These notes for “Key concepts and terms” in theDLP 2.6 sheet.GingivitisEpidemiology* Gingivitis is the mildest form of periodontal disease and affects 50% to 90% ofadults worldwide. It is ubiquitous and affects males and females, young and old.As defined by gingival bleeding adjacent to ≥1 teeth, about half of the USpopulation has gingivitis with the prevalence slightly greater in males thanfemales, and in black people and Mexican Americans than in white people. Thereis evidence that the prevalence of gingivitis has been decreasing in developedcountries over the last few decades. Globally, there appears to be considerableheterogeneity in the prevalence of gingivitis with higher prevalence reported incertain parts of the world.The prevalence of necrotising ulcerative gingivitis (NUG) varies widely, and it isfrequently reported among young HIV/AIDS patients in some countries. Studiesincluding outpatients, particularly after introduction of antiretroviral therapy, haveshown relatively low prevalence figures, similar to those of the generalpopulation. This disease is frequently seen in developing countries, especially insub-Saharan Africa, where it occurs almost exclusively among children, usuallybetween the ages of 3 and 10 years, from low socio-economic backgrounds. Itsprevalence has been reported to be about 0.3% in Swiss Army recruits and 3% ina South African population, and is as high as 27% among Nigerian children aged<12 years at a west Nigerian dental clinic. In this population, prevalence of thisdisease increases from 2% to 3% of children with good oral hygiene to 67% ofchildren with very poor oral hygiene.* In recent years, tremendous strides have been made in understanding theetiology of gingivitis. This increase in knowledge has come, for the most part,from basic research in oral microbiology, immunology, histology and pathology.Over the past decade, less progress has been made in further refining theepidemiological relationships between gingivitis and various host andenvironmental factors. The major restraint has been the great difficulty in reliablymeasuring gingival inflammation. This problem has resulted in great inter- andintra-study variation in diagnosing the prevalence and severity of gingivitis inhuman populations. Consequently, it is almost impossible to estimate longitudinaltrends in gingivitis and it is nearly as difficult to make comparisons amongdifferent population groups studied by different examiners. Nevertheless, byfocusing on the most apparent and robust epidemiological relationships, aninstructive overview of the epidemiology of gingivitis can be gained. A number ofhost and environmental factors have been studied in relation to gingivitis and
some of these will be reviewed. With respect to age, there is general concensusthat marginal gingivitis begins in early childhood, increases in prevalence andseverity to the early teenage years, thereafter subsiding slightly and leveling offfor the remainder of the second decade of life. Gingivitis during the adult period ismuch more difficult to characterize due to paucity of data. Estimates of thegeneral prevalence of adult gingivitis vary from approximately 50 to 100% fordentate subjects. In terms of gingivitis prevalence, the dentate elderly do notdeviate appreciably from the general adult pattern. When adjusted for cohorteffects, gingival disease appears to be on the decline.(ABSTRACT TRUNCATEDAT 400 WORDS)Etiology* The etiology, or cause, of plaque-induced gingivitis is bacterial plaque, whichacts to initiate the bodys host response. This, in turn, can lead to destruction ofthe gingival tissues, which may progress to destruction of the periodontalattachment apparatus. The plaque accumulates in the small gaps betweenteeth, in the gingival grooves and in areas known as plaque traps: locations thatserve to accumulate and maintain plaque. Examples of plaque traps includebulky and overhanging restorative margins, claps of removable partial denturesand calculus (tartar) that forms on teeth. Although these accumulations may betiny, the bacteria in them produce chemicals, such as degrative enzymes, andtoxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) orlipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue.This inflammation can cause an enlargement of the gingiva and subsequentformation.Risk factors* Gingivitis is very common, and anyone can develop it. Many people firstexperience gum problems during puberty and then in varying degrees throughoutlife.Factors that can increase your risk of gingivitis include:Poor oral health habitsTobacco useDiabetesOlder ageDecreased immunity as a result of leukemia, HIV/AIDS or other conditions
Certain medicationsCertain viral and fungal infectionsDry mouthHormonal changes, such as those related to pregnancy, your menstrual cycle oruse of oral contraceptivesPoor nutritionSubstance abuseIll-fitting dental restorationsManagement* Richard H. Nagelberg, DDS , says: My previous post indicated that I approachgingivitis in my general dental practice, as a non-reversible disease entitiy. I haveconluded from professional reading, dialogue with other practitioners and myclinical judgment and experience, that it is not a separate disease entity fromperiodontitis, just an early manifestation. Think about other conditions such asdiabetes. When an individual is diagnosed with Type II diabetes, which accountsfor 90-95% of all cases, they are commonly put on dietary control, not a regimenof oral meds and/or insulin, with frequent monitoring. The early manifestations ofthe disease commonly do not require intervention; however, if there is a lack ofcompliance, then more aggressive attention such as one or more medicationswill be necessary to achieve adequate glycemic control. Most importantly, acasual approach to the diabetes would be inappropriate and increase thelikelihood of disease progression. If gingivitis is pro-actively approached as anearly non-reversible manifestation of periodontitis, the likelihood of returning thepatient to health is increased considerably. Assuming the cause of the gingivitisis poor biofilm control, rather than an exaggreated host response, having thepatient describe their home care in detail is indicated, along with an examinationof their risk factors (covered in an earlier blog post). Among the most importantrecommendations, in my opinion and experience, is recommending a powertoothbrush. My preference is the Philips Sonicare Flexcare. I have seenconsistently excellent results with its usage. Other recommendations wouldinclude an antimicrobial mouthrinse, my preference being Listerine, twice daily.Interdental cleaning tools such as floss, Proxabrushes, floss picks, rubber tipstimulators and so on are indicated as needed for specific patients. A tonguecleaner is another easy tool for patients to use to help reduce the total bacterialpopulation in the mouth. Perhaps, most importantly is need for patient education.
Taking the time to educate our patients on the importance of meticulous biofilmcontrol, and the potential consequences of non-compliance will help the patientunderstand why it is so important to change home care habits. Monitoring at 30day intervals should also be considered, tweaking the home care as needed. Ifgingivitis is present despite good biofilm control, DNA testing is indicated,including testing the bacterial DNA and perhaps the patients geneticpredisposition for perio disease (PST testing). Both salivary diagnostic tests areavailable from OralDNA Labs (OralDNA.com). This scenario will be discussed ina future blog post. As always, comments are welcome.PeriodontitisEpidemiology* There is a conspicuous lack of uniformity in the definition of periodontitis usedin epidemiologic studies, and findings from different research groups are notreadily interpretable. There is a lack of studies that specifically address thedistinction between factors responsible for the onset of periodontitis versus thoseaffecting its progression. Colonization by specific bacteria at high levels,smoking, and poorly controlled diabetes have been established as risk factors forperiodontitis, while a number of putative factors, including specific genepolymorphisms, have been identified in association studies. There is a clear needfor longitudinal prospective studies that address hypotheses emerging from thecross-sectional data and include established risk factors as covariates along withnew exposures of interest. Intervention studies, fulfilling the "targeting" step ofthe risk assessment process, are particularly warranted. Obvious candidates inthis context are studies of the efficacy of elimination of specific bacterial speciesand of smoking cessation interventions as an alternative to the traditional broadanti-plaque approach in the prevention and control of periodontitis. Ideally, suchstudies should have a randomized-controlled trial design.*Unfortunately, periodontitis is extremely common, occurring in an estimated35% of U.S. residents ages 30 and older.Approximately 63% have a mild form,while the remaining 37% have moderate to severe periodontitis. Periodontaldisease is also the leading cause of tooth loss for those older than 40.3 Riskfactors for periodontitis are dental plaque, which contains microorganisms,diabetes mellitus, smoking, and possibly stress.Etiology
* Periodontitis is an inflammation of the periodontium, i.e., the tissues thatsupport the teeth. The periodontium consists of four tissues: gingiva, or gum tissue; cementum, or outer layer of the roots of teeth; alveolar bone, or the bony sockets into which the teeth are anchored; periodontal ligaments (PDLs), which are the connective tissue fibers that run between the cementum and the alveolar bone.The primary etiology (cause) of gingivitis is poor oral hygiene which leads to theaccumulation of a mycotic and bacterial matrix at the gum line, called dentalplaque. Other contributors are poor nutrition and underlying medical issues suchas diabetes. New finger nick tests have been approved by the Food and DrugAdministration in the US, and are being used in dental offices to identify andscreen patients for possible contributory causes of gum disease such asdiabetes.In some people, gingivitis progresses to periodontitis –- with the destruction ofthe gingival fibers, the gum tissues separate from the tooth and deepenedsulcus, called a periodontal pocket. Subgingival microorganism (those that existunder the gum line) colonize the periodontal pockets and cause furtherinflammation in the gum tissues and progressive bone loss. Examples ofsecondary etiology are those things that, by definition, cause microbic plaqueaccumulation, such as restoration overhangs and root proximity.Smoking is another factor that increases the occurrence of periodontitis, directlyor indirectly, and may interfere with or adversely affect its treatment.Ehlers-Danlos Syndrome is a periodontitis risk factor.If left undisturbed, microbic plaque calcifies to form calculus, which is commonlycalled tartar. Calculus above and below the gum line must be removedcompletely by the dental hygienist or dentist to treat gingivitis and periodontitis.Although the primary cause of both gingivitis and periodontitis is the microbicplaque that adheres to the tooth surface, there are many other modifying factors.A very strong risk factor is ones genetic susceptibility. Several conditions anddiseases, including Down syndrome, diabetes, and other diseases that affectones resistance to infection also increase susceptibility to periodontitis.Another factor that makes periodontitis a difficult disease to study is that humanhost response can also affect the alveolar bone resorption. Host response to thebacterial-mycotic insult is mainly determined by genetics; however, immunedevelopment may play some role in susceptibility.According to some researches periodontitis may be associated with higherstress.
Risk factors* Factors that can increase your risk of periodontitis include:GingivitisHeredityPoor oral health habitsTobacco useDiabetesOlder ageDecreased immunity, such as that occurring with leukemia or HIV/AIDS orchemotherapyPoor nutritionCertain medicationsHormonal changes, such as those related to pregnancy or menopauseSubstance abuseIll-fitting dental restorations(See also Dr.Abeer’s lectures + http://www.slideshare.net/neilpande/risk-factors-in-periodontal-disease)Management* While risk assessment for periodontal disease is largely the domain of thedental care professional, periodontal disease management (including diseaseprevention) requires the patient‘s participation. Indeed, self-care has been a keycomponent of preventive dentistry for years. Axelsson and colleagues 3conducted a long-term study of plaque control in adults that showedadministration of frequent, regular education in self-diagnosis and self-caretechniques resulted in more healthy tooth surfaces, less periodontal attachmentloss and fewer sites requiring periodontal care.As illustrated in the figure , a self-care regimen of brushing, flossing and rinsingwith an antimicrobial mouthrinse can help control dental plaque biofilm. Forpatients without periodontal disease, this three-step approach can help prevent
the onset of periodontal disease. For patients with periodontal disease, thisapproach can play a secondary preventive role in early disease control, as wellas be an important component of conservative therapy. In addition, self-care withparticular oral rinses can be important for the postsurgical management ofplaque-induced tissue inflammation.Figure. A three-step approach to daily oral health care can be part of theregimen for patients with a healthy periodontium, those with gingivitis and thosewith periodontitis. In each case, the intent is to reduce the microbial challenge.Clearly, patient motivation regarding disease management is critical if thebenefits of self-care are to be realized; this may require individualized patienteducation to ensure that each patient appreciates the relevance of self-care tothe enhancement of his or her own oral health. (For more information on patientadherence to self-care, see the article by Silverman and Wilder in thissupplement.)Host defence mechanism* Host defenses that protect against infection include natural barriers (eg, skin,mucous membranes), nonspecific immune responses (eg, phagocytic cells[neutrophils, macrophages] and their products), and specific immune responses(eg, antibodies, lymphocytes).Natural Barriers
Skin: The skin usually bars invading microorganisms unless it is physicallydisrupted (eg, by injury, IV catheter, or surgical incision). Exceptions includehuman papillomavirus, which can invade normal skin, causing warts, and someparasites (eg, Schistosoma mansoni, Strongyloides stercoralis).Mucous membranes: Many mucous membranes are bathed in secretions thathave antimicrobial properties (eg, cervical mucus, prostatic fluid, and tearscontaining lysozyme, which splits the muramic acid linkage in bacterial cell walls,especially in gram-positive organisms). Local secretions also containimmunoglobulins, principally IgG and secretory IgA, which preventmicroorganisms from attaching to host cells.Respiratory tract: The respiratory tract has upper airway filters. If invadingorganisms reach the tracheobronchial tree, the mucociliary epithelium transportsthem away from the lung. Coughing also helps remove organisms. If theorganisms reach the alveoli, alveolar macrophages and tissue histiocytes engulfthem. However, these defenses can be overcome by large numbers oforganisms or by compromised effectiveness resulting from air pollutants (eg,cigarette smoke) or interference with protective mechanisms (eg, endotrachealintubation, tracheostomy).GI tract: GI tract barriers include the acid pH of the stomach and the antibacterialactivity of pancreatic enzymes, bile, and intestinal secretions. Peristalsis and thenormal loss of epithelial cells remove microorganisms. If peristalsis is slowed (eg,because of drugs such as belladonna or opium alkaloids), this removal is delayedand prolongs some infections, such as symptomatic shigellosis. Compromised GIdefense mechanisms may predispose patients to particular infections (eg,achlorhydria predisposes to salmonellosis). Normal bowel flora can inhibitpathogens; alteration of this flora with antibiotics can allow overgrowth ofinherently pathogenic microorganisms (eg, Salmonella typhimurium) orsuperinfection with ordinarily commensal organisms (eg, Candida albicans).GU tract: GU tract barriers include the length of the urethra (20 cm) in men, theacid pH of the vagina in women, and the hypertonic state of the kidney medulla.The kidneys also produce and excrete large amounts of Tamm-Horsfallmucoprotein, which binds certain bacteria, facilitating their harmless excretion.Nonspecific Immune Responses
Cytokines (including IL-1, IL-6, tumor necrosis factor, interferon-γ) are producedprincipally by macrophages and activated lymphocytes and mediate an acute-phase response that develops regardless of the inciting microorganism (see alsoBiology of the Immune System: Cytokines). The response involves fever andincreased production of neutrophils by the bone marrow. Endothelial cells alsoproduce large amounts of IL-8, which attracts neutrophils.The inflammatory response directs immune system components to injury orinfection sites and is manifested by increased blood supply and vascularpermeability, which allows chemotactic peptides, neutrophils, and mononuclearcells to leave the intravascular compartment. Microbial spread is limited byengulfment of microorganisms by phagocytes (eg, neutrophils, macrophages).Phagocytes are drawn to microbes via chemotaxis and engulf them, releasingphagocytic lysosomal contents that help destroy microbes. Oxidative productssuch as hydrogen peroxide are generated by the phagocytes and kill ingestedmicrobes. When quantitative or qualitative defects in neutrophils result ininfection, the infection is usually prolonged and recurrent and responds slowly toantimicrobial drugs. Staphylococci, gram-negative organisms, and fungi are thepathogens usually responsible.Specific Immune ResponsesAfter infection, the host can produce a variety of antibodies, complexglycoproteins known as immunoglobulins that bind to specific microbial antigenictargets. Antibodies can help eradicate the infecting organism by attracting thehosts WBCs and activating the complement system. The complement system(see Biology of the Immune System: Complement System) destroys cell walls,usually through the classic pathway. Complement can also be activated on thesurface of some microorganisms via the alternative pathway. Antibodies can alsopromote the deposition of substances known as opsonins (eg, the complementprotein C3b) on the surface of microorganisms, which helps promotephagocytosis. Opsonization is important for eradication of encapsulatedorganisms such as pneumococci and meningococci.Control of fuel metabolism* Metabolism (pronounced: muh-tah-buh-lih-zum) is a collection of chemicalreactions that takes place in the bodys cells. Metabolism converts the fuel in thefood we eat into the energy needed to power everything we do, from moving to
thinking to growing. Specific proteins in the body control the chemical reactionsof metabolism, and each chemical reaction is coordinated with other bodyfunctions. In fact, thousands of metabolic reactions happen at the same time —all regulated by the body — to keep our cells healthy and working.Metabolism is a constant process that begins when were conceived and endswhen we die. It is a vital process for all life forms — not just humans. Ifmetabolism stops, living things die.Heres an example of how the process of metabolism works in humans — and itbegins with plants. First, a green plant takes in energy from sunlight. The plantuses this energy and a molecule called cholorophyll (which gives plants theirgreen color) to build sugars from water and carbon dioxide. This process is calledphotosynthesis, and you probably learned about it in biology class.When people and animals eat the plants (or, if theyre carnivores, they eatanimals that have eaten the plants), they take in this energy (in the form ofsugar), along with other vital cell-building chemicals. The bodys next step is tobreak the sugar down so that the energy released can be distributed to, and usedas fuel by, the bodys cells.After food is eaten, molecules in the digestive system called enzymes breakproteins down into amino acids, fats into fatty acids, and carbohydrates intosimple sugars (e.g., glucose). In addition to sugar, both amino acids and fattyacids can be used as energy sources by the body when needed. Thesecompounds are absorbed into the blood, which transports them to the cells. Afterthey enter the cells, other enzymes act to speed up or regulate the chemicalreactions involved with "metabolizing" these compounds. During theseprocesses, the energy from these compounds can be released for use by thebody or stored in body tissues, especially the liver, muscles, and body fat.A Balancing ActIn this way, the process of metabolism is really a balancing act involving twokinds of activities that go on at the same time — the building up of body tissuesand energy stores and the breaking down of body tissues and energy stores togenerate more fuel for body functions:
Anabolism (pronounced: uh-nah-buh-lih-zum), or constructive metabolism, is all about building and storing: It supports the growth of new cells, the maintenance of body tissues, and the storage of energy for use in the future. During anabolism, small molecules are changed into larger, more complex molecules of carbohydrate, protein, and fat. Catabolism (pronounced: kuh-tah-buh-lih-zum), or destructive metabolism, is the process that produces the energy required for all activity in the cells. In this process, cells break down large molecules (mostly carbohydrates and fats) to release energy. This energy release provides fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. As complex chemical units are broken down into more simple substances, the waste products released in the process of catabolism are removed from the body through the skin, kidneys, lungs, and intestines.Several of the hormones of the endocrine system are involved in controlling therate and direction of metabolism. Thyroxine (pronounced: thigh-rahk-sun), ahormone produced and released by the thyroid (pronounced: thigh-royd) gland,plays a key role in determining how fast or slow the chemical reactions ofmetabolism proceed in a persons body.Another gland, the pancreas (pronounced: pan-kree-us) secretes (gives off)hormones that help determine whether the bodys main metabolic activity at aparticular time will be anabolic or catabolic. For example, after eating a meal,usually more anabolic activity occurs because eating increases the level ofglucose — the bodys most important fuel — in the blood. The pancreas sensesthis increased level of glucose and releases the hormone insulin (pronounced:in-suh-lin), which signals cells to increase their anabolic activities.Metabolism is a complicated chemical process, so its not surprising that manypeople think of it in its simplest sense: as something that influences how easilyour bodies gain or lose weight. Thats where calories come in. A calorie is a unitthat measures how much energy a particular food provides to the body. Achocolate bar has more calories than an apple, so it provides the body with moreenergy — and sometimes that can be too much of a good thing. Just as a carstores gas in the gas tank until it is needed to fuel the engine, the body storescalories — primarily as fat. If you overfill a cars gas tank, it spills over onto the
pavement. Likewise, if a person eats too many calories, they "spill over" in theform of excess fat on the body.The number of calories a person burns in a day is affected by how much thatperson exercises, the amount of fat and muscle in his or her body, and thepersons basal metabolic rate. The basal metabolic rate, or BMR, is a measureof the rate at which a persons body "burns" energy, in the form of calories, whileat rest. The BMR can play a role in a persons tendency to gain weight. Forexample, a person with a low BMR (who therefore burns fewer calories while atrest or sleeping) will tend to gain more pounds of body fat over time, comparedwith a similar-sized person with an average BMR who eats the same amount offood and gets the same amount of exercise.What factors influence a persons BMR? To a certain extent, a persons basalmetabolic rate is inherited — passed on through the genes the person gets fromhis or her parents. Sometimes health problems can affect a persons BMR (seebelow). But people can actually change their BMR in certain ways. For example,exercising more will not only cause a person to burn more calories directly fromthe extra activity itself, but becoming more physically fit will increase BMR aswell. BMR is also influenced by body composition — people with more muscleand less fat generally have higher BMRs.Altered control of fuel metabolism in diabetesmellitus* Type 1 diabetes mellitus (pronounced: dye-uh-bee-teez meh-luh-tus). Type 1diabetes occurs when the pancreas doesnt produce and secrete enough insulin.Symptoms of this disease include excessive thirst and urination, hunger, andweight loss. Over the long term, the disease can cause kidney problems, paindue to nerve damage, blindness, and heart and blood vessel disease. Teens withtype 1 diabetes need to receive regular injections of insulin and control bloodsugar levels to reduce the risk of developing problems from diabetes.Type 2 diabetes. Type 2 diabetes happens when the body cant respondnormally to insulin. The symptoms of this disorder are similar to those of type 1diabetes. Many children and teens who develop type 2 diabetes are overweight,and this is thought to play a role in their decreased responsiveness to insulin.
Some teens can be treated successfully with dietary changes, exercise, and oralmedication, but insulin injections are necessary in other cases. Controlling bloodsugar levels reduces the risk of developing the same kinds of long-term healthproblems that occur with type 1 diabetes.Pathophysiology of diabetes mellitus Sysmtemic and oral* Diabetes mellitus is another systemic condition with oral inflammatoryconnections. One of the major complications of diabetes is periodontitis. Whilediabetes increases the probability of developing periodontal disease, periodontitisalso increases the risk of poor glycemic control in people with diabetes whencompared to those individuals with diabetes without periodontitis. Fortunately,periodontal treatment can improve glycemic control by reducing the bacterialburden and the inflammatory response.There are several biological mechanisms proposed to explain the increasedincidence and severity of periodontal disease in individuals with diabetes.Diabetes tends to increase susceptibility to infection--including oral infection--andthe disease itself decreases the effectiveness of cells that kill bacteria.Another explanation is that inflammation is enhanced in those with diabetes.Research has demonstrated elevated levels of inflammatory mediators in thegingival crevicular fluid of periodontal pockets of poorly controlled patients withdiabetes as compared to those without diabetes or those with diabetes who arewell controlled. These patients had significant periodontal destruction with anequivalent bacterial challenge. In particular, the proinflammatory cytokine, TNF-α,plays a major role in this process. TNF- α has a significant role in insulinresistance, the primary cause of type 2 diabetes. It is produced in large quantitiesby fat cells. Periodontitis has also been associated with increased levels of TNF-α. Elevated levels of TNF-α may lead to greater bone loss by killing cells thatrepair damaged connective tissue or bone and may exacerbate insulin resistanceand worsen glycemic control.It has also been hypothesized that diabetes interferes with the capacity to formnew bone after periodontal diseases have caused bone resorption. Graves, etal., studied genetically diabetic mice with type 2 diabetes and nondiabeticlittermates by injecting them with P. gingivalis. The death of osteoblasts wasmeasured, and results indicated that there was a higher and more prolonged rateof osteoblast cell death in the diabetic group. It was concluded that the capacityto repair a bony defect by producing new bone would be severely limited whenosteoblasts died prematurely. Yet further study is needed in this area to refinethis concept.
As with CVD and diabetes mellitus, there is a relationship between oral infectionand respiratory disease. In particular, chronic obstructive pulmonary disease(COPD) and pneumonia have been associated with poor oral health. It is likelythat oral biofilm serves as a reservoir of infection for respiratory bacteria.Specifically, Pseudomonas aeruginosa, Staphylococcus aureus, and entericbacteria that has been shown to colonize the teeth of patients admitted tohospitals or long-term care facilities. These bacteria may be released into salivaand then aspirated into the lower airway causing infection. Another vehicle bywhich bacteria from the oral cavity can be introduced into the respiratory systemis intubation.Management of oral health of diabetes mellituspatients* When the dental practitioner is called upon to provide dental treatment for apreviously diagnosed diabetes mellitus patient, a certain amount of detailedinformation should be gathered. The patient should be questioned regarding thetype of diabetes, the age at onset and duration of the disease; any currentmedications and their method of administration. The patient‘s degree ofcompliance and monitoring technique should be discussed.The practitioner should review any previous history of diabetic complications,determine the most recent laboratory results and record the name and address ofthe patient‘s physician(s). By gathering this information the clinician can bestrelate the patient‘s oral condition to his or her systemic status and determinewhether or not medical consultation is required. Under most circumstances itwould be prudent to obtain medical clearance prior to performing any extensivedental therapy, especially if surgery is indicated.In most instances the well-controlled type 1 or type 2 patient can be managed ina manner consistent with a healthy non-diabetic individual.Periodontal surgical procedures can be performed, although it must be assuredthat the patient can maintain a normal diet post-surgically. In the event that thetreatment procedure modifies the patient‘s dietary habits, dietary supplementsshould be recommended.Supportive therapy such as scaling and root planning should be provided atrelatively close intervals (2 to 3 months) since some studies indicate a slight butpersistent tendency to progressive periodontal destruction despite effectivemetabolic diabetes mellitus control.Management of Uncontrolled or Poorly Controlled Diabetic Patients
The uncontrolled or poorly controlled diabetic patient or the diabetes mellituspatient who does not know his or her control status should not receive electivedental treatment until the condition is stabilized or medical clearance obtained.Prophylactic antibiotic therapy should be used for performance of emergency oralor surgical procedures to minimize the potential for postoperative infections anddelayed wound healing.Any therapy other than emergency treatment may be contraindicated in thepoorly controlled diabetes mellitus patient until appropriate metabolic controlled isachieved.In many instances this may require short- or long-term prescription of insulin ororal medications by the physician.Oral Medications for Diabetic ControlFor many years, type 2 diabetes mellitus has been treated by diet control andvarious hypoglycaemic agents, usually a first- or second-generation sulfonylurea(acetohexamide, chlorpropamide, tolazamide, tolbutamide, glimepiride, glipizideor glyburide).Sulfonylurea promotes insulin secretion, and importantly, they are all capable ofinducing hypoglycaemia. Non-sulfonylurea drugs may be used as monotherapyor in combination with other oral hypoglycaemic agents or insulin.Troglitazone is a thiazolidinedione agent which improves insulin sensitivity anddecreases insulin resistance. When used as monotherapy it does not inducehypoglycaemia. It is active only in the presence of insulin.Repaglinide is a new antidiabetic agent that potentiates glucose-stimulatedinsulin secretion. It can produce hypoglycaemia, and serious cardiovascularevents have been reported.The biguanide, metformin, is often used as a monotherapy. When combined withsulfonylurea or insulin, however, it may also induce hypoglycaemia.The alpha-glycosidase inhibitors, acarbose and meglitol do not causehypoglycaemia unless given in combination with sulfonylurea.InsulinInsulin is classified as rapid, short, intermediate or long-acting. Each categoryinduces variable onset of peak activity and duration. Insulin injections are timedso that peak plasma levels coincide with peak postprandial glucose levels. It isimportant for the practitioner to know the medication regimen being used by thepatient, and any surgical therapy should be timed to avoid peak insulin activityand possible hypoglycaemic crisis
Management of Diabetic Emergencies in Dental OfficeDental practitioners must remain alert for possible complications and/oremergencies associated with diabetes mellitus.Hyperglycemia may lead to shock (diabetic coma), although the conditiondevelops relatively slowly and abrupt onset is unlikely. The hyperglycaemicpatient may become disoriented, breathing may become rapid and deep(Kussmaul‘s respiration), the skin may be hot and dry and ‗‗acetone‘‘ breath maybe evident.Severe hypotension and coma may follow. Coma is usually associated withplasma glucose levels of between 300 and 600 mg/dl. Patients experiencing thiscondition will usually remain conscious but should be transferred immediately toa hospital emergency room for evaluation.If the patient becomes unconscious, basic life support procedures should beinitiated (open airway, administration of 100% oxygen) and the emergencymedical alert system activated. If circumstances allow, non-glucose-containingintravenous fluids should be administered to prevent vascular collapse. Patientrecovery from diabetic coma may be slower than from hypoglycaemic shock.In contrast, hypoglycaemic shock is associated with relatively sudden onsetwhen plasma glucose levels drop below 40 mg/dl. It may be precipitated byexercise, diabetes mellitus drug overdose, stress or failure by the patient toproperly control his or her dietary intake.In many instances hyperglycaemic or hypoglycaemic shock may be difficult todifferentiate based on signs and symptoms. In both circumstances the patientmay experience mood changes, mental confusion, lethargy and increasinglybizarre behaviour. Although careful analysis may indicate the true nature of thepatient‘s condition, it is usually more prudent to treat unknown reactions bydiabetes mellitus patients in the dental office as though they were experiencinghypoglycaemia.Treatment should be initiated as quickly as possible since hypoglycaemia maylead to tachycardia, hypotension, hypothermia, loss of consciousness, seizuresand even death. Early treatment includes the administration of oralcarbohydrates such as orange juice, soft drinks, candy or glucola. Such agentsadministered during hyperglycaemic states will have little additional detrimentaleffects, while they may reverse hypoglycaemic status. Dextrose can beadministered intravenously to the conscious or unconscious patient, whileglucagon may be administered subcutaneously, intramuscularly, or intravenously(1 mg), followed by epinephrine (0.5 mg of 1:1000 concentration). Glucagon may
be less useful in type 2 diabetes mellitus, since its function is to stimulate insulinsecretion rather than decrease resistance.If the patient remains unresponsive, the emergency alert system should beactivated and the patient transferred to a hospital emergency room. In mostinstances, patients will become alert in response to therapy within five to tenminutes. In this event careful observation is necessary until the patient is fullystabilized. If possible the patient‘s own glucometer should be used to evaluatehis or her status. In any event the patient‘s physician should be notified.Ongoing multi centre studies of diabetic patients indicate that strict control ofblood glucose levels in both type 1 and type 2 patients close to the range ofnormal for non-diabetic individual‘s results in fewer medical complications.Consequently, increased emphasis is being placed on home monitoring andrigorous efforts by patients to maintain strict blood sugar control. Although, onbalance these efforts may greatly benefit the diabetes mellitus patient, there isalso strong evidence to suggest that maintenance of blood glucose levels closeto the range of normal can lead to an increased incidence of hypoglycaemia.Elderly diabetes mellitus patients are prone to develop insidious hypoglycaemiaand any diabetes mellitus patient may develop hypoglycaemia without displayingor sensing the common signs and symptoms.The dental practitioner must remain constantly alert for evidence of the conditionduring therapy and take steps to prevent its occurrence.Role of dentist in diagnosing systemic diseases* The oral systemic connection is more clearly understood, dentists who are trained indiagnosing oral and periodontal disease will play a greater role in the overall health oftheir patients. Many times, the first signs of unnatural systemic health conditions revealthemselves in changes within the oral cavity. Medical histories should be carefullyreviewed when ―at risk‖ patients are identified. A comprehensive Periodontal RiskEvaluation should be performed and results should be sent to the patient‘s treatingphysician(s).Physicians will play a more active role in the oral systemic connection. They will screen atrisk patients for the common signs of periodontal disease, which include bleeding gums,swollen gums, pus, shifting teeth, chronic bad breath and family history of periodontaldisease. When appropriate, they will refer them to dentists and Periodontists who areuniquely qualified to evaluate and treat their patient‘s oral conditions. This new era ofinterdisciplinary dental/medical cooperation will undoubtedly result in improved patienthealth, as well as an improvement in overall patient longevity.(Note: every * is from different website)