12. Epidemiology
• Severe periodontitis : Diabetic > non-diabetics.
study.Taylor et al, J Perio 96)
(Pima
• Destructive periodontitis occurred much earlier in
life in the diabetics (27% of diabetics 15-19 years
old). (Pima study.Taylor et al, J Perio 96)
• Higher-aged diabetic had greater periodontal
attachment and bone loss than younger. (R.G. Nelson, M.
Shlossman, L.M. Budding et al.Periodontal disease and NIDDM in Pima Indians.
Diabetes Care 1990)
•Diabetic complications increased susceptibility to
periodontal disease with increased attachment loss
(B.L. Mealey. Diabetes and periodontal disease: two sides of a coin.Compend
20. Pseudomembranous candidiasis (thrush)
Impairment of the immune system, chemotherapy, Sjögren
syndrome, and diabetes mellitus can also contribute to the
proliferation of C albicans.
Lynch DP. Oral examination. http://emedicine.medscape.com/article/1080850-
30. Generally in periodontal patients is noticed
the presence of
◦ Porphyromonas gingivalis
◦ Tannerella forsythia
◦ Actinobacillus actinomycetemcomitans
Sometime, other bacteria, such as
◦ Treponema denticola
◦ Treponema socranskii
L. MARIGO, R. CERRETO, M. GIULIANI, F. SOMMA, C. LAJOLO, M. CORDARO,
31. DM patients
◦ Candida albicans
In type 1 DM patients
◦ Capnocytophaga spp :most frequent
bacteria
◦ Porphyromonas gingivalis
◦ Prevotella intermedia
L. MARIGO, R. CERRETO, M. GIULIANI, F. SOMMA, C. LAJOLO, M. CORDARO,
32. In type 2 DM patients
◦ Capnocytophaga spp. : most frequent
bacteria
◦ Prevotella intermedia
◦ Campylobacter rectus
◦ Porphyromonas gingivalis
◦ Actinobacillus actinomycetemcomitans.
L. MARIGO, R. CERRETO, M. GIULIANI, F. SOMMA, C. LAJOLO, M. CORDARO,
42. Attachment and Bone Loss
AGE-Bone :
Bone metabolism
Bone turnover
: cellular , structural , functional
characteristic
American Academy of
Periodontology,2006
43. Attachment and Bone Loss
Attachment and Bone loss
◦
tissue metabolism
◦ Bone healing
Bone Turnover rate
◦
proliferation of Osteoblast
◦
collagen
◦
apoptosis
fibroblast
Osteoblast
attachment and bone loss
American Academy of
Periodontology,2006
57. Uncontrolled patient and
Poorly control patient
Only emergency care
antibiotic therapy
oral infection
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
58. Well-controlled patient
complete periodontal therapy
surgical procedures
the presence of medical complications
associated with diabetes mellitus should be
carefully evaluated and considered in any
periodontal therapeutic decision
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
61. Hyperglycemic
•breathing may become rapid and deep
(Kussmaul’s respiration)
•hot and dry skin
•‘‘acetone’’ breath may be evident.
•Severe hypotension
•coma may follow. Coma is usually associated with
plasma glucose levels of between 300 and 600
mg/dl.
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
62. conscious
hyperglycemic
hospital emergency room
basic life support procedures
unconscious
open airway
administration of 100% oxygen
non-glucose-containing intravenous
fluids should be administered to prevent
vascular collapse.
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
63. Hypoglycemic shock
plasma glucose levels drop below 40
mg/dl.
◦ exercise
◦ diabetes mellitus drug overdose,
◦ stress or failure by the patient to properly
control his or her dietary Intake.
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
65. orange juice
administration of
oral carbohydrates
candy
Early treatment
soft drinks
Treatment
patient remains
unresponsive
hospital emergency room
Terry D. Rees. Periodontal management of the patient with diabetes mellitus.
Figure 1. Mechanisms of diabetes-mediated periodontal tissue destruction. The hyperglycemic status can directly provide favorable environment for the growth of Gram-negative periodontal pathogens, impair cellular function and host defense, and induce overproduction of proinflammatory cytokines and secretion of collagenolytic enzymes (black lines). By facilitating the formation of advanced glycation end products (AGEs), diabetes can also indirectly alter the crosslink of the extracellular matrix (gray lines) as well as the cellular activities to amplify inflammatory reactions and decrease cell viability, leading to further wound healing impairment and potential vascular change (dash black lines) in periodontal tissue (gray box).
There is evidence that exposing serum from periodontitis patients to LPS of periodontal pathogens leads to increased triglycerides and lower levels of high-density lipoprotein (HDL),132 and 133 which suggests that local infection, such as periodontitis, can alter systemic lipid metabolism. The mechanism is possibly due to activation of the ‘cytokine cascade’ in response to LPS. The elevation of serum lipids may also influence immune cell function by upregulatingproinflammatory cytokines and superoxide production by PMNs and altering surface marker antigens of monocytes.134 In the meanwhile, periodontitis can potentially induce insulin resistance by the overproduction of systemic proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6. These cytokines will further ameliorate insulin insensitivity by destroying pancreatic β-cells, antagonizing insulin action, or altering intracellular insulin signaling through the NF-κB and c-Jun N-terminal kinase (JNK) axes.13, 40, 135 and 136