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Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. Related Stories. Study questions certain treatments for diabetic patients at high risk for heart disease Oct 25, Oct 19, Sep 29, Low levels of vitamin D3 and periodontitis may trigger the onset of Type 2 diabetes Aug 20, Jun 13, May 21, Recommended for you. Biliopancreatic diversion improves insulin sensitivity, but some concerns remain 12 hours ago.
Oct 03, Nonsalvageable teeth are extracted. These sites are debrided, lavaged, and closed with absorbable monofilament suture.
Extractions will cause a transient decrease in appetite when compared to preoperative appetite, but after a brief recuperative period, the appetite will return to normal and sometimes better than normal. Occasionally, I will send a diabetic cat home on the day of the procedure if I feel that the patient is too stressed and will do better at home.
During the postoperative period, close attention to food intake is critical. Excessive insulin supplementation in the face of a faltering appetite may result in hypoglycemia. Lack of insulin supplementation may result in ketoacidosis. When glucose is unable to enter cells due to lack of insulin, the body breaks down fat as an alternative energy source, releasing free fatty acids into the bloodstream.
The liver subsequently converts FFAs to triglycerides and ketone bodies. Predisposing diseases and exposure to stressful situations e. To increase the chances of an uncomplicated recovery, oral surgery should be efficient and effective in removing any source of oral pain. A case report in the Journal of Veterinary Dentistry described complications associated with poorly performed extractions in a diabetic cat. During a second dental procedure, 22 retained tooth roots were removed. After nearly two weeks in the hospital, the cat was doing well enough to be discharged from the hospital.
What are the symptoms of gum disease?
Do diabetic cats and dogs heal less well after oral surgery? It may depend at least in part on the level of glycemic control of the individual patient, but I personally do not see an increased likelihood of dehiscence of oral surgery sites in diabetic patients compared to nondiabetic patients. However, I do use simple interrupted suture patterns for both diabetics and nondiabetics, so this may help decrease dehiscence over continuous patterns. The mouth has an excellent blood supply and tends to heal rapidly, even in diabetic patients. Tartar creates a strong bond that can only be removed professionally.
Oral bacteria passing through the bloodstream can permanently damage the kidneys, heart, liver, and lungs. Dentists have long been aware of the importance of a diagnosis of diabetes in their patients, and various oral conditions are associated with diabetes, including xerostomia and candidal infections as well as periodontitis. Periodontitis clinical appearance in a year-old man with poorly controlled type 1 diabetes and severe periodontitis. Note the generalised inflammation, abnormal gingival anatomy owing to tissue destruction, gingival recession, swelling and inflammation, spontaneous bleeding and abundant plaque deposits.
The periodontal tissues around the lower incisors are particularly severely affected. Periodontitis radiographic appearance. Some of the teeth have lost nearly all their supporting alveolar bone as a result of periodontitis progression, e.
Alveolar bone levels are normal, with the crest of the alveolar bone being in close proximity to the cemento-enamel junction the boundary between the enamel crown and the root. Contrast with appearance in Fig. Other lifestyle factors such as obesity, physical activity and diet are also likely to affect the risk of periodontitis.
One of the first studies to show an effect of obesity on periodontitis identified that obese rats with periodontitis had more alveolar bone loss compared with non-obese rats [ 19 ]. Adiposity can be regarded as a systemic disease that predisposes individuals to a variety of comorbidities and complications, and a number of studies have reported associations between obesity and periodontitis [ 20 ]. A recent meta-analysis revealed a significant association between periodontitis and obesity OR 1.
These findings raise the question of whether increased physical activity can reduce periodontitis risk. In the US Health Professionals Follow-up Study of 39, health professionals, an inverse linear relationship was identified between sustained physical activity and periodontitis, independent of known risk factors [ 24 ]. Another analysis of NHANES III data revealed that adults with higher levels of physical activity had significantly lower risk of periodontitis, with associations being strongest in non-smokers but no association in smokers, suggesting that the harmful effects of smoking outweighed any benefit of physical activity [ 25 ].
Prospective cohort studies are required to evaluate this area further. That is, not only is diabetes a risk factor for periodontitis, but periodontitis could have a negative effect on glycaemic control. The first clear evidence to support this hypothesis came from investigations of individuals in the Gila River Indian community. In addition, various studies have reported that the prevalence and severity of non-oral diabetes-related complications, including retinopathy, diabetic neuropathy, proteinuria and cardiovascular complications, are correlated with the severity of periodontitis [ 28 — 31 ].
Further studies of the Gila River Indian Community investigated the effect of periodontitis on the development of overt nephropathy, defined as macroalbuminuria and end-stage renal disease ESRD , in type 2 diabetes mellitus [ 32 ]. A total of individuals developed macroalbuminuria over a median follow-up of 9.
After adjusting for age, sex, diabetes duration, BMI and smoking, the incidences of macroalbuminuria were 2. The incidences of ESRD were 2. The same researchers also investigated the effect of periodontitis on deaths from cardiovascular disease and diabetic nephropathy. After adjusting for age, sex, diabetes duration, HbA 1c , macroalbuminuria, BMI, cholesterol, hypertension, electrocardiogram abnormalities and smoking, diabetic individuals with severe periodontitis had 3.
Acknowledging that the above studies were conducted in a specific, defined population, more recent research has investigated the impact of oral disease on subsequent cardiovascular disease in a general population of people with type 2 diabetes mellitus [ 34 ]. A total of 10, participants responded to two questions about the presence of oral disease the number of natural teeth in their mouth, and the approximate number of days their gums had bled in the previous year [ 35 ]; a lower number of remaining natural teeth and higher number of bleeding days were taken as indicators of poorer oral health.
The authors of the paper postulated that inflammation resulting from poor oral health may have been implicated in the development of cardiovascular disease. An intriguing area of recent investigation has focused on whether periodontitis plays a role in the incidence of diabetes. In unadjusted analyses, moderate pockets 3. Periodontitis is a complex chronic inflammatory disease in which inflammation in the periodontal tissues is stimulated by the long-term presence of the subgingival biofilm dental plaque.
The inflammatory response is characterised by dysregulated secretion of host-derived mediators of inflammation and tissue breakdown. IL, IL and the chemokines [ 38 ]. The complexity of cytokine networks in periodontal pathogenesis is becoming increasingly apparent, and it is clear that there is considerable heterogeneity in the nature of the inflammatory response between individuals. This heterogeneity exists not only between individuals, but also within individuals over time, and is influenced by genetic, epigenetic and environmental factors.
The sum total of the inflammatory response in the periodontal tissues determines the pattern and rate of disease progression [ 39 ]. Both type 1 and type 2 diabetes mellitus are associated with elevated levels of systemic markers of inflammation [ 40 ].watch
Treating gum disease may help manage Type 2 diabetes
The elevated inflammatory state in diabetes contributes to both microvascular and macrovascular complications, and it is clear that hyperglycaemia can result in the activation of pathways that increase inflammation, oxidative stress and apoptosis [ 41 ]. Elevated levels of CRP are also associated with insulin resistance, type 2 diabetes mellitus and cardiovascular disease [ 43 ]. Serum levels of IL-6 and CRP are also raised in patients with periodontitis, with IL-6 levels correlating with the extent of disease [ 46 , 47 ].
The systemic inflammation that is associated with periodontal disease may therefore enhance the diabetic state. Diabetes increases inflammation in the periodontal tissues. Furthermore, studies have consistently demonstrated defects in polymorphonuclear leucocyte PMN activity in patients with diabetes, including impaired chemotaxis, phagocytosis and microbicidal functions [ 52 ]. PMNs require energy to function and these defects may be related to the metabolic changes that occur in diabetes [ 53 ].
Diabetic patients with severe periodontitis have been shown to have depressed PMN chemotaxis compared with diabetic individuals with mild periodontitis [ 54 ], as well as defective PMN apoptosis [ 55 ], which may lead to increased retention of PMNs in the periodontal tissue, leading to more tissue destruction by continued release of MMPs and reactive oxygen species ROS.
Accumulation of AGEs in the periodontal tissues is also likely to play a role in upregulating periodontal inflammation in individuals with diabetes. AGE formation results in the production of ROS and enhances oxidant stress, and the subsequent endothelial cell changes that occur contribute to the vascular injury implicated in many diabetes complications [ 62 ].
AGEs also enhance the respiratory burst in PMNs [ 63 ], which has the potential to significantly increase local tissue damage in periodontitis. Furthermore, AGEs have detrimental effects on bone metabolism, leading to impaired repair and bone formation [ 64 ] and decreased extracellular matrix production [ 65 ].
Apoptosis may also play a role in the increased susceptibility to periodontitis associated with diabetes, and apoptosis of matrix-producing cells may limit the opportunities for repair in inflamed tissues. Induction of tissue injury by inoculation with P. The various inflammatory pathways postulated to link diabetes and periodontitis are illustrated in Fig.
Schematic representation of the proposed two-way relationship between diabetes and periodontitis. Exacerbated and dysregulated inflammatory responses are at the heart of the proposed two-way interaction between diabetes and periodontitis purple box , and the hyperglycaemic state results in various proinflammatory effects that impact on multiple body systems, including the periodontal tissues.
The hyperglycaemic state results in deposition of AGEs in the periodontal tissues as well as elsewhere in the body , and binding of the receptor for AGE RAGE results in local cytokine release and altered inflammatory responses. Neutrophil function is also altered in the diabetic state, resulting in enhancement of the respiratory burst and delayed apoptosis leading to increased periodontal tissue destruction.
Diabetes and gum disease | Diabetes UK
Local production of cytokines in the periodontal tissues may, in turn, affect glycaemic control through systemic exposure and an impact on insulin signalling dotted arrow. All of these factors combine to contribute to dysregulated inflammatory responses that develop in the periodontal tissues in response to the chronic challenge by bacteria in the subgingival biofilm, and which are further exacerbated by smoking.
Compared with the large number of studies that have investigated the role of inflammatory mechanisms in the link between periodontitis and diabetes, relatively few have investigated relationships between the oral microbiota and diabetes.