5. Etiology and pathogenesis of inflammatory periodontal diseases. The contribution of domestic scientists. ( E.V. Udovytska, G.M. Vyshniak, M.F. Danylevskyy, P.T. Maksymenko, I.S. Maschenko). Papillitis. Clinical features, diagnosis, treatment and prevention.
Periodontal disease is progressive and episodic iature, with tissue destruction resulting from the host response to bacterial antigens and irritants. Risk factors encompass systemic influences, external influences, intrinsic factors and local factors. An individual patient’s responsiveness to treatment also depends on the host response and the presence of risk factors. Adjunctive systemic and/or local therapy can positively impact periodontal therapy. Considerations in determining which to select in- clude clinical preference and efficacy.
Periodontal disease is an inflammatory process involving progressive, episodic loss of the periodontal attachment apparatus, resulting ultimately in tooth loss in susceptible patients. From the 1999-2004 National Health and Nutrition Examination Survey III (NHANES III) data, Eke and Barker estimated that the prevalence of moderate and severe periodontal disease was less than 1% in the under-35 age group, with increasing prevalence in older age groups. In the 75-and-older age group, it is estimated that the prevalence in the United States is approximately 18% for moderate periodontitis and 7% for severe periodontitis
Biofilm and periodontal disease
Dental biofilm, also known as plaque, develops and matures over a period of several weeks, initially developing supra gingiva with mainly aerobic bacteria. Over time, the flora changes from predominantly gram-positive to gram-negative, from facultative aerobes to strictly anaerobic species, with more motile forms pres- ent. Mature subgingival biofilm takes up to 12 weeks to develop. As biofilm accumulates, gingivitis develops over a period of several days in the presence of periodontal bacteria. Gingivitis may be a nonspecific bacterial infection dependent on the level of plaque present.
It should be noted that no individual is truly biofilm free; there is either a healthy biofilm in place or a pathogenic biofilm contributing to caries and periodontal disease. The supragingival biofilm forms a reservoir for periodontal bacteria and the development of subgingival biofilm. As the biofilm matures, the concentration and virulence of the periodontal bacteria change.
A recent study on supragingival plaque by Haffajee et al. in 187 subjects found that, over a period of seven days from baseline after pro- fessional prophylaxis, plaque regrowth resulted in the development of bacterial complexes similar to subgingival biofilm. The amount of supragingival plaque changed the flora composition. The heaviest plaques were found to harbor a higher proportion of green and orange complexes, and the lighter plaque harbored yellow, orange and purple bacterial complexes. The total number of bacteria was associated with the level of gingival inflammation, recession and pocket depth.
Mature subgingival biofilm is dynamic, well organized and structured as a solid mass with fluid-filled channels within it; protects bacteria in its depth with diffusion barriers; and enables the migration and colonization of periodontal bacteria at adjacent periodontal sites and in periodontal tissues themselves. This is a key point, as biofilm disruption is a necessary step when using either local or systemic antibiotic therapy. Undisrupted biofilm may decrease the efficacy of antimicrobial therapy. Subgingival bacteria were classified by Socransky and Haffajee and grouped into five major complexes of varying virulence. Across all subjects with periodontal disease, the first complex (the red complex) was consistently associated with periodontal disease, as evidenced by bleeding upon probing and pocket depth measurements.
This red complex includes Tannerella forsythia (T. forsythia, previously known as Bacteroides forsythus), Porphyromonas gingivalis (P. gingivalis) and Treponema denticola (T. denticola). Research the same year by Dibart et al. in 51 individuals determined that in clinically healthy subjects the majority of sites were associ– ated with the presence of Streptococcus oralis (S. oralis), while in diseased sites greater numbers of T. forsythia (B. forsythus), Prevotella intermedia (P. intermedia), Capnocytophaga ochracea and Campylobacter rectus were found.
Virulent periodontal bacteria, specifically P. gingivalis and Actinobacillus actinomycetemcomitans (now Aggregatibacter actinomycetemcomitans), are commonly found in patients with periodontal disease and rarely found in patients with a healthy periodontium. Van Winkelhoff et al. found a significantly greater presence of specific bacteria in patients with periodontal disease: A. actinomycetemcomitans, P. gingivalis, T. forsythia (B. forsythus), P. intermedia, Fusobacterium nucleatum and Peptostreptococcus micros. They concluded that the presence of these bacteria is a marker for destructive periodontal disease.
The current concept concerning the etiology of periodontal disease considers 3 groups of factors, which determine whether active periodontal disease will occur:
1. a susceptible host,
2. the presence of pathogenic species,
3. the absence of so-called “beneficial bacteria”.
It is generally accepted that the oral biofilm in association with anaerobic bacteria is the main etiological factor in periodontal disease.
The oral biofilm consists mainly of microbes and host proteins that adhere to teeth within minutes of a dental oral hygiene procedure. Healthy gingival sulcus has a flora dominated by equal proportions of Gram positive cocci, especially Streptococcus spp, and Actinomuces sp. Later, plaque “matures” resulting in a flora consisting from facultative anaerobic microorganisms, spirochaetes and motile rods. The proportions of strict anaerobic, Gram negative and motile organisms increase significantly in accordance with increasing severity of disease. Disease activity in periodontal disease may range from slow, chronic, progressive destruction to brief and acute episodic bursts with varying intensity and duration.
The composition of the subgingival microbial flora and the level of pathogenic species differ from subject to subject as well as from site to site. The search for the pathogens of periodontal diseases has been underway for more than 100 years, and continues up today.
The currently recognized key Gram negative periodontopathogens include:
Porphyromonas gingivalis (P.g),
Prevotella intermedia (P.i),
Bacteroides forsythus (B.f),
Aggregatibacter actinomycetemcomitans (A.a),
Fuso- bacterium nucleatum (F.n),
Capnocytophaga species (C.sp),
Campylobacter rectus (C.r).
Also, the following bacteria could be isolated: Eubacterium spp, Peptostreptococcus micros, Selenomonas spp, Spirochaetes. The range of putative pathogens has been ex- tended to include not only cultivated bacteria but also non-cultivated bacteria and viruses. A correlation was found between P.g, P.i, C.r, Eikenella corrodens, Selenomonas sp, Bacteroides species, Spirochetes and adult or refractory periodontal disease.
The microorganisms could produce disease directly, by invasion on the tissues, or indirectly by bacterial enzymes and toxins.
In order to be a periodontal pathogen, a microorganism is must have the following:
1. • the organism must occur at higher numbers in disease-active sites than at disease-inactive sites
2. • elimination of the organism should arrest disease progression
3. • the organism should possess virulence factors relevant to the disease process
4. the organism should elicit a humoral or cellular immune response animal pathogenicity testing should infer disease potential.
5. the innate immune response could be attacked directly.
A.a endotoxin has the potential to modulate host responses and contribute to tissue destruction. The ability of the Aa lipopolysaccharide to stimulate macrophages to release interleukin IL-1, IL-1β, and tumor necrosis factor (TNF) is of big importance. These cytokines, among other their activities, are capable of stimulating bone resorption . P.g and A.a are suggested to represent exogenous microorganisms based on their low levels in periodontally healthy subjects. It has been suggested that periodontal infections associated with these pathogens represent “true infection”.
Prevotella intermedia
Prevotella intermedia, former Bacteroides intermedius, is a black pigmented Gram negative bacterium. This species resists phagocytosis, probably by virtue of its capsule. P.i is an important periodontal pathogen, in association with P.g and A.a .
Fusobacterium nucleatum
F.n. is an important periodontal pathogen, particularly in the beginning of the rapidly progressive periodontal disease. It creates very strong lipopoysaccharide as well as butyric acid as a metabolic end product.
Bacteroides forsythus
Tannerella forsythensis (T.f) – formerly Bacteroides forsythus – is a non-pigmented saccharolytic anaerobic gram-negative rod. T. f possesses several virulence factors including the production of a trypsin-like protease and lipopolysaccharide but recently, its ability to penetrate into host cells or induce apoptosis.
Capnocytophaga species
Capnocytophaga are micro-aerophilic Gram negative rods. There are three species – C.ochracea (formerly Bacteroides ochracea), C.sputigena and C.gingivalis. C.ochracea is implicated in the beginning of a juvenile periodontal disease, and adult periodontal disease. This bacterium produces lipopolysaccharide with activity on alveolar bone, extracellular proteases which could damage immunoglobulins.
Peptostreptococcus micros
Peptostreptococcus micros (P.m) is an anaerobic, Gram positive bacterium which is associated with periodontal disease as well as several other polymicro– bial infections in other systemic diseases . The prevalence of P.m in advanced adult periodontitis
Porphyromonas gingivalis
This bacterium, previously known as Bacteroides gingivalis, is a strictly anaerobic, Gram negative rod. It is a black-pigmented microorganism which produces a black pigment. Many virulence mechanisms have been identified. P.g. has a carbohydrate capsule on its outer surface which prevents opsonization by complement and inhibits phagocytosis and killing by neutrophils. The lipopolysaccharide which is produced is not very strong, but it could inhibit chemotaxis and killing by leucocytes. This organism possesses several putative virulence factors (including proteases which degrade immunoglobulin, complement, collagen fibres, hyalu– ronic acid; adhesins, endotoxins, and cytotoxins) that can directly affect the periodontium or elicit host func– tions that result in the gingival tissue and bone damage typical for periodontal disease. Pg expresses three major virulence factors-fimbriae, gingvipains and lipopolysaccharides.
P.g is a one of the major periodontopathogen with the ability to adhere, and to invade oral epithelia in vitro. Differences exist in the adhesion capacity of P.g among laboratory and clinical strains . This has been attributed to the differences in the surface characteristics between strains, espe– cially the presence of fimbriae .
The lipopolysaccharide of Pg is unique, based on the chemical structure of its core polysaccharide and lipid A regions and in its biological activity .
Its importance as a periodontal pathogen is also highlighted by the research efforts aimed at developing a vaccine aimed at immunization against this bacterial species and thus preventing a chronic periodontal disease ..
Aggregatibacter actinomycetemcomitans
A.a., previously Actinobacillus actinomycetem– comitans, is a Gram negative facultative non motile coccoid bacillus. Its presence in the periodontal pocket is associated with preadolescent, localized juvenile and advanced adult aggressive periodontal disease. Several virulence factors are reported: the leukotoxin is the most important, cytolethal distending toxin, immunosuppression factors, inhibition of PMNS functions etc.
Leukotoxin, is an RTX (Repeats in Toxin) toxin and shares sequence similarity with the α-hemolysin from Escherichia coli, the cytolysin from Pasteurella haemolytica and the leukotoxin from Actinobacillus pleuropneumoniae. Leukotoxin from A.a could kill human and non-human primate polimorphopnuclear leukocytes and peripheral blood monocytes.
Spirochaetes
Spirochaetes are motile spiral-shaped microorganisms with flagella. They are not associated with locaized juvenile periodontal disease, but two important species – Treponema denticola (T.d) and Treponema vincentii. They could be implicated in periodontal dis- ease. Both of them produce a lipopolysaccharide, and unusual metabolic end products, like indole, hydrogen sulphide, ammonia, which are potentially toxic to host cells.
Spirochetes were observed in a higher proportion of patients with periodontal disease than in periodontally healthy patients .
T.d is frequently isolated from severely diseased sites in patients with a periodontal disease . Many studies have attempted to elucidate the role of T.d in periodontitis . T.d has been shown to attach to human gingival fibroblasts, basement membrane proteins, as well as other substrates by specific attachment mechanisms, the binding of the spirochete to human gingival fibroblasts resulted in cytotoxicity and cell death due to enzymes and other proteins.
Takeuchi et al 2001 found that Treponema socransky (T.s), T.d and P.g. were frequently detected in patients with a periodontal disease by PCR technique in plaque and saliva samples. They also found that the presence of T.s was associated with periodontitis, as well as that T.socranskii was more frequently detected in plaque samples from aggressive or chronic periodontitis patients than from healthy subjects. T.s were detected more frequently at sites where a severe periodontal tissue destruction was observed.
Human viruses
Human viruses have also been implicated in periodontitis. Recent findings have begun to provide a basis for a causal link between herpes viruses and aggressive periodontitis. One theory is that herpes viruses cooper- ate with specific bacteria in the etiopathogenesis of the disease. Namely, periodontal herpes viruses comprise an important source for triggering periodontal tissue de- struction . In cross sectional studies, viruses in Herpes family have been isolated from the lesions of periodontitis patients . Their genomes have been found in chronic periodontal disease , aggressive periodontal disease and periodontal disease associated with systemic diseases.
Herpes virus productive infection may initiate or accelerate periodontal tissue destruction due to a virally mediated release of cytokines and chemokines from inflammatory and non-inflammatory host cells, or a virally induced impairment of the periodontal defense resulting in a heightened virulence of resident pathogenic bacteria . Human cytomegalovirus and Epstein-Barr virus occur frequently in aggressive periodontitis site. Also, the periodontal presence of Human cytomegalovirus has been linked to a high occurrence of subgingival P. g , Dialister pneumosintes and other periodontal pathogens.
In addition to these bacteria and viruses, a few new cultivated species are associated with a periodontal disease. These include Eubacterium saphenum and Mogi- bacterium timidum ; Prevotella corporis, Prevotella distens and Peptostreptococcus magnus , Eubacterium nodatum and Slackia exigua , Strepto– coccus faecalis, Escherichia colli and Bartonela sp..
Bacteria presented in the periodontal pockets could be detected by microbiological culture techniques, detection of the certain microbial enzymes, immunological methods, DNA/RNA probes . Bacteria recognized in periodontal pockets could be successfully treated by antibiotics. This is one of the main aims in the treatment of periodontal disease.
Conclusion
A full understanding of the microbial factors, their pathogenicity as well as host factors are of the essential importance for pathogenesis of periodontal disease. In this way it could be possible to treat the periodontal patients adequately.
Pathogenesis of periodontal diseases and chronic inflammation
The inflammatory response in periodontal disease includes the activation of leucocytes, neutrophils, T-lymphocytes and plasma cells and the release of antibodies, lipopolysaccharides and chemical inflammatory mediators that include cytokines, chemokines and C-reactive protein. The lipopolysaccharides are present in the gram-negative bacterial cell walls and act as powerful stimulants for the complex host response. The initial increased presence of neutrophils at the site is followed by the release of cytokines by neutrophils and macrophages. Chemical mediators released include tumor necrosis factor alpha (TNF- a), interleukin-1 (IL-1) and prostaglandins. The inflammatory process includes the stimulation of fibroblasts by IL-1 and the secretion of matrix metalloproteinases (MMPs, of which collage- nase is the most prominent) by polymorphonuclear neutrophils. MMPs are responsible for increased collagen breakdown, and TNF-a is primarily responsible for increased osteoclast activity resulting in bone resorption. MMPs can also activate cytokines and chemokines, exacerbating the destructive process. Collagen production is inhibited by the reduced activity of fibroblasts in response to TNF-a.
The lymphocytes release antibodies as protective mechanisms but also activate the osteoclasts, resulting in bone loss. T-lymphocytes secrete receptor activator of nuclear factor kappa-B ligand (RANKL), which is involved in osteoclast activity and therefore bone resorption. These destructive inflammatory mediators are inhibited by the secretion of osteoprotegerin and tissue inhibitors of metalloproteinases (TIMPs).
The level of periodontal destruction depends on the balance be- tween destructive and protective inflammatory mediators. While periodontal bacteria are required for infective periodontal disease, individual response determines disease progression. In vitro, it has been found that individual response is affected by genetic signaling pathways that influence the expression of inflammatory mediators in response to bacterial lipopolysaccharides.
Gum disease is an infection of the tissues and bones that support and surround the teeth. Plaque contains food, bacteria and bacterial waste products that accumulate on your teeth after eating. If it is left on your teeth, your gums become irritated. When plaque builds up and hardens into tartar (also known as calculus) the bone structures around the teeth become affected. The early stage of gum disease is known as gingivitis – this is when gums can become red and swollen and bleed easily, often during tooth brushing.
If gingivitis is left untreated, it can progress to peridontitis where the inner layer of the gum and bone recede from the teeth and form pockets.
The spaces between the teeth and gums become infected, and bacterial toxins begin to break down the bone and connective tissue that hold the teeth together. Over time, the pockets deepen and destroy bone and gum tissue.
Eventually, teeth start to feel unsteady and fall out. It is therefore essential to brush and floss your teeth daily, visit the dentist regularly, eat healthy foods and limit your intake of sweets to maintain good oral hygiene.
Symptoms and signs
The common symptoms and signs of gum disease include:
● Receding gums
● Bleeding gums
● Red, swollen and tender gums
● Discoloration of gums
● Formation of spaces between teeth and gums
● Loose teeth
● Changes in the way teeth fit together on biting, or the way dentures fit together
● Continuous bad breath or bad taste in the mouth (halitosis)
Periodontal Disease
Periodontal diseases are generally divided into two groups:
1. Gingivitis, which causes lesions (inflammatory abnormalities) that affect the gums, is a milder form of gum disease.
2. Periodontitis, which damages the bone and connective tissue that support the teeth, is a more serious form of gum disease.
3. Gum disease develops as a result of a plaque build up because of poor oral hygiene – not brushing and flossing teeth regularly and visiting the dentist.
Gingivitis
Gingivitis is an inflammation of the gingiva, or gums. It is characterized by tender, red, swollen gums that bleed easily and may cause bad breath (halitosis). Gingivitis can be treated by good dental hygiene, proper diet, and stopping smoking. Untreated gingivitis can lead to periodontitis.
Periodontitis
Periodontitis occurs when the gum tissues separate from the tooth and sulcus, forming periodontal pockets.
Periodontitis is characterized by:
1. Gum inflammation, with redness and bleeding
2. Deep pockets (greater than 3 mm in depth) that form between the gum and the tooth
3. Loose teeth, caused by loss of connective tissue structures and bone
There are different forms of periodontal disease.
They include:
Chronic Periodontitis. Chronic periodontitis is the most common type of periodontitis. It can begin in adolescence but the disease usually does not become clinically significant until people reach their mid-30s.
Aggressive Periodontitis. Aggressive periodontitis is a subtype of chronic periodontitis that can occur as early as childhood. It can lead to severe bone loss by the time patients reach their early 20s.
Disease-Related Periodontitis. Periodontitis can also be associated with a number of systemic diseases, including type 1 diabetes, Down syndrome, AIDS, and several rare disorders of white blood cells.
Necrotizing Periodontal Disease. Necrotizing periodontal disease is an uncommon acute infection of the gum tissue. It is characterized by painful and bleeding gums, bad breath, and rapid onset of pain. If left untreated, necrotizing periodontal disease can spread throughout the facial areas (cheeks, jaw) and cause extensive damage. Necrotizing periodontal disease is usually associated with systemic health conditions such as AIDS or malnutrition.
Causes
Periodontal disease is caused by plaque, which is formed from harmful bacteria. The mouth is full of bacteria but they tend to be harmless varieties. Periodontal disease usually develops because of an increase in bacteria quantity in the oral cavity and a change in balance of bacterial types from harmless to disease-causing bacteria. These harmful bacteria increase in mass and thickness until they form a sticky film called plaque.
In healthy mouths, plaque actually provides some barrier against outside bacterial invasion. When it accumulates to excessive levels, however, bacterial plaque sticks to the surfaces of the teeth and adjacent gums and causes infection with subsequent swelling, redness, and warmth.
When plaque is allowed to remain in the periodontal area, it transforms into calculus (commonly known as tartar). This material has a rock-like consistency and grabs onto the tooth surface. Tartar is much more difficult to remove than plaque, which is a soft mass. Once tartar has formed, it must be professionally removed by a dental practitioner.
Risk Factors
Most American adults have some form of gum disease but are unaware of it. The main risk factors for periodontal disease include:
1. Age
2. Smoking or tobacco use
3. Female hormonal changes
4. Illnesses such as diabetes or HIV/AIDS, and the medications used to treat some conditions
5. Genetic factors
Age
Periodontitis typically occurs as people get older and is most common after age 35.
Lifestyle Factors
Smoking. Smoking is the major preventable risk factor for periodontal disease. Smoking can cause bone loss and gum recession even in the absence of periodontal disease. The risk of periodontal disease increases with the number of cigarettes smoked per day. Smoking cigars and pipes carries the same risks as smoking cigarettes.
Substance Abuse. Long-term abuse of alcohol and certain types of illegal drugs (amphetamines) can damage gums and teeth.
Diet. A healthy diet, including eating fruits and vegetables rich in vitamin C, is important for good oral health. Malnutrition is a risk factor for periodontal disease.
Stress. Psychological stress can cause the body to release inflammatory hormones that may trigger or worsen periodontal disease.
Female Hormones
Female hormones affect the gums, and women are particularly susceptible to periodontal problems. Hormone-influenced gingivitis appears in some adolescents, in some pregnant women, and is occasionally a side effect of birth control medication.
Menstruation. Gingivitis may flare up in some women a few days before they menstruate, when progesterone levels are high. Gum inflammation may also occur during ovulation. Progesterone dilates blood vessels causing inflammation, and blocks the repair of collagen, the structural protein that supports the gums.
Pregnancy. Hormonal changes during pregnancy can aggravate existing gingivitis, which typically worsens around the second month and reaches a peak in the eighth month. Any pregnancy-related gingivitis usually resolves within a few months of delivery. Because periodontal disease may increase the risk for low-weight infants and cause other complications, it is important for pregnant women to see a dentist.
Menopause.Estrogen deficiency after menopause reduces bone mineral density, which can lead to bone loss. Bone loss is associated with both periodontal disease and osteoporosis (loss of bone density). The hormonal changes associated with menopause can cause dry mouth, which can lead to tooth and gum problems.
Genetic Factors
Periodontal disease often occurs in members of the same family. Genetic factors play a role in making some people more susceptible to periodontal disease.
Medical Conditions Associated with Periodontal Disease
Diabetes. There is a strong association between diabetes (both type 1 and 2) and periodontal disease. Diabetes causes changes in blood vessels, and high levels of specific inflammatory chemicals such as interleukins, that significantly increase the chances of developing periodontal disease.
Heart Disease. Periodontal disease and heart disease share common risk factors (smoking, older age, diabetes) but it is not yet clear if having one condition increases the risk for developing the other (see Complications section of this report).
Other Medical Conditions. A number of medical conditions can increase the risk of developing gingivitis and periodontal disease. They include conditions that affect the immune system such as HIV/AIDS, leukemia, and possibly autoimmune disorders (Crohn’s disease, multiple sclerosis, rheumatoid arthritis, lupus erythematosus).
Prescription Medications. Gingival overgrowth can be a side effect of many drugs including certain types of oral contraceptives, antidepressants, and heart medications. Any drug that has a side effect of dry mouth can increase the risk for gum disease.
If you take a bisphosphonate drug such as alendronate (Fosamax, generic) discuss with your dentist any potential risks from dental procedures (such as extractions and implants) that involve the jawbone. Oral bisphosphanates, which are used to treat osteoporosis, have in rare cases caused osteonecrosis (bone destruction) of the jaw. (Intravenous bisphosphantes, which are used in cancer treatment, are more likely to cause osteonecrosis.) Your dentist or oral surgeon may need to take special precautions when performing dental surgery. In any case, be sure to inform your dentist of all medications you are taking.
Oral Health Risk Factors
Oral Hygiene. Lack of oral hygiene, such as not brushing or flossing regularly, encourages bacterial buildup and plaque formation.
Poorly Contoured Restorations. Poorly contoured restorations (fillings or crowns) that provide traps for debris and plaque can also contribute to periodontitis.
Tooth Structure . Abnormal tooth structure can increase the risk of periodontal disease.
Wisdom Teeth. Wisdom teeth, also called third molars, can be a major breeding ground for the bacteria that cause periodontal disease. Periodontitis can occur in wisdom teeth that have broken through the gum as well as teeth that are impacted (buried). Adolescents and young adults with wisdom teeth should have a dentist check for signs of periodontal disease.
Complications
Effect on Heart Disease
Researchers are studying the association between periodontal disease and heart disease. These two conditions share common risk factors (such as smoking and diabetes). However, some studies suggest that the link between periodontal disease and heart disease involves more than shared risk factors. An inflammatory response, which occurs in both periodontal disease and heart disease, may be the common element.
According to the American Heart Association, there is currently not enough evidence to prove that periodontal disease increases the risk for heart disease or stroke, or that treating gum disease can help prevent these cardiac conditions. The U.S. Preventive Services Task Force does not recommend including periodontal disease among the factors used for estimating a healthy person’s risk of developing heart disease.
Cardiologists and periodontists currently encourage each other to monitor both conditions in their patients. Periodontists recommend that patients who have periodontal disease and at least one risk factor for heart disease have an annual medical exam to check their heart health. Cardiologists suggest that patients with atherosclerosis and heart disease have regular periodontal exams.
Effect on Diabetes
Diabetes is not only a risk factor for periodontal disease. Periodontal disease itself can worsen diabetes and make it more difficult to control blood sugar.
Effect on Respiratory Disease
Bacteria that reproduce in the mouth can also be carried into the airways in the throat and lungs, increasing the risks for respiratory diseases such as pneumonia and worsening chronic lung conditions, such as emphysema.
Effect on Pregnancy
Bacterial infections that cause moderate-to-severe periodontal disease in pregnant women may increase the risk for premature delivery and low birth weight infants. The bacteria from gum disease and tooth decay may trigger the same factors in the immune system that cause premature dilation and contractions.
Women should have a periodontal examination before becoming pregnant or as soon as possible thereafter. Because women with diabetes are at higher risk for periodontal disease, it is especially important that they see a dentist early in pregnancy. Doctors are still not sure if treating periodontal disease can improve birth outcomes. In any case, periodontal treatment is safe for pregnant women.
How is Gum Disease diagnosed?
The diagnosis of gum disease is based on a thorough examination of your mouth by a dentist. Your gums are checked for swelling bleeding or firmness while your teeth and bite are also assessed.
A full mouth x-ray is taken to determine the extent of gum disease.
If gum disease has progressed to periodontitis, you may be referred to a periodontist – a specialist in gum care disease.
Help and treatment for Gum Disease
The treatment of gum disease generally depends on the severity of the condition. Treatment options include healthy eating, proper brushing and flossing, regular visits to the dentist, non-surgical therapy and surgery. If you have developed gingivitis, your dentist or oral hygienist will clean your teeth using a scaler to remove plaque as well as an electric toothbrush with grainy toothpaste. Your dentist will usually recommend an antiseptic mouthwash such as chlorhexidine and also teach you how to brush and floss your teeth properly. If periodontitis develops, scaling or root planning is performed to scrape and remove plaque and tartar from teeth above and below the gum line. Antibiotics in the form of medicated mouthwashes or antibiotic containing gels may be applied to kill off bacteria.
More severe episodes of periodontitis may require surgery or gingival grafting where healthy gum tissue is removed from another part of the mouth to replace diseased tissue.
Natural remedies
Natural and holistic treatments have been used for centuries to treat the symptoms of gum disease and overall dental health. Treatments such as herbal remedies are a much safer, more natural alternative to use in the mouth without the harmful side effects of conventional medication.
Herbal ingredients such as Hypoxis Rooperi (extract of African Potato), Mentha Piperita, Viscum Album, Astralagus Membranaceus and Agathosma Betulina (also known as buchu) are excellent for the immune system, acting as a supportive tonic and natural antiseptic. In addition, Chamomile, Echinacea, and Myrrh can also provide anti-inflammatory and antimicrobial actions that are beneficial for the treatment of gum disease.
Standard nonsurgical treatment
The key goal of periodontal treatment is the removal of pathogenic bacteria, correction of reversible risk factors, and then the prevention of recolonization in order to prevent disease recurrence. The desired clinical outcomes are to favorably influence clinical attachment levels, pocket probing depths and other clinical parameters such as bleeding on probing, mobility and furcation involvement. The standard nonsurgical treatment for periodontal disease is scaling and root planning (SRP). Meticulous removal of bacteria is required, together with removal of calculus and debris from the periodontal tissues and tooth surfaces to minimize bacterial retention. Recently, lasers have been advocated as an alternative or adjunctive therapy to reduce levels of periodontal bacteria and for “pocket disinfection.”
While it has been demonstrated that it is the removal and reduction of bacteria that are key, removal of calculus reduces the opportunity for bacterial reattachment and colonization and also removes the bacteria and toxins contained in the calculus. Certain bacteria may remain in the soft tissues and anatomical niches following scaling and root planning. It is difficult to completely remove bacteria, calculus and debris, given the anatomy of periodontal pockets. Virulent bacteria, which are more prevalent in deeper pockets, can rapidly recolonize periodontal sites, with the potential for recurrence of active periodontal disease and renewed tissue destruction Quantitative polymerase chain reaction (PCR) in one study found an association between the P. gingivalis count and both pocket depth and attachment loss, but no such relationship for P. intermedia or A. actinomycetemcomitans. Nonsurgical scaling and root planning were found to substantially reduce the levels of all three bacteria but did not eliminate any of them completely. Scaling and root plan- ing have been found to effectively reduce the levels of IL-1-B, MMPs and elastase activity in gingival crevicular fluid in both healthy and diabetic patients, although the diabetic group had less reduction of elastase activity. Scaling and root planing are effective at reducing the levels of bacteria and improving clinical parameters in responsive patients.
Responsiveness to treatment
The presence and level of virulent periodontal bacteria influence treatment outcomes. Smoking status in particular influences responsiveness. Following periodontal therapy, probing depth reductions and clinical attachment level gains are less in smokers thaonsmokers. Darby et al. found that the reduction in peri– odontal bacteria was less in smokers thaonsmokers following scaling and root planing therapy, possibly a result of the deeper pockets found in the smokers’ group prior to treatment. Smokers account for the majority of cases of refractory periodontitis. In investigating the effects of nonsurgical scaling and root planing over a nine-month period post-treatment, Haffajee et al. found significant decreases in the levels of P. gingivalis, T. denticola and T. forsythia (B. forsythus) as well as their prevalence in the 57 subjects, and increases in A. viscosus, in particular, at the deepest pocket sites. In the responders, they found that modest reductions in periodontal bacteria were sufficient for clinical improvement. The greatest improvements following scaling and root planing were at the sites that were most severe and had the highest peri– odontal bacterial loads. A recent study of type 2 diabetics found that while clinical parameters improved following SRP, the levels of TNF-a and IL-6 actually increased. Type 1 diabetics with poor disease control experience more attachment loss as a result of periodontal disease than diabetics with moderate and good control. As discussed earlier, genetics and genotype influence responsiveness by influencing the presence of specific bacteria; the immune response, involving signaling pathways; and chemical inflammatory mediator production. The importance of obtaining a response and an improvement in periodontal clinical and bacterial parameters has been heightened with the increasing amount of research demonstrating an association between periodontal and systemic disease.
Systemic and local treatment adjuncts
Adjunctive systemic and/or local antibiotic/antimicrobial treat- ment has been found to positively impact periodontal therapy outcomes. Indications include when a patient’s risk factors suggest that he or she may otherwise be nonresponsive, when a patient has received periodontal therapy and the response was unfavorable, or when there is a recurrence of disease. With increasing evidence of the role of genetics and inflammatory mediators, biomarkers may in the future offer definitive predictive value for responsiveness and aid preemptive case selection or adjunctive therapy. Systemic therapy can be utilized for host modulation or bacterial elimination (control), while local treatments have been shown to be successful at controlling the bacterial environment.
Systemic Therapy – Host Modulation
Host modulation is the purposeful redirection of the inflammatory host response. Nonsteroidal anti-inflammatory drugs, bisphosphonates and antibiotics have all been explored as host modulation agents. Due to complications of long-term use of the first two classes of drugs, to date only systemic doxycycline has had any clinical utility. Sub antimicrobial dose doxycycline (SDD) has been used adjunctively in periodontal disease therapy for almost two decades. Doxycycline hyclate at a dose of 20 mg twice daily (Periostat®), is effective at reducing pocket depths and gingival indices and has been found to help prevent collagen breakdown and influence the levels of inflammatory mediators. Doxycycline inhibits the enzyme collagenase, helping to prevent collagen breakdown. It has been shown to reduce pocket depths by up to 79%, depending on the pre-treatment depth of the pockets. Low- dose doxycycline also modulates the host response in other ways. A randomized, double-blind, placebo-controlled study found that low-dose doxycycline given twice daily (20 mg per dose) resulted in greater pocket depth reductions and gingival indices than were seen in the control group. Levels of MMP-8 have been found to be lower compared to a control group. The levels of Ln-5 gamma2 chain fragments of laminin-5, which are mediated by MMPs and have been found to aid pocket development, are also lower with adjunctive low-dose doxycycline. Another study found increases in the level of growth factor-B1 in the gingival crevicular fluid in the adjunctive low-dose doxycycline test group compared to the control group, which received only scaling and root planing and a placebo. A combination of low-dose doxycycline and NSAIDs has been found to suppress MMP activity more than low-dose doxycycline alone.
Bacterial resistance associated with low-dose doxycyline therapy has not been seen. Studies of up to 12 months’ duration have been completed. One common clinical question is, How long should a patient be on this medication? As host modula– tion is used when all other approaches have failed to control attachment loss, the answer is probably for an indefinite period. Some clinicians suggest placing patients on SDD for a time, next having them enter a “resting” phase and then reinstituting host modulation therapy.
Systemic Therapy – Antimicrobials
Systemic antibiotics have been used to treat periodontal disease. One of the first was metronidazole (Flagyl®), used for three days to treat what was then known as acute ulcerative gingivitis and is now known as acute necrotizing ulcerative gingivitis. Systemic antibiotics proven to help periodontal disease include amoxicil– lin, ciprofloxacin, metronidazole, tetracyclines/doxycyclines, erythromycin and clindamycin. Indications for the use of systemic antibiotics include the following: the treatment of aggressive forms of periodontitis, especially when A. actinomycetemcomitans is present; treatment of recurrent/refractory disease forms of perio– dontitis, especially when multiple sites are involved; treatment of patients prone to infection, such as unstable diabetics and patients with other immune compromise such as chemotherapy or HIV infection. One disadvantage of using systemic antibiotics is that the level needed to treat periodontal disease is high, because the concentration that reaches the periodontal tissues after systemic ingestion is low; additionally, overuse of systemic antibiotics to treat disease has contributed to an increasing level of antibiotic resistance worldwide. These disadvantages are absent with the use of locally applied antimicrobials. Systemic antibiotics have been used to treat aggressive forms of periodontitis and recurrent/refractory disease in brittle diabetics and empirically when the amount of in- flammation is severe compared to the amount of etiology present, as well as for the current prophylaxis indications. It is critical to remember that biofilm throughout the mouth must be disrupted at the onset of systemic or local antibiotic therapy.
Specific dosing is at the practitioner’s discretion. The Ameri– can Academy of Periodontology has published suggested systemic antibiotic dosages.62 Pallasch has presented criteria for antibiotic dosing and suggests employing high doses for a short duration, using an oral antibiotic loading dose, frequent dosing intervals, achieving blood levels of the antibiotic at two to eight times the minimum inhibitory concentration and determining the duration of therapy by the remission of disease.63
Local Therapy – Locally Applied Antimicrobial Agents
Locally applied antimicrobial agents (LAAs) enable targeted use of antimicrobials, with a lower dose than would be required if given systemically, and release the antimicrobial in a controlled manner at or above the minimum inhibitory concentration (MIC) over a period of several days. In addition to being effective at a lower dose,
no antibiotic resistance has been found following the use of LAAs. Studies have found improved clinical parameters with the use of LAAs.64 Available agents in the United States include doxycycline hyclate, minocycline hydrochloride and chlorhexidine gluconate. In a comparative study of doxycycline hyclate, chlorhexidine gluconate chip and Elyzol® (metronidazole gel, available in Europe), it was found that all three resulted in a statistically significant reduction in pocket probing depths, while only doxycycline hyclate resulted in a statistically significant improvement in clinical attachment level. Killoy addressed five requirements for a local delivery system to be effective. These are that the agent must reach the site to be treated, have an adequate concentration at the site, remain at the site long enough to be effective, inhibit or kill the putative bacteria and, lastly, do no harm. These requirements should be considered when selecting an agent.
Doxycycline hyclate
Ten percent doxycycline hyclate (ATRIDOX®) is applied as a gel directly to the pockets, using a syringe. Upon application, the polymer sets in the presence of moisture, releases the antimicrobial for 21 days at doses higher than the MIC and is bioabsorbable. Novak et al. conducted a multicenter, randomized, blinded study on SRP plus adjunctive use of both low-dose systemic doxycyline hyclate and 10% doxycyline hyclate gel (ATRIDOX®). The combination of SRP and both adjuncts resulted in greater reductions in bleeding upon probing and greater gains in clinical attachment levels than SRP alone, and based on other studies it was also concluded that this combination was more effective than using SRP plus low-dose systemic doxycycline hyclate or SRP plus 10% doxycycline gel.
Ten percent doxycycline hyclate has been found to be effective as an adjunct to SRP in both smokers and nonsmokers. It has also been found to be effective in smokers in the absence of scaling and root planing. ATRIDOX® is approved for application prior to, during or after SRP. In smokers and type 1 diabetics, the use of 10% doxycycline hyclate has resulted in improvements in post-therapy clinical parameters. In one study of smokers, the level of P. gingivalis three months post-therapy was significantly reduced with SRP and use of doxycycline hyclate compared to only SRP. At 18 and 24 months following therapy using SRP and doxycyline hyclate, greater reductions in pocket depth and improved clinical attachment levels were found compared to the control group receiving only SRP, with the magnitude of change depending on the initial depth of the pockets. At 24 months, rela– tive attachment gains of 2 mm or greater were observed in 34.4% of sites receiving doxycycline hyclate, compared to 18.1% of sites in the control group.70 In 16 patients who were smokers, the pro- portion of sites with no remaining T. forsythia (B. forsythus) three months following adjunctive treatment with doxycycline hyclate was 53% versus 9% for SRP alone, and for P. gingivalis 82% versus 40%. A trial comparing doxycycline hyclate use with SRP found the clinical results of both protocols to be the same, with no statis– tical differences. Probing depth reductions of at least 2 mm were found in 41% of sites treated with doxycycline hyclate and in 43% of SRP sites. From a clinical perspective, it is interesting to note that the doxycycline gel penetrates the topographical complexities
of the periodontal pockets. If the material is removed after 10 days instead of being left to resorb, the complexities of the pocket wall are evident in the residual polymer. In addition to adaptation of the polymer to the pocket wall, one syringe of ATRIDOX® may be used to treat several pockets.
Minocycline hydrochloride
Minocycline hydrochloride 1 mg (Arestin®), which is also applied in a syringe (one syringe per site pocket), consists of microspheres that are applied as a dry powder that hydrolyzes and sets when ex- posed to gingival crevicular fluid and remains in the pocket for 14 days. Minocycline hydrochloride is used adjunctively with SRP. Williams et al. found a 22% greater reduction in mean pocket probing depths (with a mean clinical difference of 0.24 mm) with its use compared to SRP only.73 Minocycline hydrochloride use has been found to result in improved clinical parameters nine months following treatment in smokers compared to SRP only, with a 32% greater reduction in pocket depths.74 Adjunctive use of minocycline hydrochloride together with mechanical debride- ment of peri-implantitis sites has been found to result in reduced probing depths compared to the control treatment without ad- junctive LAA therapy, when repeated application of LAA was provided at baseline, 30 and 90 days.75 In smokers and nonsmok– ers, adjunctive therapy with minocycline hydrochloride resulted in reduced levels of red complex bacteria for up to one month. In the same study, SRP alone did not reduce the levels of red complex bacteria in smokers.76 In one study, in type 1 diabetics, adjunctive application of minocycline hydrochloride resulted in greater reductions in pocket probing depths and improved gains in clinical attachment level compared to SRP alone.77
Chlorhexidine gluconate
Chlorhexidine gluconate is used as an LAA in the form of a 2.5 mg hard chip that is a biodegradable matrix of gelatin and glutaraldehyde inserted into the periodontal pocket. While it is also a controlled-release vehicle, it releases the first 40% of the chlorhexidine within 24 hours and the remainder over the one- week treatment period. The released cationic chlorhexidine has a broad antimicrobial effect and, as with chlorhexidine rinses, adheres to the cell wall surfaces, which are anionic, and causes cell apoptosis and death. The use of chlorhexidine gluconate chips has been found to be superior to only SRP.78
Case treatment
Considerations in the decision to use adjunctive LAAs include the patient’s predicted responsiveness – whether the patient is a smoker or diabetic, has a genotype favoring periodontal disease, or did not respond to prior therapy. Further considerations in determining which LAA to use include clinical preference, efficacy, ease of ap– plication, and number of sites that can be treated with one packet or syringe. The case below shows the use of doxycycline hyclate.
The patient was a 38-year old woman. There was nothing ab– normal in her medical history and she did not smoke. On examina– tion and probing, twelve sites with probing depths greater than 5 mm were found. Following scaling and root planing, a number of sites required adjunctive therapy.
Prior to use, the polymer and doxycycline components must be mixed. When this is accomplished, a blunt end cannula is attached to the syringe and the material is slowly applied into the pocket. As moisture acts as the catalyst to set the polymer, it may be helpful to have an instrument handy to separate the last of the material from the cannula.
Both systemic and local antibiotic/antimicrobial approaches have their place in periodontal therapy. The main questions faced by clinicians are: when are systemic and local antibiotic/antimicrobial approaches indicated, at what dose and for how long, and which drug/product to choose. While there is no one answer to each of the above questions, basic principles and experiences can guide the decision-making process. Indications for the use of local antibiotic/ antimicrobial therapy include the presence of one or several areas that have either not responded to therapy or have been discovered during a maintenance appointment to be breaking down; and, the number of sites to be treated and the cost of material to treat the se- lected sites. The availability of locally-applied antimicrobials and subantimicrobial doses of antibiotics has increased the therapeutic options available to treat patients with periodontal disease.
Tips to prevent gum disease
There are several effective ways to prevent gum disease and ensure healthier gums and teeth:
● Floss your teeth daily before brushing to remove plaque from those hard-toreach places in your mouth
● Brush your teeth properly twice a day for at least two minutes
● Use a toothpaste that contains fluoride to help fight gum disease and prevents plaque build up
● Use an electric toothbrush for more thorough cleaning as they are more effective than manual toothbrushes and are able to remove plaque below the gum line
● Eat a healthy diet packed with vegetables and fruit
● Limit your intake of sweets and sugary foods
● Replace toothbrushes every three months because new toothbrushes remove plaque more easily than used ones
● Stop smoking as it destroys gum tissue, causes tartar formation and bone loss
● Avoid long term use of certain drugs such as antidepressants, antihistamines or muscle relaxants as they dry out the mouth and can cause tooth decay and gum disease
● Visit your dentist every six months for routine checkups
The Natural Approach
While Western medicine has become the norm in many cultures, it is not the only treatment option. Conventional western medicine, often called allopathic medicine, is the system of medicine taught at most medical schools and most pharmaceutical and synthetic medicines are manufactured and marketed according to the principles of allopathic medicine. Allopathic medicine is also sometimes called orthodox medicine.
Because most of us in the Western world have grown up in a society in which allopathic medicine is the prevailing norm, we forget that, only a few decades ago, homeopathic, herbal and other natural medicines were commonly available – and freely used even by conventional doctors. While there are often heated debates about which system of medicine is ‘better’ than the other, many responsible doctors (whether they are allopathic or not) recognize that both have a role to play in the treatment program.
Natural medicine has often been frowned on by conventional doctors, especially by those who did not have sufficient knowledge of these medicines. However, it is encouraging to note that some medical schools are now beginning to re-introduce it into their course work, thereby providing doctors with a wider range of treatment options from which to choose. In many countries, especially in Europe, India and China, natural and homeopathic medicines are commonly prescribed by conventional doctors and represent a significant part of the total annual drug sales. Naturopathy is a branch of medicine (just as allopathy is a branch of medicine) which operates according to the underlying philosophy that the body has an innate capacity to heal itself. While natural medicines are often called ‘alternative’ or ‘complimentary’ medicines, they are, in fact, a unique and independent form of medicine in their own right, well able to treat a variety of conditions. Perhaps the term ‘holistic’ medicine is more apt, given the broad range of treatment options
