These notes for “Key concepts and terms” in the

DLP 2.6 sheet.

Gingivitis

Epidemiology

* Gingivitis is the mildest form of periodontal disease and affects 50% to 90% of

adults 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 US population has gingivitis with the prevalence slightly greater in males than females, and in black people and Mexican Americans than in white people. There is evidence that the prevalence of gingivitis has been decreasing in developed countries over the last few decades. Globally, there appears to be considerable heterogeneity in the prevalence of gingivitis with higher prevalence reported in certain parts of the world.

The prevalence of necrotising ulcerative gingivitis (NUG) varies widely, and it is frequently reported among young HIV/AIDS patients in some countries. Studies including outpatients, particularly after introduction of antiretroviral therapy, have shown relatively low prevalence figures, similar to those of the general population. This disease is frequently seen in developing countries, especially in sub-Saharan Africa, where it occurs almost exclusively among children, usually between the ages of 3 and 10 years, from low socio-economic backgrounds. Its prevalence has been reported to be about 0.3% in Swiss Army recruits and 3% in a 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 this disease increases from 2% to 3% of children with good oral hygiene to 67% of children with very poor oral hygiene.

* In recent years, tremendous strides have been made in understanding the

etiology 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 the epidemiological relationships between gingivitis and various host and environmental factors. The major restraint has been the great difficulty in reliably measuring gingival inflammation. This problem has resulted in great inter- and intra-study variation in diagnosing the prevalence and severity of gingivitis in human populations. Consequently, it is almost impossible to estimate longitudinal trends in gingivitis and it is nearly as difficult to make comparisons among different population groups studied by different examiners. Nevertheless, by focusing on the most apparent and robust epidemiological relationships, an instructive overview of the epidemiology of gingivitis can be gained. A number of host and environmental factors have been studied in relation to gingivitis and

some of these will be reviewed. With respect to age, there is general concensus that marginal gingivitis begins in early childhood, increases in prevalence and severity to the early teenage years, thereafter subsiding slightly and leveling off for the remainder of the second decade of life. Gingivitis during the adult period is much more difficult to characterize due to paucity of data. Estimates of the general prevalence of adult gingivitis vary from approximately 50 to 100% for dentate subjects. In terms of gingivitis prevalence, the dentate elderly do not deviate appreciably from the general adult pattern. When adjusted for cohort effects, gingival disease appears to be on the decline.(ABSTRACT TRUNCATED AT 400 WORDS)

Etiology

* The etiology, or cause, of plaque-induced gingivitis is bacterial plaque, which

acts to initiate the body's host response. This, in turn, can lead to destruction of

the gingival tissues, which may progress to destruction of the periodontal

attachment apparatus.[6] The plaque accumulates in the small gaps between

teeth, in the gingival grooves and in areas known as plaque traps: locations that

serve to accumulate and maintain plaque. Examples of plaque traps include

bulky and overhanging restorative margins, claps of removable partial dentures

and calculus (tartar) that forms on teeth. Although these accumulations may be

tiny, the bacteria in them produce chemicals, such as degrative enzymes, and

toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or

lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue.

This inflammation can cause an enlargement of the gingiva and subsequent

formation.

Risk factors

* Gingivitis is very common, and anyone can develop it. Many people first

experience gum problems during puberty and then in varying degrees throughout life.

Factors that can increase your risk of gingivitis include:

Poor oral health habits

Tobacco use

Diabetes

Older age

Decreased immunity as a result of leukemia, HIV/AIDS or other conditions

Certain medications

Certain viral and fungal infections

Dry mouth

Hormonal changes, such as those related to pregnancy, your menstrual cycle or

use of oral contraceptives

Poor nutrition

Substance abuse

Ill-fitting dental restorations

Management

* Richard H. Nagelberg, DDS , says: My previous post indicated that I approach

gingivitis in my general dental practice, as a non-reversible disease entitiy. I have

conluded from professional reading, dialogue with other practitioners and my

clinical judgment and experience, that it is not a separate disease entity from

periodontitis, just an early manifestation. Think about other conditions such as

diabetes. When an individual is diagnosed with Type II diabetes, which accounts

for 90-95% of all cases, they are commonly put on dietary control, not a regimen

of oral meds and/or insulin, with frequent monitoring. The early manifestations of

the disease commonly do not require intervention; however, if there is a lack of

compliance, then more aggressive attention such as one or more medications

will be necessary to achieve adequate glycemic control. Most importantly, a

casual approach to the diabetes would be inappropriate and increase the

likelihood of disease progression. If gingivitis is pro-actively approached as an

early non-reversible manifestation of periodontitis, the likelihood of returning the

patient to health is increased considerably. Assuming the cause of the gingivitis

is poor biofilm control, rather than an exaggreated host response, having the

patient describe their home care in detail is indicated, along with an examination

of their risk factors (covered in an earlier blog post). Among the most important

recommendations, in my opinion and experience, is recommending a power

toothbrush. My preference is the Philips Sonicare Flexcare. I have seen

consistently excellent results with its usage. Other recommendations would

include an antimicrobial mouthrinse, my preference being Listerine, twice daily.

Interdental cleaning tools such as floss, Proxabrushes, floss picks, rubber tip

stimulators and so on are indicated as needed for specific patients. A tongue

cleaner is another easy tool for patients to use to help reduce the total bacterial

population in the mouth. Perhaps, most importantly is need for patient education.

Taking the time to educate our patients on the importance of meticulous biofilm

control, and the potential consequences of non-compliance will help the patient

understand why it is so important to change home care habits. Monitoring at 30

day intervals should also be considered, tweaking the home care as needed. If

gingivitis is present despite good biofilm control, DNA testing is indicated,

including testing the bacterial DNA and perhaps the patient's genetic

predisposition for perio disease (PST testing). Both salivary diagnostic tests are

available from OralDNA Labs (OralDNA.com). This scenario will be discussed in

a future blog post. As always, comments are welcome.

Periodontitis

Epidemiology

* There is a conspicuous lack of uniformity in the definition of periodontitis used

in epidemiologic studies, and findings from different research groups are not

readily interpretable. There is a lack of studies that specifically address the

distinction between factors responsible for the onset of periodontitis versus those

affecting its progression. Colonization by specific bacteria at high levels,

smoking, and poorly controlled diabetes have been established as risk factors for

periodontitis, while a number of putative factors, including specific gene

polymorphisms, have been identified in association studies. There is a clear need

for longitudinal prospective studies that address hypotheses emerging from the

cross-sectional data and include established risk factors as covariates along with

new exposures of interest. Intervention studies, fulfilling the "targeting" step of

the risk assessment process, are particularly warranted. Obvious candidates in

this context are studies of the efficacy of elimination of specific bacterial species

and of smoking cessation interventions as an alternative to the traditional broad

anti-plaque approach in the prevention and control of periodontitis. Ideally, such

studies should have a randomized-controlled trial design.

*Unfortunately, periodontitis is extremely common, occurring in an estimated

35% of U.S. residents ages 30 and older.Approximately 63% have a mild form,

while the remaining 37% have moderate to severe periodontitis. Periodontal

disease is also the leading cause of tooth loss for those older than 40.3 Risk

factors 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 that

support 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 the accumulation of a mycotic and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes. New finger nick tests have been approved by the Food and Drug Administration in the US, and are being used in dental offices to identify and screen patients for possible contributory causes of gum disease such as diabetes.

In some people, gingivitis progresses to periodontitis –- with the destruction of the gingival fibers, the gum tissues separate from the tooth and deepened sulcus, called a periodontal pocket. Subgingival microorganism (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples of secondary etiology are those things that, by definition, cause microbic plaque accumulation, such as restoration overhangs and root proximity.

Smoking is another factor that increases the occurrence of periodontitis, directly or 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 commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbic plaque that adheres to the tooth surface, there are many other modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one's resistance to infection also increase susceptibility to periodontitis.

Another factor that makes periodontitis a difficult disease to study is that human host response can also affect the alveolar bone resorption. Host response to the bacterial-mycotic insult is mainly determined by genetics; however, immune development may play some role in susceptibility.

According to some researches periodontitis may be associated with higher stress.

Risk factors

* Factors that can increase your risk of periodontitis include:

Gingivitis

Heredity

Poor oral health habits

Tobacco use

Diabetes

Older age

Decreased immunity, such as that occurring with leukemia or HIV/AIDS or

chemotherapy

Poor nutrition

Certain medications

Hormonal changes, such as those related to pregnancy or menopause

Substance abuse

Ill-fitting dental restorations

(See also Dr.Abeer’s lectures + the PowerPoint of “Risk factors associated

with periodontal disease)

Management

* While risk assessment for periodontal disease is largely the domain of the

dental care professional, periodontal disease management (including disease prevention) requires the patient‘s participation. Indeed, self-care has been a key component of preventive dentistry for years. Axelsson and colleagues3 conducted a long-term study of plaque control in adults that showed administration of frequent, regular education in self-diagnosis and self-care techniques resulted in more healthy tooth surfaces, less periodontal attachment loss and fewer sites requiring periodontal care.

As illustrated in the figure , a self-care regimen of brushing, flossing and rinsing with an antimicrobial mouthrinse can help control dental plaque biofilm. For patients without periodontal disease, this three-step approach can help prevent

the onset of periodontal disease. For patients with periodontal disease, this approach can play a secondary preventive role in early disease control, as well as be an important component of conservative therapy. In addition, self-care with particular oral rinses can be important for the postsurgical management of plaque-induced tissue inflammation.

Figure. A three-step approach to daily oral health care can be part of the regimen for patients with a healthy periodontium, those with gingivitis and those with periodontitis. In each case, the intent is to reduce the microbial challenge.

Clearly, patient motivation regarding disease management is critical if the benefits of self-care are to be realized; this may require individualized patient education to ensure that each patient appreciates the relevance of self-care to the enhancement of his or her own oral health. (For more information on patient adherence to self-care, see the article by Silverman and Wilder in this supplement.)

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 physically

disrupted (eg, by injury, IV catheter, or surgical incision). Exceptions include

human papillomavirus, which can invade normal skin, causing warts, and some

parasites (eg, Schistosoma mansoni, Strongyloides stercoralis).

Mucous membranes: Many mucous membranes are bathed in secretions that

have antimicrobial properties (eg, cervical mucus, prostatic fluid, and tears

containing lysozyme, which splits the muramic acid linkage in bacterial cell walls,

especially in gram-positive organisms). Local secretions also contain

immunoglobulins, principally IgG and secretory IgA, which prevent

microorganisms from attaching to host cells.

Respiratory tract: The respiratory tract has upper airway filters. If invading

organisms reach the tracheobronchial tree, the mucociliary epithelium transports

them away from the lung. Coughing also helps remove organisms. If the

organisms reach the alveoli, alveolar macrophages and tissue histiocytes engulf

them. However, these defenses can be overcome by large numbers of

organisms or by compromised effectiveness resulting from air pollutants (eg,

cigarette smoke) or interference with protective mechanisms (eg, endotracheal

intubation, tracheostomy).

GI tract: GI tract barriers include the acid pH of the stomach and the antibacterial

activity of pancreatic enzymes, bile, and intestinal secretions. Peristalsis and the

normal loss of epithelial cells remove microorganisms. If peristalsis is slowed (eg,

because of drugs such as belladonna or opium alkaloids), this removal is delayed

and prolongs some infections, such as symptomatic shigellosis. Compromised GI

defense mechanisms may predispose patients to particular infections (eg,

achlorhydria predisposes to salmonellosis). Normal bowel flora can inhibit

pathogens; alteration of this flora with antibiotics can allow overgrowth of

inherently pathogenic microorganisms (eg, Salmonella typhimurium) or

superinfection with ordinarily commensal organisms (eg, Candida albicans).

GU tract: GU tract barriers include the length of the urethra (20 cm) in men, the

acid pH of the vagina in women, and the hypertonic state of the kidney medulla.

The kidneys also produce and excrete large amounts of Tamm-Horsfall

mucoprotein, which binds certain bacteria, facilitating their harmless excretion.

Nonspecific Immune Responses

Cytokines (including IL-1, IL-6, tumor necrosis factor, interferon-γ) are produced

principally by macrophages and activated lymphocytes and mediate an acute-

phase response that develops regardless of the inciting microorganism (see also

Biology of the Immune System: Cytokines). The response involves fever and

increased production of neutrophils by the bone marrow. Endothelial cells also

produce large amounts of IL-8, which attracts neutrophils.

The inflammatory response directs immune system components to injury or

infection sites and is manifested by increased blood supply and vascular

permeability, which allows chemotactic peptides, neutrophils, and mononuclear

cells to leave the intravascular compartment. Microbial spread is limited by

engulfment of microorganisms by phagocytes (eg, neutrophils, macrophages).

Phagocytes are drawn to microbes via chemotaxis and engulf them, releasing

phagocytic lysosomal contents that help destroy microbes. Oxidative products

such as hydrogen peroxide are generated by the phagocytes and kill ingested

microbes. When quantitative or qualitative defects in neutrophils result in

infection, the infection is usually prolonged and recurrent and responds slowly to

antimicrobial drugs. Staphylococci, gram-negative organisms, and fungi are the

pathogens usually responsible.

Specific Immune Responses

After infection, the host can produce a variety of antibodies, complex

glycoproteins known as immunoglobulins that bind to specific microbial antigenic

targets. Antibodies can help eradicate the infecting organism by attracting the

host's 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 the

surface of some microorganisms via the alternative pathway. Antibodies can also

promote the deposition of substances known as opsonins (eg, the complement

protein C3b) on the surface of microorganisms, which helps promote

phagocytosis. Opsonization is important for eradication of encapsulated

organisms such as pneumococci and meningococci.

Control of fuel metabolism

* Metabolism (pronounced: muh-tah-buh-lih-zum) is a collection of chemical

reactions that takes place in the body's cells. Metabolism converts the fuel in the

food 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 reactions

of metabolism, and each chemical reaction is coordinated with other body

functions. 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 we're conceived and ends

when we die. It is a vital process for all life forms — not just humans. If

metabolism stops, living things die.

Here's an example of how the process of metabolism works in humans — and it

begins with plants. First, a green plant takes in energy from sunlight. The plant

uses this energy and a molecule called cholorophyll (which gives plants their

green color) to build sugars from water and carbon dioxide. This process is called

photosynthesis, and you probably learned about it in biology class.

When people and animals eat the plants (or, if they're carnivores, they eat

animals that have eaten the plants), they take in this energy (in the form of

sugar), along with other vital cell-building chemicals. The body's next step is to

break the sugar down so that the energy released can be distributed to, and used

as fuel by, the body's cells.

After food is eaten, molecules in the digestive system called enzymes break

proteins down into amino acids, fats into fatty acids, and carbohydrates into

simple sugars (e.g., glucose). In addition to sugar, both amino acids and fatty

acids can be used as energy sources by the body when needed. These

compounds are absorbed into the blood, which transports them to the cells. After

they enter the cells, other enzymes act to speed up or regulate the chemical

reactions involved with "metabolizing" these compounds. During these

processes, the energy from these compounds can be released for use by the

body or stored in body tissues, especially the liver, muscles, and body fat.

A Balancing Act

In this way, the process of metabolism is really a balancing act involving two

kinds of activities that go on at the same time — the building up of body tissues

and energy stores and the breaking down of body tissues and energy stores to

generate 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 the

rate and direction of metabolism. Thyroxine (pronounced: thigh-rahk-sun), a

hormone produced and released by the thyroid (pronounced: thigh-royd) gland,

plays a key role in determining how fast or slow the chemical reactions of

metabolism proceed in a person's body.

Another gland, the pancreas (pronounced: pan-kree-us) secretes (gives off)

hormones that help determine whether the body's main metabolic activity at a

particular time will be anabolic or catabolic. For example, after eating a meal,

usually more anabolic activity occurs because eating increases the level of

glucose — the body's most important fuel — in the blood. The pancreas senses

this 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 it's not surprising that many

people think of it in its simplest sense: as something that influences how easily

our bodies gain or lose weight. That's where calories come in. A calorie is a unit

that measures how much energy a particular food provides to the body. A

chocolate bar has more calories than an apple, so it provides the body with more

energy — and sometimes that can be too much of a good thing. Just as a car

stores gas in the gas tank until it is needed to fuel the engine, the body stores

calories — primarily as fat. If you overfill a car's gas tank, it spills over onto the

pavement. Likewise, if a person eats too many calories, they "spill over" in the

form of excess fat on the body.

The number of calories a person burns in a day is affected by how much that

person exercises, the amount of fat and muscle in his or her body, and the

person's basal metabolic rate. The basal metabolic rate, or BMR, is a measure

of the rate at which a person's body "burns" energy, in the form of calories, while

at rest. The BMR can play a role in a person's tendency to gain weight. For

example, a person with a low BMR (who therefore burns fewer calories while at

rest or sleeping) will tend to gain more pounds of body fat over time, compared

with a similar-sized person with an average BMR who eats the same amount of

food and gets the same amount of exercise.

What factors influence a person's BMR? To a certain extent, a person's basal

metabolic rate is inherited — passed on through the genes the person gets from

his or her parents. Sometimes health problems can affect a person's BMR (see

below). 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 from

the extra activity itself, but becoming more physically fit will increase BMR as

well. BMR is also influenced by body composition — people with more muscle

and less fat generally have higher BMRs.

Altered control of fuel metabolism in diabetes

mellitus

* Type 1 diabetes mellitus (pronounced: dye-uh-bee-teez meh-luh-tus). Type 1

diabetes occurs when the pancreas doesn't produce and secrete enough insulin.

Symptoms of this disease include excessive thirst and urination, hunger, and

weight loss. Over the long term, the disease can cause kidney problems, pain

due to nerve damage, blindness, and heart and blood vessel disease. Teens with

type 1 diabetes need to receive regular injections of insulin and control blood

sugar levels to reduce the risk of developing problems from diabetes.

Type 2 diabetes. Type 2 diabetes happens when the body can't respond

normally to insulin. The symptoms of this disorder are similar to those of type 1

diabetes. 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 oral

medication, but insulin injections are necessary in other cases. Controlling blood

sugar levels reduces the risk of developing the same kinds of long-term health

problems that occur with type 1 diabetes.

Pathophysiology of diabetes mellitus

Sysmtemic and oral

* Diabetes mellitus is another systemic condition with oral inflammatory

connections. One of the major complications of diabetes is periodontitis. While diabetes increases the probability of developing periodontal disease, periodontitis also increases the risk of poor glycemic control in people with diabetes when compared to those individuals with diabetes without periodontitis. Fortunately, periodontal treatment can improve glycemic control by reducing the bacterial burden and the inflammatory response.

There are several biological mechanisms proposed to explain the increased incidence and severity of periodontal disease in individuals with diabetes. Diabetes tends to increase susceptibility to infection--including oral infection--and the 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 the gingival crevicular fluid of periodontal pockets of poorly controlled patients with diabetes as compared to those without diabetes or those with diabetes who are well controlled. These patients had significant periodontal destruction with an equivalent bacterial challenge. In particular, the proinflammatory cytokine, TNF-α, plays a major role in this process. TNF- α has a significant role in insulin resistance, the primary cause of type 2 diabetes. It is produced in large quantities by 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 that repair damaged connective tissue or bone and may exacerbate insulin resistance and worsen glycemic control.

It has also been hypothesized that diabetes interferes with the capacity to form new bone after periodontal diseases have caused bone resorption. Graves, et al., studied genetically diabetic mice with type 2 diabetes and nondiabetic littermates by injecting them with P. gingivalis. The death of osteoblasts was measured, and results indicated that there was a higher and more prolonged rate of osteoblast cell death in the diabetic group. It was concluded that the capacity to repair a bony defect by producing new bone would be severely limited when osteoblasts died prematurely. Yet further study is needed in this area to refine this concept.

As with CVD and diabetes mellitus, there is a relationship between oral infection and respiratory disease. In particular, chronic obstructive pulmonary disease (COPD) and pneumonia have been associated with poor oral health. It is likely that oral biofilm serves as a reservoir of infection for respiratory bacteria. Specifically, Pseudomonas aeruginosa, Staphylococcus aureus, and enteric bacteria that has been shown to colonize the teeth of patients admitted to hospitals or long-term care facilities. These bacteria may be released into saliva and then aspirated into the lower airway causing infection. Another vehicle by which bacteria from the oral cavity can be introduced into the respiratory system is intubation.

Management of oral health of diabetes mellitus patients

* When the dental practitioner is called upon to provide dental treatment for a

previously diagnosed diabetes mellitus patient, a certain amount of detailed information should be gathered. The patient should be questioned regarding the type of diabetes, the age at onset and duration of the disease; any current medications and their method of administration. The patient‘s degree of compliance 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 of the patient‘s physician(s). By gathering this information the clinician can best relate the patient‘s oral condition to his or her systemic status and determine whether or not medical consultation is required. Under most circumstances it would be prudent to obtain medical clearance prior to performing any extensive dental therapy, especially if surgery is indicated.

In most instances the well-controlled type 1 or type 2 patient can be managed in a manner consistent with a healthy non-diabetic individual.

Periodontal surgical procedures can be performed, although it must be assured that the patient can maintain a normal diet post-surgically. In the event that the treatment procedure modifies the patient‘s dietary habits, dietary supplements should be recommended.

Supportive therapy such as scaling and root planning should be provided at relatively close intervals (2 to 3 months) since some studies indicate a slight but persistent tendency to progressive periodontal destruction despite effective metabolic diabetes mellitus control.

Management of Uncontrolled or Poorly Controlled Diabetic Patients

The uncontrolled or poorly controlled diabetic patient or the diabetes mellitus patient who does not know his or her control status should not receive elective dental treatment until the condition is stabilized or medical clearance obtained.

Prophylactic antibiotic therapy should be used for performance of emergency oral or surgical procedures to minimize the potential for postoperative infections and delayed wound healing.

Any therapy other than emergency treatment may be contraindicated in the poorly controlled diabetes mellitus patient until appropriate metabolic controlled is achieved.

In many instances this may require short- or long-term prescription of insulin or oral medications by the physician.

Oral Medications for Diabetic Control

For many years, type 2 diabetes mellitus has been treated by diet control and various hypoglycaemic agents, usually a first- or second-generation sulfonylurea (acetohexamide, chlorpropamide, tolazamide, tolbutamide, glimepiride, glipizide or glyburide).

Sulfonylurea promotes insulin secretion, and importantly, they are all capable of inducing hypoglycaemia. Non-sulfonylurea drugs may be used as monotherapy or in combination with other oral hypoglycaemic agents or insulin.

Troglitazone is a thiazolidinedione agent which improves insulin sensitivity and decreases insulin resistance. When used as monotherapy it does not induce hypoglycaemia. It is active only in the presence of insulin.

Repaglinide is a new antidiabetic agent that potentiates glucose-stimulated insulin secretion. It can produce hypoglycaemia, and serious cardiovascular events have been reported.

The biguanide, metformin, is often used as a monotherapy. When combined with sulfonylurea or insulin, however, it may also induce hypoglycaemia.

The alpha-glycosidase inhibitors, acarbose and meglitol do not cause hypoglycaemia unless given in combination with sulfonylurea.

Insulin

Insulin is classified as rapid, short, intermediate or long-acting. Each category induces variable onset of peak activity and duration. Insulin injections are timed so that peak plasma levels coincide with peak postprandial glucose levels. It is important for the practitioner to know the medication regimen being used by the patient, and any surgical therapy should be timed to avoid peak insulin activity and possible hypoglycaemic crisis

Management of Diabetic Emergencies in Dental Office

Dental practitioners must remain alert for possible complications and/or emergencies associated with diabetes mellitus.

Hyperglycemia may lead to shock (diabetic coma), although the condition develops relatively slowly and abrupt onset is unlikely. The hyperglycaemic patient may become disoriented, breathing may become rapid and deep (Kussmaul‘s respiration), the skin may be hot and dry and ‗‗acetone‘‘ breath may be evident.

Severe hypotension and coma may follow. Coma is usually associated with plasma glucose levels of between 300 and 600 mg/dl. Patients experiencing this condition will usually remain conscious but should be transferred immediately to a hospital emergency room for evaluation.

If the patient becomes unconscious, basic life support procedures should be initiated (open airway, administration of 100% oxygen) and the emergency medical alert system activated. If circumstances allow, non-glucose-containing intravenous fluids should be administered to prevent vascular collapse. Patient recovery from diabetic coma may be slower than from hypoglycaemic shock.

In contrast, hypoglycaemic shock is associated with relatively sudden onset when plasma glucose levels drop below 40 mg/dl. It may be precipitated by exercise, diabetes mellitus drug overdose, stress or failure by the patient to properly control his or her dietary intake.

In many instances hyperglycaemic or hypoglycaemic shock may be difficult to differentiate based on signs and symptoms. In both circumstances the patient may experience mood changes, mental confusion, lethargy and increasingly bizarre behaviour. Although careful analysis may indicate the true nature of the patient‘s condition, it is usually more prudent to treat unknown reactions by diabetes mellitus patients in the dental office as though they were experiencing hypoglycaemia.

Treatment should be initiated as quickly as possible since hypoglycaemia may lead to tachycardia, hypotension, hypothermia, loss of consciousness, seizures and even death. Early treatment includes the administration of oral carbohydrates such as orange juice, soft drinks, candy or glucola. Such agents administered during hyperglycaemic states will have little additional detrimental effects, while they may reverse hypoglycaemic status. Dextrose can be administered intravenously to the conscious or unconscious patient, while glucagon 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 insulin secretion rather than decrease resistance.

If the patient remains unresponsive, the emergency alert system should be activated and the patient transferred to a hospital emergency room. In most instances, patients will become alert in response to therapy within five to ten minutes. In this event careful observation is necessary until the patient is fully stabilized. If possible the patient‘s own glucometer should be used to evaluate his or her status. In any event the patient‘s physician should be notified.

Ongoing multi centre studies of diabetic patients indicate that strict control of blood glucose levels in both type 1 and type 2 patients close to the range of normal for non-diabetic individual‘s results in fewer medical complications. Consequently, increased emphasis is being placed on home monitoring and rigorous efforts by patients to maintain strict blood sugar control. Although, on balance these efforts may greatly benefit the diabetes mellitus patient, there is also strong evidence to suggest that maintenance of blood glucose levels close to the range of normal can lead to an increased incidence of hypoglycaemia.

Elderly diabetes mellitus patients are prone to develop insidious hypoglycaemia and any diabetes mellitus patient may develop hypoglycaemia without displaying or sensing the common signs and symptoms.

The dental practitioner must remain constantly alert for evidence of the condition during 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 in

diagnosing oral and periodontal disease will play a greater role in the overall health of their patients. Many times, the first signs of unnatural systemic health conditions reveal themselves in changes within the oral cavity. Medical histories should be carefully reviewed when ―at risk‖ patients are identified. A comprehensive Periodontal Risk Evaluation should be performed and results should be sent to the patient‘s treating physician(s). Physicians will play a more active role in the oral systemic connection. They will screen at risk patients for the common signs of periodontal disease, which include bleeding gums, swollen gums, pus, shifting teeth, chronic bad breath and family history of periodontal disease. When appropriate, they will refer them to dentists and Periodontists who are uniquely qualified to evaluate and treat their patient‘s oral conditions. This new era of interdisciplinary dental/medical cooperation will undoubtedly result in improved patient health, as well as an improvement in overall patient longevity.

(Note: every * is from different website)