life  **SYSTEMIC DISEASES → PERIODONTITIS** More than a 100 systemic diseases/conditions and 500 medications have oral manifestations. *Kane, 2017* **SYSTEMIC DISEASES ← PERIODONTITIS** **EFP** European Federation of Periodontology DOSSIER ON PERIODONTAL DISEASE Periodontal Health for a Better Life A labelled diagram illustrating the systemic effects of periodontal disease. The image features a central vertical cross-section of a tooth and gingiva. An orange line extends from the gum tissue to various organ icons representing different body systems, including the heart, lungs, stomach/intestines, and joints, visually demonstrating that 'Periodontal Disease can cause tooth loss and affect the rest of the body'. On the left side, there is a logo for the European Federation of Periodontology (EFP) with the text 'DOSSIER ON PERIODONTAL DISEASE'. On the right, a circular inset provides a magnified view of the periodontal pocket area. # DIABETES ## The University of Western Australia High level of blood glucose due to absolute or relative lack of hormone insulin ### **TYPE 1 DM** * Autoimmune destruction of pancreatic β-cells * Leads to total loss of insulin production * Usually diagnosed in children and adolescents ### **TYPE 2 DM** * Develop resistance to insulin with reduced β-cell function * Reduced insulin production, but retains ability for some insulin production * After 40 years old & associated with obesity GESTATIONAL (unspecified) (Imagine the logo as if it were the text on the page) The University of Western Australia High level of blood glucose due to absolute or relative lack of hormone insulin #### Type 1 DM - Autoimmune destruction of pancreatic β-cells - Leads to total loss of insulin production - Usually diagnosed in children and adolescents #### Type 2 DM - Develop resistance to insulin with reduced β-cell function - Reduced insulin production, but retains ability for some insulin production - After 40 years old & associated with obesity #### Gestational (unspecified) The official logo of The University of Western Australia, featuring a shield with a swan emblem and the university name in blue text. # PREVALENCE OF DIABETES - Over 250 million worldwide (2007) - Rates have doubled over past 20 years www.worlddiabetesday.org **11**  - Over 250 million worldwide (2007) - Rates have doubled over past 20 years Bar chart titled 'PREVALENCE OF DIABETES' showing diabetes prevalence rates in various regions. The chart includes a legend indicating light blue bars represent the year 2000 and dark blue bars represent 2005. Regions shown include United States and Canada, Europe, Middle East, Sub-Saharan Africa, Latin America and the Caribbean, India, Southeast Asia, China, Australia, and others with corresponding percentage values. - FATIGUE - INFECTIONS - VISION ALTERATION - WEAKNESS - HYPERGLYCEMIA - PRURITUS (Itchy) - POLYPHAGIA (xs eating) - POLYURIA <img>A diabetes awareness graphic showing symptoms including fatigue, infections, blurred vision, weight loss, slow-healing wounds, frequent urination, hunger, sexual problems, vaginal infections, and numbness. <img>  - FATIGUE - INFECTIONS - VISION ALTERATION - WEAKNESS - HYPERGLYCEMIA - PRURITUS (Itchy) - POLYPHAGIA (xs eating) - POLYURIA Educational figure composed of a grid of nine panels illustrating clinical symptoms of diabetes. The main title 'DIABETES' is prominent at the top with the subtitle 'KNOW THE SYMPTOMS'. Panels depict: 'Always tired' (fatigue), 'Frequent urination' (polyuria), 'Sudden weight loss', 'Wounds that won't heal' (infections/weakness), 'Always hungry' (polyphagia), 'Sexual problems', 'Blurry vision' (vision alteration), 'Vaginal infections' (infections/pruritus), and 'Numb or tingling hands or feet' (neuropathy). <br> <br> **PERIODONTAL ABSCCESS** <br> <br> <br> <br> <br> <br> <br> Diabetics are more susceptible to periodontal abcesses (Ueta et al 1993) <br> <br> 13  **PERIODONTAL ABSCESS** Diabetics are more susceptible to periodontal abscesses (Ueta et al 1993) Clinical photograph showing an anterior view of upper teeth and gingiva. The image displays a periodontal abscess characterized by localized swelling (edema) on the attached gingiva above the lateral incisor/canine region. There is visible erythema and a small area of bleeding or ulceration associated with the abscess site. **DIAGNOSIS & SCREENING** **HbA1c (percent)** **Fasting Plasma** **Glucose** **(mg/dL)** **Oral Glucose** **Tolerance Test** **(mg/dL)** | | HbA1c | Fasting Plasma Glucose | Oral Glucose Tolerance Test | |---|---|---|---| | **Diabetes** | ≥ 6.5 | ≥ 126 | ≥ 200 | | **Prediabetes** | 5.7 – 6.4 | 100 - 125 | 140 – 199 | | **Normal** | ~ 5.7 | ≤ 99 | ≤ 139 | 14  **DIAGNOSIS & SCREENING** | | HbA1c | Fasting Plasma Glucose (mg/dL) | Oral Glucose Tolerance Test (mg/dL) | |---|---|---|---| | **Diabetes** | ≥ 6.5 | ≥ 126 | ≥ 200 | | **Prediabetes** | 5.7 – 6.4 | 100 - 125 | 140 – 199 | | **Normal** | ~ 5.7 | ≤ 99 | ≤ 139 | A clinical table titled 'DIAGNOSIS & SCREENING' showing diagnostic criteria for Diabetes, Prediabetes, and Normal ranges. The table has columns for HbA1c (percent), Fasting Plasma Glucose (mg/dL), and Oral Glucose Tolerance Test (mg/dL). Rows show: Diabetes (HbA1c ≥ 6.5, FPG ≥ 126, OGTT ≥ 200); Prediabetes (HbA1c 5.7–6.4, FPG 100–125, OGTT 140–199); Normal (~5.7, ≤99, ≤139). <table style="width:100%;text-align:left;font-family:Arial,sans-serif;font-size:14px;vertical-align:middle;"> <tr> <td colspan="2"><strong>HOW TO MEASURE GLYCEMIC CONTROL</strong></td> </tr> <tr> <td colspan="2" style="text-align:right;"><a href="#"><img src="https://upload.wikimedia.org/wikipedia/commons/thumb/c/c6/The_University_of_Western_Australia_coat_of_arms.svg/440px-The_University_of_Western_Australia_coat_of_arms.svg.png" width="80" height="42" style="margin-bottom:5px;"></a></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:10px;"></td> </tr> <tr> <td colspan="2" style="height:15px;"></td> </tr> <tr> <td colspan="2"><strong>GLYCOSYLATED HAEMOGLOBIN MOLECULE <br>(HbA1c)</strong></td> </tr> <tr> <td colspan="2"><strong>BINDING OF GLUCOSE TO HEMOGLOBIN</strong></td> </tr> <tr> <td colspan="2"><strong>% HbA1c INCREASES WITH HIGHER SERUM <br>GLUCOSE DURING LIFE OF RBC</strong></td> </tr> <tr> <td colspan="2"><strong>LIFE SPAN OF RBC – 100-120 DAYS</strong></td> </tr> <tr> <td colspan="2"><strong>New measurements at 3-4 months</strong></td> </tr> <tr> <td colspan="2" style="height:16px;"></td> </tr> <tr> <td colspan="2" style="height:16px;"></td> </tr> <tr> <td colspan="2" style="height:16px;"></td> </tr> <tr> <td colspan="2" style="height:16px;"></td> </tr> <tr> <td colspan="2" style="height:16px;"></td> </tr> <tr> <td colspan="2"><strong><span style="font-weight:400; font-style:italic;">15</span></strong></td> </tr> </table>  **HOW TO MEASURE GLYCEMIC CONTROL** **GLYCOSYLATED HAEMOGLOBIN MOLECULE (HbA1c)** **BINDING OF GLUCOSE TO HEMOGLOBIN** **% HbA1c INCREASES WITH HIGHER SERUM GLUCOSE DURING LIFE OF RBC** **LIFE SPAN OF RBC – 100-120 DAYS** **New measurements at 3-4 months** A vertical diagram illustrating A1c Test Results. It features a central column with three colored targets (red at the top, yellow in the middle, green at the bottom) connected by arrows pointing upwards and downwards. Each target is labeled with a category and percentage range: 'Diabetes 6.5% or higher' (red), 'Prediabetes 5.7 to 6.4%' (yellow), and 'Normal Below 5.7%' (green). The diagram visually represents the scale of glycemic control. <b>COMPLICATIONS AND TREATMENT</b> <b>PERIODONTAL DISEASE</b> has been called the 6th complication of diabetes (Löe 1993) Tratamento • Redução das taxas de glicose a fim de prevenir sinais/sintomas e complicações – Controle glicêmico - manutenção de níveis controlados a fim de prevenir complicações 16  **COMPLICATIONS AND TREATMENT** **PERIODONTAL DISEASE** has been called the 6th complication of diabetes (Löe 1993) **Treatment** - Redução das taxas de glicose a fim de prevenir sinais/sintomas e complicações – Controle glicêmico - manutenção de níveis controlados a fim de prevenir complicações Medical diagram titled 'Diabetes' and 'Complications of Chronic Hyperglycemia'. It features a central illustration of the human body with highlighted vascular systems. Yellow callout boxes point to specific regions: 'Retinopathy' (pointing to the head/eye area), 'Stroke', 'Heart disease' (pointing to the chest), 'Nephropathy' (pointing to the kidneys), 'Peripheral neuropathy' (pointing to the legs), and 'Autonomic neuropathy' (pointing to the torso). Each box lists associated symptoms or conditions. # RELATIONSHIP BETWEEN DIABETES & PERIODONTAL DISEASE 17  Clinical photo showing inflamed gingival tissue with erythema and edema surrounding the cervical areas of multiple teeth. A tooth is marked with an asterisk (*), indicating a specific site of interest or pathology related to periodontal disease. # RELATIONSHIP BETWEEN DIABETES & PERIODONTAL DISEASE **The University of Western Australia** * Approximately **40%** of adult Pima Indians in Arizona have type 2 diabetes. * A comparison of individuals with and without diabetes in this Native American tribe showed a clear increase in the prevalence of destructive periodontitis as well as a **15%** increase in edentulousness among patients with diabetes 18   - Approximately **40%** of adult Pima Indians in Arizona have type 2 diabetes. - A comparison of individuals with and without diabetes in this Native American tribe showed a clear increase in the prevalence of destructive periodontitis as well as a **15%** increase in edentulousness among patients with diabetes. Black and white historical photo showing two Pima Indians in Arizona. One is seated on a large rock by a riverbank, while the other stands nearby. The image illustrates the demographic group discussed in the text regarding diabetes prevalence. Black and white historical photo showing a person sitting in front of a traditional thatched dwelling or hut. This visual provides context for the lifestyle and environment of the Native American tribe mentioned in the study. # RELATIONSHIP BETWEEN DIABETES & PERIODONTAL DISEASE * Periodontitis' prevalence is increased in diabetics * **2.8-3.4**X increase in risk for periodontitis * Poorly controlled (type 2 DM) had **X11** increased risk for periodontitis compared to non-diabetic * Glycemic control is related to periodontitis in a dose-response manner (the level of hyperglycemia is related to periodontitis) * Diabetics with complications have poorer periodontal conditions * Well controlled diabetics had similar risk for periodontitis to non-diabetics   - Periodontitis' prevalence is increased in diabetics. - **2.8-3.4**X increase in risk for periodontitis. - Poorly controlled (type 2 DM) had **X11** increased risk for periodontitis compared to non-diabetic. - Glycemic control is related to periodontitis in a dose-response manner (the level of hyperglycemia is related to periodontitis). - Diabetics with complications have poorer periodontal conditions. - Well controlled diabetics had similar risk for periodontitis to non-diabetics. Graphic illustration showing an 'X11' multiplier symbol with explosive effects, visually representing the 11-fold increased risk for periodontitis in poorly controlled Type 2 diabetics mentioned in the adjacent text. Clinical photograph of a human mouth displaying severe periodontitis, characterized by inflamed red gingiva and visible calculus deposits on the teeth. - Degree of glycemic/metabolic control - Age - Duration of DM - Severity of DM - Complications     - Degree of glycemic/metabolic control - Age - Duration of DM - Severity of DM - Complications A conceptual flow diagram illustrating the relationship between two conditions. On the left is a green rectangular box labeled 'Diabetes', and on the right is a blue rectangular box labeled 'Periodontitis'. A large orange arrow points from the Diabetes box to the Periodontitis box, indicating a causal link or progression. A text-based list of risk factors associated with the condition shown in the diagram above. The list includes: Degree of glycemic/metabolic control, Age, Duration of DM, and Severity of DM - Complications. A clinical photograph showing a close-up view of teeth with significant periodontal disease. The gingiva appears red, swollen, and inflamed, particularly at the gum line. There is visible recession exposing the tooth roots and darkened pockets between the teeth, consistent with severe periodontitis. A second clinical photograph, positioned next to the first one, also depicting severe periodontitis. It shows similar signs of inflammation, redness, and gingival recession around the teeth, providing visual evidence of the condition discussed in the slide. # WHY ARE DIABETICS MORE SUSCEPTIBLE TO PERIODONTAL DISEASE? 21 University logo for The University of Western Australia, featuring a shield with a swan and text. # DO DIABETICS HAVE DIFFERENT BACTERIA? * Earlier studies in 1980s & 1990s (using culture) found higher levels of **SPIROCHETES** & **MOTILE RODS** in diabetics (vs healthy controls) * More recent studies (using molecular techniques such as PCR) found similar levels of putative periodontal pathogens between diabetics & non-diabetics * **CONCLUDE: increase in susceptibility to periodontal disease in diabetics is NOT due to differences in composition of the microbiota**  - Earlier studies in 1980s & 1990s (using culture) found higher levels of **SPIROCHETES** & **MOTILE RODS** in diabetics (vs healthy controls). - More recent studies (using molecular techniques such as PCR) found similar levels of putative periodontal pathogens between diabetics & non-diabetics. - **CONCLUDE: increase in susceptibility to periodontal disease in diabetics is NOT due to differences in composition of the microbiota.** A circular microscopic image showing several green-stained rod-shaped bacteria (bacteroids), illustrating the subject of periodontal pathogens mentioned in the text. **HOST RESPONSE IN DIABETICS** Impaired neutrophil function: • Impaired neutrophil adherence, chemotaxis & phagocytosis (produce less oxygen radicals) • **Bacteria persists in periodontal pocket** <p align="right">23</p> **Impaired neutrophil function:** - Impaired neutrophil adherence, chemotaxis & phagocytosis (produce less oxygen radicals). - **Bacteria persists in periodontal pocket.** Polymorphonuclear Leukocyte Function **The increased susceptibility of patients with diabetes to infection has been hypothesized as being caused by polymorphonuclear leukocyte (PMN) deficiencies that result in impaired chemotaxis, defective phagocytosis, or impaired adherence.** In patients with poorly controlled diabetes, the functions of PMNs, monocytes, and **macrophages** are impaired. As a result, the primary defense mounted by PMNs against periodontal pathogens is diminished, and bacterial proliferation is more likely. No alteration of **immunoglobulin A (IgA)**, G (IgG), or M (IgM) has been found in patients with diabetes. **Polymorphonuclear Leukocyte Function** The increased susceptibility of patients with diabetes to infection has been hypothesized as being caused by polymorphonuclear leukocyte (PMN) deficiencies that result in impaired chemotaxis, defective phagocytosis, or impaired adherence. In patients with poorly controlled diabetes, the functions of PMNs, monocytes, and **macrophages** are impaired. As a result, the primary defense mounted by PMNs against periodontal pathogens is diminished, and bacterial proliferation is more likely. No alteration of **immunoglobulin A (IgA)**, G (IgG), or M (IgM) has been found in patients with diabetes. University logo for The University of Western Australia. - Impaired immune response in periodontium of diabetics suggested in 1960s - Structural changes: with sustained hyperglycemia, proteins become **irreversibly glycated** to form **advanced glycation end products (AGEs)** - Formation of AGEs also occurs in the periodontium - Higher levels found in diabetic patients - AGEs activate a receptor known as "**receptor for AGEs**" (RAGE) found on the surface of smooth muscle cells, endothelial cells & monocytes/macrophages & gingival tissues of type 2 diabetics - Hyperglycemia results in increased RAGE expression (Frantzis et al. 1971; Schmidt et al. 1996; 1999) - Impaired immune response in periodontium of diabetics suggested in 1960s. - Structural changes: with sustained hyperglycemia, proteins become **irreversibly glycated** to form **advanced glycation end products (AGEs)**. - Formation of AGEs also occurs in the periodontium. - Higher levels found in diabetic patients. - AGEs activate a receptor known as "**receptor for AGEs**" (RAGE) found on the surface of smooth muscle cells, endothelial cells & monocytes/macrophages & gingival tissues of type 2 diabetics. - Hyperglycemia results in increased RAGE expression. (Frantzis et al. 1971; Schmidt et al. 1996; 1999) The University of Western Australia logo featuring a shield with a swan and text. **Altered Collagen Metabolism** Chronic hyperglycemia **impairs** *collagen* structure and function, which may directly impact the integrity of the periodontium. **Decreased** collagen synthesis, osteoporosis, and a **reduction** in alveolar bone height have been demonstrated in diabetic animals. 97, 233 **Altered Collagen Metabolism** Chronic hyperglycemia **impairs** *collagen* structure and function, which may directly impact the integrity of the periodontium. **Decreased** collagen synthesis, osteoporosis, and a **reduction** in alveolar bone height have been demonstrated in diabetic animals. 97, 233 University logo for The University of Western Australia located in the top right corner. Chronic hyperglycemia **adversely affects** the synthesis, maturation, and maintenance of collagen and extracellular matrix. In the hyper-glycemic state, numerous proteins and matrix molecules undergo a nonenzymatic glycosylation, thereby resulting in *advanced gly-compression end-products (AGEs)*. The formation of AGEs occurs at normal glucose levels as well; however, in hyperglycemic environments, AGE formation is excessive. Many types of molecules are affected, including proteins, lipids, and carbohydrates. Collagen is cross-linked by AGE formation, which makes the collagen less soluble and less likely to be normally repaired or replaced. Cellular migration through cross-linked collagen is impeded, and, perhaps more importantly, tissue integrity is impaired as a result of damaged collagen that remains in the tissues for longer periods (i.e., collagen is not renewed at a normal rate).$^{113}$ As a result, collagen in the tissues of patients with poorly controlled diabetes is older and more susceptible to pathogenic breakdown (i.e., less resistant to destruction by periodontal infections). Chronic hyperglycemia **adversely affects** the synthesis, maturation, and maintenance of collagen and extracellular matrix. In the hyper-glycemic state, numerous proteins and matrix molecules undergo a nonenzymatic glycosylation, thereby resulting in *advanced gly-compression end-products (AGEs)*. The formation of AGEs occurs at normal glucose levels as well; however, in hyperglycemic environments, AGE formation is excessive. Many types of molecules are affected, including proteins, lipids, and carbohydrates. Collagen is cross-linked by AGE formation, which makes the collagen less soluble and less likely to be normally repaired or replaced. Cellular migration through cross-linked collagen is impeded, and, perhaps more importantly, tissue integrity is impaired as a result of damaged collagen that remains in the tissues for longer periods (i.e., collagen is not renewed at a normal rate).$^{113}$ As a result, collagen in the tissues of patients with poorly controlled diabetes is older and more susceptible to pathogenic breakdown (i.e., less resistant to destruction by periodontal infections). AGEs and receptors for AGEs (RAGEs) play a central role in the classic complications of diabetes,$^{36}$ and they may play a significant role in the progression of periodontal disease as well. Poor glycemic control, with the associated increase in AGEs, renders the periodontal tissues more susceptible to destruction.$^{232}$ The cumulative effects of altered cellular response to local factors, impaired tissue integrity, and altered collagen metabolism undoubtedly play a significant role in the susceptibility of patients with diabetes to infections and destructive periodontal disease. AGEs and receptors for AGEs (RAGEs) play a central role in the classic complications of diabetes,$^{36}$ and they may play a significant role in the progression of periodontal disease as well. Poor glycemic control, with the associated increase in AGEs, renders the periodontal tissues more susceptible to destruction.$^{232}$ The cumulative effects of altered cellular response to local factors, impaired tissue integrity, and altered collagen metabolism undoubtedly play a significant role in the susceptibility of patients with diabetes to infections and destructive periodontal disease. The logo for The University of Western Australia, featuring a blue shield with a swan and open books. **Stimulates monocytes & macrophages to proliferate,** **upregulate pro-inflammatory cytokines such as IL-1β,** **PgE2 and TNF-α & produce free O2 radicals** These free O2 radicals & pro-inflammatory cytokines contribute to the pathogenesis of periodontal disease Direct cell/host damage (Schmidt et al. 1996; 1999; Engebretson et al. 2004; Katz et al. 2005) 29 **Stimulates monocytes & macrophages to proliferate, upregulate pro-inflammatory cytokines such as IL-1β, PgE2 and TNF-α & produce free O2 radicals** These free O2 radicals & pro-inflammatory cytokines contribute to the pathogenesis of periodontal disease. Direct cell/host damage. (Schmidt et al. 1996; 1999; Engebretson et al. 2004; Katz et al. 2005) The University of Western Australia institutional logo featuring a shield with a swan and open books. **HOST RESPONSE IN DIABETICS** Higher levels of inflammatory cytokines & mediators found in GCF of diabetics Monocytes & macrophages with a destructive phenotype  Higher levels of inflammatory cytokines & mediators found in GCF of diabetics. Monocytes & macrophages with a destructive phenotype. Microscopic image showing a large, textured red cell (likely a macrophage) surrounded by smaller green rod-shaped bacteria, illustrating the interaction between host cells and pathogens.  Labelled conceptual diagram illustrating the bidirectional relationship between Diabetes mellitus and Periodontitis. The diagram is organized into two main pathways originating from 'Diabetes mellitus' (top) and converging on 'Periodontitis' (bottom). The left pathway details the effects of Insulin resistance leading to inflammatory cytokines (IL-1, IL-6, TNF-α), which are influenced by Bacterial Factors (LPS). The right pathway shows Hyperglycemia leading to oxidative stress markers (ROS, AGEs) and systemic inflammation, resulting in an Exaggerated Immune response and Glycation. A central box labeled 'Common risks' lists shared contributors: Obesity, age, sex, genetic, smoking, and socio economic factors. Arrows indicate feedback loops and causal relationships between these nodes. **HEALING RESPONSE** THE UNIVERSITY OF WESTERN AUSTRALIA In a hyperglycemic state, repair process in periodontium is compromised due to: - Gingival fibroblasts produce less collagen & more MMPs - Recently synthesized collagen is rapidly degraded by elevated levels of active MMPs - Decreased osteoblast proliferation & collagen production - Increased rate of apoptosis of fibroblasts & osteoblasts (Loder 1988; Inaba et al. 1999; Lu et al. 2003; Gooch et al. 2000; He et al. 2004; Liu et al. 2004) 32 **HEALING RESPONSE** In a hyperglycemic state, repair process in periodontium is compromised due to: - Gingival fibroblasts produce less collagen & more MMPs. - Recently synthesized collagen is rapidly degraded by elevated levels of active MMPs. - Decreased osteoblast proliferation & collagen production. - Increased rate of apoptosis of fibroblasts & osteoblasts. (Loder 1988; Inaba et al. 1999; Lu et al. 2003; Gooch et al. 2000; He et al. 2004; Liu et al. 2004) University logo for The University of Western Australia. # HEALING RESPONSE 33   Clinical photo showing a wound on the sole and heel of a foot with a scale bar attached. Clinical photo showing a large wound on a leg with a scale bar attached. # HOST RESPONSE IN DIABETICS **Together, the impaired immune response, poorer healing & increased destruction may explain the greater propensity of diabetics to have more severe periodontal disease** (Loder 1988; Inaba et al. 1999; Lu et al. 2003; Gooch et al. 2000; He et al. 2004; Liu et al. 2004) 34  Together, the impaired immune response, poorer healing & increased destruction may explain the greater propensity of diabetics to have more severe periodontal disease. (Loder 1988; Inaba et al. 1999; Lu et al. 2003; Gooch et al. 2000; He et al. 2004; Liu et al. 2004) A cartoon illustration featuring a green anthropomorphic hand with glasses and a tie in the foreground. A speech bubble from the hand contains text reading 'don't let AGE RAGE claim you! watch for the signs'. In the background, a pink cat-like character wearing a party hat sits on an office chair. INFLUENCE OF **PERIODONTAL DISEASE** ON **DIABETES** --- **35**  **Influence of Periodontal Disease on Diabetes** Clinical photograph of a patient's anterior dentition demonstrating severe periodontal disease. The image shows significant gingival inflammation (redness), recession exposing root surfaces, and heavy accumulation of supra- and subgingival calculus (tartar) on the teeth. The University of Western Australia INFLUENCE OF PERIODONTAL DISEASE ON DIABETES **Proposed mechanism:** periodontal infection may add to systemic inflammation which induces insulin resistance **High levels of cytokines** can affect efficacy of insulin receptor Insulin Glucose Insulin receptors Glut-4 Defect in signaling to Glut-4 Diamond muscle cells Glucose transporters Diminished glucose uptake 36   **Proposed mechanism:** periodontal infection may add to systemic inflammation which induces insulin resistance **High levels of cytokines** can affect efficacy of insulin receptor - Insulin - Glucose - Insulin receptors - Glut-4 - Defect in signaling to Glut-4 - Diamond muscle cells - Glucose transporters - Diminished glucose uptake Clinical photograph of a tooth exhibiting severe periodontal disease. The image shows the gum line receding significantly below the crown of the tooth, exposing the root surface. There appears to be inflammation (redness) in the surrounding tissue and potential calculus or plaque accumulation near the base of the tooth. Biological diagram illustrating the mechanism of insulin resistance in Type 2 diabetes within muscle cells. The diagram depicts 'Insulin' molecules interacting with 'Insulin receptors'. A red 'X' indicates a 'Defect in signaling to Glut-4', preventing the activation of 'Glucose transporters'. This results in 'Diminished glucose uptake' by the cell from the surrounding environment containing 'Glucose'. Periodontitis Modified by Systemic Factors **Diabetes Mellitus** The University of Western Australia **eFig. 7.109** Severe gingival inflammation and periodontal abscess occurred in a 26-year-old woman with type 1 **diabetes mellitus**. Notice the extrusion of the maxillary left central incisor caused by alveolar bone loss. **eFig. 7.110** Severe inflammation, pus formation, and periodontal breakdown occurred in a 34-year-old man with uncontrolled type 1 **diabetes mellitus**.   #### Periodontitis Modified by Systemic Factors: Diabetes Mellitus **eFig. 7.109** Severe gingival inflammation and periodontal abscess occurred in a 26-year-old woman with type 1 **diabetes mellitus**. Notice the extrusion of the maxillary left central incisor caused by alveolar bone loss. **eFig. 7.110** Severe inflammation, pus formation, and periodontal breakdown occurred in a 34-year-old man with uncontrolled type 1 **diabetes mellitus**. Clinical photo showing severe gingival inflammation and a periodontal abscess on the upper front teeth of a patient with type 1 diabetes. The caption notes the extrusion of the maxillary left central incisor due to bone loss. Clinical photo showing severe inflammation, pus formation, and periodontal breakdown in the mouth of a 34-year-old man with uncontrolled type 1 diabetes mellitus. **THE UNIVERSITY OF WESTERN AUSTRALIA** **eFig. 7.111** Two views show the dentition of a 14-year-old girl who was referred with a complaint of tooth mobility. She had spontaneous loss of teeth #11, #31, #41, and #46 in the past 2 years. The patient had advanced bone loss despite a minimal amount of bacterial plaque and degree 3 mobility of many teeth. She was diagnosed with type 1 diabetes mellitus on consultation.    **eFig. 7.111** Two views show the dentition of a 14-year-old girl who was referred with a complaint of tooth mobility. She had spontaneous loss of teeth #11, #31, #41, and #46 in the past 2 years. The patient had advanced bone loss despite a minimal amount of bacterial plaque and degree 3 mobility of many teeth. She was diagnosed with type 1 diabetes mellitus on consultation. Clinical intraoral photograph showing the anterior maxillary dentition of a patient exhibiting significant gingival inflammation (redness) and severe tooth mobility/displacement. The central incisors are tilted and crowded. Dental panoramic radiograph (OPG) showing the mandibular and maxillary arches. The image reveals advanced periodontal bone loss and evidence of spontaneous tooth loss in the anterior regions, consistent with the clinical presentation described in the caption. Figure caption describing the case study presented in the images above, noting the diagnosis of Type 1 Diabetes Mellitus as a cause for the severe periodontitis symptoms in a 14-year-old female. **INFLUENCE OF PERIODONTAL DISEASE ON DIABETES** - Periodontal infection contributes to poorer glycaemic control & increased risk for diabetic complications in diabetics (Thorstensson et al. 1996; Saremi et al. 2005; Schultis et al. 2007)  - Periodontal infection contributes to poorer glycaemic control & increased risk for diabetic complications in diabetics (Thorstensson et al. 1996; Saremi et al. 2005; Schultis et al. 2007) A complex flowchart illustrating the bidirectional relationship between Periodontitis and Diabetes. The diagram includes labeled boxes for Obesity (orange), Adipokines, RANKL/OPG ratio, AGE/RAGE interaction, Altered PMN function, ROS, Microvascular damage, CVD, PVD, Retinopathy, Nephropathy, Neuropathy, Smoking, Periodontal Microbiota, Citokines (IL-1, IL-6, PGE2, TNF-α), Matrix Metalloproteinases, and Diabetes. Arrows indicate causal or correlational links between these elements. **Cukurova University, Periodontology Dept. Archive** **THE UNIVERSITY OF** **WESTERN** **AUSTRALIA** ©Cukurova University, Periodontology Dept. Archive ©Cukurova University, Periodontology Dept. Archive **eFig. 7.112** Three views show alveolar bone loss and severe inflammation with spontaneous bleeding, pus formation, and abscess in a 56-year-old man with *type 2 diabetes* mellitus who used external insulin for 12 years.    **eFig. 7.112** Three views show alveolar bone loss and severe inflammation with spontaneous bleeding, pus formation, and abscess in a 56-year-old man with *type 2 diabetes* mellitus who used external insulin for 12 years. Clinical photo showing severe periodontal inflammation with spontaneous bleeding and pus formation in a patient with type 2 diabetes. Close-up clinical photo of an abscess or severe gingival swelling with visible bleeding, demonstrating advanced periodontal disease. Dental radiograph (panoramic X-ray) showing alveolar bone loss and severe periodontal destruction consistent with the clinical findings. **THE UNIVERSITY OF WESTERN AUSTRALIA** A ©Gukurova University, Periodontology Dept. Archive B ©Cukurova University, Periodontology Dept. Archive C ©Gukurova University, Periodontology Dept. Archive D ©Gukurova University, Periodontology Dept. Archive **eFig. 7.113** A 28-year-old woman with uncontrolled type 1 **diabetes** mellitus was referred with complaints of rapid mobility of teeth, severe pain, spontaneous pus, and several abscesses. Her fasting glucose level was 486 mg/dL on the day of referral. (A) Although the lesions resembled abscesses of periodontal origin, the pocket depths and attachment levels were within normal levels. (B) The computed tomography findings and consultation with the infection department confirmed the diagnosis of osteomyelitis. (C) View of the patient after 1 week of blood glucose control in the intensive care unit and hyperbaric oxygen therapy. (D) Although the lesions healed uneventfully, severe malocclusion was evident at the 1-year follow-up examination.     **eFig. 7.113** A 28-year-old woman with uncontrolled type 1 **diabetes** mellitus was referred with complaints of rapid mobility of teeth, severe pain, spontaneous pus, and several abscesses. Her fasting glucose level was 486 mg/dL on the day of referral. (A) Although the lesions resembled abscesses of periodontal origin, the pocket depths and attachment levels were within normal levels. (B) The computed tomography findings and consultation with the infection department confirmed the diagnosis of osteomyelitis. (C) View of the patient after 1 week of blood glucose control in the intensive care unit and hyperbaric oxygen therapy. (D) Although the lesions healed uneventfully, severe malocclusion was evident at the 1-year follow-up examination. Clinical photo showing the patient's upper and lower dentition. The image highlights severe gingival inflammation with multiple abscesses (pus-filled swellings) on the maxillary anterior gum line. There is a significant gap in the central incisors. Computed tomography (CT) scan cross-section of the jaw. The image shows a large, dark radiolucent lesion (indicating bone loss/infection) in the maxilla, confirming the diagnosis of osteomyelitis mentioned in the text. Clinical photo taken after 1 week of treatment. The acute abscesses seen in panel A have resolved, but the gingiva remains red and inflamed. The teeth are still present. Clinical photo at the 1-year follow-up examination. Although the lesions healed uneventfully as stated in the caption, there is severe malocclusion evident due to missing teeth and spacing issues.  Clinical photograph showing a set of dental periodontal instruments (likely explorers or probes) arranged in a row. The handles are wrapped in various colors including grey, purple, pink, blue, green, yellow, orange, and red, while the working ends are metallic. **THE UNIVERSITY OF WESTERN AUSTRALIA** EFFECT OF PERIODONTAL TREATMENT IN DIABETICS • Limited evidence Non-surgical periodontal treatment: • Short-term studies suggest healing response to be similar in diabetics (well-controlled) compared to non-diabetics • Greater risk for relapse in poorly-controlled diabetics  #### Non-Surgical Periodontal Treatment - Limited evidence - Short-term studies suggest healing response to be similar in diabetics (well-controlled) compared to non-diabetics - Greater risk for relapse in poorly-controlled diabetics Clinical photo showing a close-up view of teeth with inflamed red gingiva and plaque accumulation being examined by a dental probe. The image illustrates the subject matter discussed in the text regarding periodontal treatment. **EFFECT OF PERIODONTAL TREATMENT IN DIABETICS** * Limited evidence Surgical periodontal treatment: * Healing response similar in diabetics (well-controlled) compared to non-diabetics * But diabetics may have an increased risk for post-surgical infection & impaired wound healing * No studies on efficacy of regenerative treatment in diabetics (since they are often excluded in clinical trials)  #### Surgical Periodontal Treatment - Limited evidence - Healing response similar in diabetics (well-controlled) compared to non-diabetics - But diabetics may have an increased risk for post-surgical infection & impaired wound healing - No studies on efficacy of regenerative treatment in diabetics (since they are often excluded in clinical trials) Clinical photograph showing a surgical periodontal procedure. The image displays an intraoral view with a dental instrument being used on exposed gingival tissue and a tooth root, illustrating the context of the text regarding healing response and post-surgical infection risks. INFLUENCE OF PERIODONTAL TREATMENT ON DIABETES 45 INFLUENCE OF PERIODONTAL TREATMENT ON DIABETES <file_utils.image2text:image2text> INTERVENTION TRIALS THE UNIVERSITY OF WESTERN AUSTRALIA • More studies (4/7) reported significant benefit of periodontal treatment • Improvements in glycaemic control after SRP +/- adjunctive systemic antibiotics of approx 1% in HbA1c (eg. 9 to 8%) 42 </file_utils.image2text> **INTERVENTION TRIALS** The University of Western Australia * More studies (4/7) reported significant benefit of periodontal treatment * Improvements in glycaemic control after SRP +/- adjunctive systemic antibiotics of approx 1% in HbA1c (eg. 9 to 8%) 42  #### Intervention Trials - More studies (4/7) reported significant benefit of periodontal treatment - Improvements in glycaemic control after SRP +/- adjunctive systemic antibiotics of approx 1% in HbA1c (eg. 9 to 8%) Clinical photo showing a dental professional in a white coat and mask performing a procedure on a patient reclined in a dental chair. **IMPACT OF CHANGE IN HbA1c LEVELS** **The University of Western Australia** • UK Prospective Diabetes Study (1993, 1998) showed that every percentage point decrease in HbA1c (eg. 9 to 8%) was associated with 25% reduction in diabetes-related deaths  #### Impact of Change in HbA1c Levels - UK Prospective Diabetes Study (1993, 1998) showed that every percentage point decrease in HbA1c (eg. 9 to 8%) was associated with 25% reduction in diabetes-related deaths Bar chart titled 'Lowering HbA1c Reduces Risk of Diabetic Complications: UKPDS'. The vertical axis represents 'Risk reduction (%) per 1% decrease in HbA1c' ranging from 0 to -50. Five colored bars display risk reduction values for specific endpoints: green bar for 'Any diabetes endpoint' (-12), orange bar for 'Microvascular endpoint' (-25), yellow bar for 'Myocardial infarction' (-16), purple bar for 'Retinopathy 0-12 years' (-21), and cyan bar for 'Albuminuria at 12 years' (-34). Each bar is accompanied by a P-value indicating statistical significance. Source cited at bottom: UK Prospective Diabetes Study Group. Lancet. 1998;352:837-853. **PERIODONTAL MANAGEMENT OF THE DIABETIC PATIENT** **The University of Western Australia** **Educate patients & their physicians:** * Diabetes (Type I, II & GDM) can affect periodontal health * Depends on diabetic control * Uncontrolled diabetics are at higher risk of periodontal destruction & also present with more severe periodontal disease * Diabetics have an altered host response to bacteria & poorer healing response * Periodontal infections can worsen glycaemic control & increase risk for diabetic complications * **2 way relationship** #### Educate Patients & Their Physicians - Diabetes (Type I, II & GDM) can affect periodontal health - Depends on diabetic control - Uncontrolled diabetics are at higher risk of periodontal destruction & also present with more severe periodontal disease - Diabetics have an altered host response to bacteria & poorer healing response - Periodontal infections can worsen glycaemic control & increase risk for diabetic complications - **2 way relationship** The official logo of The University of Western Australia, featuring a shield with a swan and open books. **PERIODONTAL MANAGEMENT OF THE DIABETIC PATIENT** • Evidence is limited, but with periodontal treatment diabetics heal just as well as non-diabetics • Disease recurrence may be higher in diabetics especially in patients with uncontrolled diabetes • **PRA risk assessment – increase frequency of SPT (3/12)** • Treatment of periodontal infections in diabetics MAY have a significant role in improving glycaemic control & **POTENTIALLY** reduce the burden of diabetic complications Tervonen et al. 1991; Wesfelt et al. 1996; Tervonen & Karjalainen 1997; Christgau et al. 1998, da Cruz et al. 2008 - Evidence is limited, but with periodontal treatment diabetics heal just as well as non-diabetics - Disease recurrence may be higher in diabetics especially in patients with uncontrolled diabetes - **PRA risk assessment – increase frequency of SPT (3/12)** - Treatment of periodontal infections in diabetics MAY have a significant role in improving glycaemic control & **POTENTIALLY** reduce the burden of diabetic complications Tervonen et al. 1991; Wesfelt et al. 1996; Tervonen & Karjalainen 1997; Christgau et al. 1998, da Cruz et al. 2008 University logo for The University of Western Australia, featuring the university crest and name in blue text. **Emerging evidence that diabetics have more chance to develop biological complications (mucositis and peri-implantitis).** Higher failure rates. No evidence of contra-indication to implant placement (unless uncontrolled diabetes) Glycemic control should be maintained. - Emerging evidence that diabetics have more chance to develop biological complications (mucositis and peri-implantitis). - Higher failure rates. - No evidence of contra-indication to implant placement (unless uncontrolled diabetes) - Glycemic control should be maintained. The University of Western Australia logo featuring a shield with a swan and the university name. Wagner *et al*. **International Journal of Implant Dentistry** (2022) 8:1 https://doi.org/10.1186/s40729-021-00399-8 International Journal of Implant Dentistry REVIEW Open Access Systematic review on diabetes mellitus and dental implants: an update Juliane Wagner* , Johannes H. Spille, Jörg Wiltfang and Hendrik Naujokat * Dental implant procedures represent a safe way of oral rehabilitation in patients with prediabetes or diabetes mellitus, as long as appropriate precautions can be adhered to. Accordingly, **under controlled conditions there is still no contraindication** for dental implant surgery in patients with diabetes mellitus or prediabetic conditions. 1528 10.1186/s40729-021-00399-8 **©** THE UNIVERSITY OF WESTERN AUSTRALIA Wagner *et al*. **International Journal of Implant Dentistry** (2022) 8:1 https://doi.org/10.1186/s40729-021-00399-8 **REVIEW** **Systematic review on diabetes mellitus and dental implants: an update** Juliane Wagner* , Johannes H. Spille, Jörg Wiltfang and Hendrik Naujokat - Dental implant procedures represent a safe way of oral rehabilitation in patients with prediabetes or diabetes mellitus, as long as appropriate precautions can be adhered to. - Accordingly, **under controlled conditions there is still no contraindication** for dental implant surgery in patients with diabetes mellitus or prediabetic conditions. The University of Western Australia logo featuring a shield with a swan and the university name. # Our lecture today… Our lecture today… The official logo of The University of Western Australia. It features a shield containing three open books above a black swan (the university's mascot) on a yellow background, with the motto 'Sine die' visible below the shield. Thank you!!! THE UNIVERSITY OF WESTERN AUSTRALIA SEEK WISDOM Thank you!!! THE UNIVERSITY OF WESTERN AUSTRALIA SEEK WISDOM The University of Western Australia institutional logo featuring a shield with a swan and books, alongside the text 'THE UNIVERSITY OF WESTERN AUSTRALIA' and the motto 'SEEK WISDOM'. [^1]: Original PDF page 1: [[L12 PerioDiabetes.pdf#page=1|L12 PerioDiabetes, p.1]] [^2]: Original PDF page 2: [[L12 PerioDiabetes.pdf#page=2|L12 PerioDiabetes, p.2]] [^3]: Original PDF page 3: [[L12 PerioDiabetes.pdf#page=3|L12 PerioDiabetes, p.3]] [^4]: Original PDF page 4: [[L12 PerioDiabetes.pdf#page=4|L12 PerioDiabetes, p.4]] [^5]: Original PDF page 5: [[L12 PerioDiabetes.pdf#page=5|L12 PerioDiabetes, p.5]] [^6]: Original PDF page 6: [[L12 PerioDiabetes.pdf#page=6|L12 PerioDiabetes, p.6]] [^7]: Original PDF page 7: [[L12 PerioDiabetes.pdf#page=7|L12 PerioDiabetes, p.7]] [^8]: Original PDF page 8: [[L12 PerioDiabetes.pdf#page=8|L12 PerioDiabetes, p.8]] [^9]: Original PDF page 9: [[L12 PerioDiabetes.pdf#page=9|L12 PerioDiabetes, p.9]] [^10]: Original PDF page 10: [[L12 PerioDiabetes.pdf#page=10|L12 PerioDiabetes, p.10]] [^11]: Original PDF page 11: [[L12 PerioDiabetes.pdf#page=11|L12 PerioDiabetes, p.11]] [^12]: Original PDF page 12: [[L12 PerioDiabetes.pdf#page=12|L12 PerioDiabetes, p.12]] [^13]: Original PDF page 13: [[L12 PerioDiabetes.pdf#page=13|L12 PerioDiabetes, p.13]] [^14]: Original PDF page 14: [[L12 PerioDiabetes.pdf#page=14|L12 PerioDiabetes, p.14]] [^15]: Original PDF page 15: [[L12 PerioDiabetes.pdf#page=15|L12 PerioDiabetes, p.15]] [^16]: Original PDF page 16: [[L12 PerioDiabetes.pdf#page=16|L12 PerioDiabetes, p.16]] [^17]: Original PDF page 17: [[L12 PerioDiabetes.pdf#page=17|L12 PerioDiabetes, p.17]] [^18]: Original PDF page 18: [[L12 PerioDiabetes.pdf#page=18|L12 PerioDiabetes, p.18]] [^19]: Original PDF page 19: [[L12 PerioDiabetes.pdf#page=19|L12 PerioDiabetes, p.19]] [^20]: Original PDF page 20: [[L12 PerioDiabetes.pdf#page=20|L12 PerioDiabetes, p.20]] [^21]: Original PDF page 21: [[L12 PerioDiabetes.pdf#page=21|L12 PerioDiabetes, p.21]] [^22]: Original PDF page 22: [[L12 PerioDiabetes.pdf#page=22|L12 PerioDiabetes, p.22]] [^23]: Original PDF page 23: [[L12 PerioDiabetes.pdf#page=23|L12 PerioDiabetes, p.23]] [^24]: Original PDF page 24: [[L12 PerioDiabetes.pdf#page=24|L12 PerioDiabetes, p.24]] [^25]: Original PDF page 25: [[L12 PerioDiabetes.pdf#page=25|L12 PerioDiabetes, p.25]] [^26]: Original PDF page 26: [[L12 PerioDiabetes.pdf#page=26|L12 PerioDiabetes, p.26]] [^27]: Original PDF page 27: [[L12 PerioDiabetes.pdf#page=27|L12 PerioDiabetes, p.27]] [^28]: Original PDF page 28: [[L12 PerioDiabetes.pdf#page=28|L12 PerioDiabetes, p.28]] [^29]: Original PDF page 29: [[L12 PerioDiabetes.pdf#page=29|L12 PerioDiabetes, p.29]] [^30]: Original PDF page 30: [[L12 PerioDiabetes.pdf#page=30|L12 PerioDiabetes, p.30]] [^31]: Original PDF page 31: [[L12 PerioDiabetes.pdf#page=31|L12 PerioDiabetes, p.31]] [^32]: Original PDF page 32: [[L12 PerioDiabetes.pdf#page=32|L12 PerioDiabetes, p.32]] [^33]: Original PDF page 33: [[L12 PerioDiabetes.pdf#page=33|L12 PerioDiabetes, p.33]] [^34]: Original PDF page 34: [[L12 PerioDiabetes.pdf#page=34|L12 PerioDiabetes, p.34]] [^35]: Original PDF page 35: [[L12 PerioDiabetes.pdf#page=35|L12 PerioDiabetes, p.35]] [^36]: Original PDF page 36: [[L12 PerioDiabetes.pdf#page=36|L12 PerioDiabetes, p.36]] [^37]: Original PDF page 37: [[L12 PerioDiabetes.pdf#page=37|L12 PerioDiabetes, p.37]] [^38]: Original PDF page 38: [[L12 PerioDiabetes.pdf#page=38|L12 PerioDiabetes, p.38]] [^39]: Original PDF page 39: [[L12 PerioDiabetes.pdf#page=39|L12 PerioDiabetes, p.39]] [^40]: Original PDF page 40: [[L12 PerioDiabetes.pdf#page=40|L12 PerioDiabetes, p.40]] [^41]: Original PDF page 41: [[L12 PerioDiabetes.pdf#page=41|L12 PerioDiabetes, p.41]] [^42]: Original PDF page 42: [[L12 PerioDiabetes.pdf#page=42|L12 PerioDiabetes, p.42]] [^43]: Original PDF page 43: [[L12 PerioDiabetes.pdf#page=43|L12 PerioDiabetes, p.43]] [^44]: Original PDF page 44: [[L12 PerioDiabetes.pdf#page=44|L12 PerioDiabetes, p.44]] [^45]: Original PDF page 45: [[L12 PerioDiabetes.pdf#page=45|L12 PerioDiabetes, p.45]] [^46]: Original PDF page 46: [[L12 PerioDiabetes.pdf#page=46|L12 PerioDiabetes, p.46]] [^47]: Original PDF page 47: [[L12 PerioDiabetes.pdf#page=47|L12 PerioDiabetes, p.47]] [^48]: Original PDF page 48: [[L12 PerioDiabetes.pdf#page=48|L12 PerioDiabetes, p.48]] [^49]: Original PDF page 49: [[L12 PerioDiabetes.pdf#page=49|L12 PerioDiabetes, p.49]] [^50]: Original PDF page 50: [[L12 PerioDiabetes.pdf#page=50|L12 PerioDiabetes, p.50]] [^51]: Original PDF page 51: [[L12 PerioDiabetes.pdf#page=51|L12 PerioDiabetes, p.51]] [^52]: Original PDF page 52: [[L12 PerioDiabetes.pdf#page=52|L12 PerioDiabetes, p.52]] [^53]: Original PDF page 53: [[L12 PerioDiabetes.pdf#page=53|L12 PerioDiabetes, p.53]]