Changing Periodontal Concepts: Treatment Considerations

Abstract: Many clinical trials conducted during the last decade have clarified controversial issues and resulted in changed periodontal paradigms. These modified concepts have therapeutic implications. Some salient altered periodontal concepts include the following: The mere presence of pathogens will not initiate periodontal diseases. Most subgingival bacteria reside in biofilms. Periodontal diseases are infections. Periodontal pathogens can be transferred between family members. The host response can be protective and destructive. Gingivitis does not usually proceed to periodontitis. Risk factors in conjunction with bacteria and the host response can affect the severity of disease, patterns of destruction, and the response to therapy. Many medical conditions (eg, diabetes, smoking, and HIV infection) may predispose patients to periodontitis. Associations between periodontitis and a number of systemic ailments (eg, diabetes, adverse pregnancy outcomes, and cardiovascular disease) have been detected and are being investigated to determine if there is a cause-and-effect relationship. Diagnostic and therapeutic implications of these altered paradigms are addressed throughout the article.

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Gary Greenstein, DDS, MS
Clinical Professor Department of Periodontology University of Medicine and Dentistry of New Jersey Newark, New Jersey Private practice Freehold, New Jersey

any paradigms related to periodontal therapy have changed, which have therapeutic implications. Integration of altered perceptions into the daily management of patients with regard to the bacterial etiology, pathogenesis, and risk factors for periodontal diseases and risk of systemic effects for periodontal diseases will facilitate improved patient treatment. This review article addresses many concepts that have been modified and suggests how they can be incorporated into daily periodontal therapy.

Learning Objectives:
After reading this article, the reader should be able to: discuss changed periodontal paradigms. explain the therapeutic implications of this information. describe new information regarding the relationships between systemic diseases and periodontal diseases.

Bacteria: Etiologic Role in the Development of Periodontal Diseases Periodontal Pathogens

Over 500 types of bacteria have been found within the oral cavity; 1 however, only about 10 are commonly associated with bacterial infections (Table 1).2,3 In 1998, Socransky and colleagues reported that Bacteroides forsythus (now reclassified as Tannerella forsythensis) , Porphyromonas gingivalis, and Treponema denticola were closely associated with clinical assessments of periodontal disease, particularly probing depth and bleeding on probing.3 In general, periodontal diseases are caused by mixed infections, and patients who do not respond to conventional therapy may need adjunctive local or systemic antibiotic therapy.4,5 Culture and sensitivity testing can be used to ensure that an appropriate antibiotic is selected.
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Table 1Most Common Bacterial Pathogens: Ranked by Strength of Association with Periodontitis2
Very Strong A actinomycetemcomitans P gingivalis B forsythus Strong P intermedia C rectus E nodatum Treponema sp Eubacterium sp Moderate S intermedius P micros F nucleatum E corrodens

Infection
Periodontal diseases are infections that can destroy the periodontium.2 By definition, an infection occurs when there is a bacterial etiology and an immune response.6 The term disease denotes that there is destruction of the tissues.6 In general, the continuous bacterial challenge found supragingivally and subgingivally is contained by the host response and usually there are subclinical infections that never result in disease. Therefore, it is important to promote efficient personal plaque control by patients and to provide maintenance after therapy to reduce the bacterial challenge, thereby facilitating stabilization of the hostparasite equilibrium.7

These ecologic communities develop an exopolysaccharide matrix for their mutual protection. This protective mechanism inhibits drugs from penetrating the biofilm and killing the bacteria. It has been suggested that a 500 times greater antibiotic strength may be needed to be effective against biofilms vs free-floating bacteria.12 Thus, it is prudent to disrupt subgingival biofilms with root planing before administering local drug delivery because it facilitates the drug contacting the pathogens.

Bacterial Load
Certain bacteria are associated with periodontitis (Table 1), but it is not possible to predict which patients or sites will develop periodontal disease. Nevertheless, if specific pathogens exceed specific bacterial thresholds, it often reflects an increased risk that a site will deteriorate. For example, it is advantageous to maintain bacterial levels below 105 P gingivalis (mean counts in subgingival plaque samples) and 105 Aa because at these levels the relative risk for 2.5 mm of clinical attachment loss within 2 months is respectively 2.2 and 3.2 times greater than if the bacterial levels were 103.2 At a level of 106 for P gingivalis or A a, the relative risk of attachment loss increases to 4.1 and 4.3, respectively.2 Accordingly, it may be advantageous to culture high-risk patients (eg, those with recurrent severe chronic periodontitis) after therapy to determine if levels of alleged pathogens were reduced below risk thresholds.

Tissue Invasive Bacteria

Actinobacillus actinomycetemcomitans (Aa), P gingivalis, and a variety of other bacteria have been detected within cells of the gingival tissues.8 However, the relevance of this finding with regard to disease initiation or progression is unclear.8 Nevertheless, it is recognized that infections caused by invasive bacteria may not respond well to scaling and root planing.9 Accordingly, a microbiologic assessment (eg, culturing) can be used to identify infecting pathogens and aid in directing therapy. For example, Aa infections respond well to conventional therapy and a combination of antibiotics (eg, amoxicillin/clavulanate and metronidazole).10 When Aa is present, adjunctive drug delivery is administered systemically because local delivery does not provide an effective serum level to impact on bacteria within the connective tissue.9

Subspecies of Bacteria
Genetically different subspecies of bacteria that exist within a species are called clonal types. For example, there are 32 clonal types of P gingivalis13 and 10 clonal types of Aa.14 The finding of multiple clonal types of specific bacVol. 26, No. 2

Biofilms
Bacterial aggregates found supragingivally and subgingivally are called biofilms.11
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teria provides a possible explanation as to why different individuals colonized with the same species of bacteria may or may not develop periodontitis. It is possible that some clonal types are virulent and others are not. This creates a problem because culture assessments do not differentiate between clonal types and they do not evaluate bacterial pathogenicity. Therefore, clinicians must primarily assess whether therapy is needed based on clinical findings. In general, most pathogens associated with p e r i odontal diseases are considered endogenous (part of the normal flora)15 and they have multiple clonal types.13,14 Because it is difficult to eradicate endogenous bacteria, therapy usually needs to be directed at their suppression. In contrast, if a bacterium is considered exogenous (not part of normal flora), then treatment needs to be focused on its eradication. Currently, it is still unresolved as to whether P gingivalis and Aa are endogenous or exogenous bacteria.15,16 It also is possible that some clonal types may be endogenous and others exogenous.

Table 2Summary of New Classifications for Periodontal Diseases34

Gingivitis associated with plaque not plaque induced modified by systemic factors modified by medications modified by malnutrition Chronic Periodontitis (formerly adult periodontitis) Localized and generalized forms Localized affects < 30% of the dentition Severity: mild (< 3 mm CAL), moderate (3 mm to 4 mm CAL), severe ( 5 mm CAL), or Class II and Class III furcation involvement* Amount of destruction consistent with local factors Slow to moderate rate disease progression rate, but may be rapid destruction Can occur at any age Aggressive Periodontitis (formerly early onset periodontitis, and included juvenile periodontitis, rapid progressive periodontitis, and prepubertal periodontitis) Localized and generalized forms Localized aggressive periodontitis affects molars and incisors Generalized aggressive periodontitis affects molars, incisors, and at least 3 other teeth Familial aggregation Rapid attachment loss and bone destruction frequently associated with Actinobacillus actinomycetemcomitans infections, amounts of microbial deposits inconsistent with severity of the tissue destruction Periodontitis as a Manifestation of Systemic Diseases (eg, hematological disorders, genetic disorders) Periodontitis Associated with Endodontic Lesions Necrotizing Ulcerative Periodontitis

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Transfer of Bacteria
Colonization of the oral cavity begins after birth and there is evidence to indicate that bacteria can be passed between parents and children 17,18 and between spouses.19,20 However, it varies how often bacterial transfer between family members occurs. Furthermore, if it happens, it is unknown if the bacteria will colonize and survive. In addition, even if an alleged pathogen colonizes a site, it should not be assumed that disease will develop. Thus, periodontal diseases should not be considered contagious because bacteria are not easily transmitted, transfer of microbes does not necessarily result in disease, and many healthy individuals have subgingival bacterial pathogens.15 On the other hand, it may be prudent to increase monitoring of patients when there has been an extended history of increased susceptibility to period o n t i t i s among family members.

Periodontal Disease Pathogenesis Current Model for Disease Pathogenesis

Historically, it was believed that bacteria were directly responsible for destroying the periodontium via the release of enzymes and toxins.21 Currently, it is understood that the host response can be both protective and
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Developmental or Acquired Deformities (eg, mucogingival deformities)

*Severity characterized by the extent of CAL (clinical attachment loss)

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Table 3Results Attained After Using Different Therapiesa

Procedure SC/RP 80 Pockets 4 mm to 6 mm Pockets 7 mm Tetracycline fibers and SC/RP Pockets 4 mm to 6 mm Pockets 7 mm Chlorhexidine chipd and SC/RP85 Doxycycline polymer Pockets 5 mm Pockets 6 mm Subantimicrobial doxycyclineg and SC/RP23 Pockets 4 mm to 6 mm Pockets 7 mm Metronidazole and SC/RP Pockets 7 mm Metronidazole and SC/RP89 Pockets 4 mm to 6 mm Pockets 7 mm Augmentin and SC/RP90 Open flap debridement bone grafth,93 Guided tissue regenerationsh,93 Enamel matrix proteini,j,94
a

Pocket Reduction 1.29 2.16

84

Gain of CAL 0.55 1.29 1.10 1.20 0.65 0.80 ---

Bone Fill
b

--------

1.00 2.10 0.95 1.30 1.32 1.46

e,86

Minocycline spheresf and SC/RP87

1.03 1.68

0.95 1.55 0.38 1.69 0.40 0.86 2.00 1.50

-------1.10

88

Pockets 4 mm to 6 mm

1.19 2.83 0.75 1.91 2.50 3.00

h,93

Demineralized freeze-dried 5.20 4.0 4.20 3.2 3.20 0.7-3.1k

means based on data from large clinical trials. data not reported. c Tetracycline fiber, Actisite, not available. d Chlorhexidine chip, Periochip, Astra Pharmaceuticals, Wayne, PA 10967. e Doxycycline chip, Atridox, Collagenex, Warminster, PA. f Minocycline spheres, Arestin, OraPharma Inc, Warminster, PA. g Subantimicrobial doxycycline, Periostat, Collagenex, Warminster, PA. h mean results are based on a meta-analysis. i enamel matrix protein, Emdogain, Biora, Malmo, Sweden. j results based on meta-analysis of data from many studies. k range of results from many studies.
b

destructive.22 If the neutrophils cannot contain the bacterial challenge, then monocytes and macrophages release cytokines, which are inflammatory mediators (such as interleukins). These mediators recruit normal cells of the period o ntium (such as fibroblasts and epithelial cells), which in turn release prostaglandins and matrix metalloprotein-ases. Prostaglandins are associated with bone destruction, and matrix metalloproteinases are involved in the destruction of col84
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lagen. An awareness of how the host plays a role in the destruction of the periodontium has stimulated the development of drugs (subantimicrobial dose doxycycline) to inhibit the host response and possibly help in the management of patients with periodontitis.23,24

Models of Disease Progression

During the past decade, several patterns of disease progression have been described.25-27 In
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the past, it was assumed that periodontal disease progression was slow and continuous. More recently, the episodic model was proposed, which indicated that disease progression proceeded during short episodic intervals followed by periods of remission. However, this pattern also has been questioned.28,29 Today, it is recognized that linear disease progression can occur and there may be episodes of tissue destruction. 26,29 Different patterns of disease progression can occur at various sites within the same mouth or at a particular location at a different time. It also is accepted that gingivitis does not usually proceed to periodontitis.30 However, gingivitis is frequently associated with periodontitis and gingivitis usually precedes periodontitis.30 In this regard, it has been noted that the absence of bleeding on probing is a good negative predictor for future disease progression,31 therefore, it is prudent to eliminate all inflammation and control identifiable risk factors to inhibit periodontal disease initiation.

localized and generalized aggressive periodontitis (Table 2). The term aggressive denotes a fast rate of disease progression found among some patients. The classification of refractory periodontitis as a separate disease entity has been eliminated. However, a patient can be categorized as having refractory chronic periodontitis. Two other new categories are periodontitis as a manifestation of systemic disease and necrotizing periodontal diseases.

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Epidemiology of Periodontal Diseases Prevalence

Gingivitis around more than 6 teeth affects about 50% of adults over 18 years of age.35 According to the National Health and Nutritional Examination Survey (NHANES III), among dentate individuals who are 30 years of age or older with 6 teeth, the following distribution of periodontitis was found: 3.1% had advanced periodontitis, 9.5% had moderate periodontitis, and 21.8% had mild periodontitis.36 These percentages are probably an underestimation of the prevalence of disease in the general population because measurements in epidemiological studies are frequently done at the line angles of teeth and not interproximally, which usually manifests 1 mm greater loss of clinical attachment than line angles.37

Modifying Factors
Bacteria are essential to initiate periodontal diseases; however, the mere presence of pathogens is insufficient to induce disease.2 For disease to be initiated, the host must be susceptible, the bacteria must be virulent, and the bacteria must overwhelm the host response and other antagonistic bacteria.2 The disease process also may be modified by environmental, genetic, and acquired factors (eg, diabetes).32,33

Risk Factors
People are not equally susceptible to periodontal disease, and clinical manifestations of disease can be modified by risk factors.38,39 Emerging data suggest that some systemic conditions may predispose patients to the initiation and progression of periodontal diseases. Conversely, periodontal infections may be risk factors for certain systemic diseases. These concepts reflect an emerging area of interest referred to as periodontal medicine.

Classification of Periodontal Diseases

In 1999, a workshop was conducted to reclassify periodontal diseases. Several disease categories were added and others were deleted.34 Major alterations of the classification scheme are noted in Table 2. New categories were added to reflect gingivitis associated with and without plaque and gingivitis modified by systemic factors, medications, and malnutrition. Adult periodontitis was reclassified as chronic periodontitis because periodontitis can affect young people and the previous classification indicated it only affected adults. Forms of early onset periodontitis (eg, juvenile periodontitis, rapid progressive periodontitis) were reclassified as
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Diabetes
Untreated diabetics develop periodontitis 2 to 3 times more frequently than nondiabetics and do not respond well to periodontal therapy.40,41 In contrast, diabetics who are medically managed are not more prone to periodontitis and respond normally to treatment.42 It is believed that diabetics respond differently to pathogens because their host defenses are impaired.40,41 In general, clinicians should be suspicious of a possible diaCompendium / February 2005

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betic condition if there is a rapid deterioration in p e r i odontal status.

Smoking
Smokers have a 2.8 greater chance of developing periodontitis compared with nonsmokers.43 They respond less well to therapy and have a greater recurrence of periodontitis than nonsmokers.44 The exact mechanism for this is unclear, but it is known that smokers have impaired chemotaxis and phagocytosis by neutrophils.41 Furthermore, increased levels of subgingival pathogens are detected in smokers, which may be the result of reduced oxygen tension, encouraging the growth of subgingival pathogens.45 Smokers should be encouraged to stop smoking and they may need increased monitoring and more frequent maintenance visits than nonsmokers.

gene may be useful in forecasting which individuals will be susceptible to chronic periodontitis.51 However, periodontitis is a multifactorial disease and it does not appear that any individual genetic polymorphism (altered gene) will be able to forecast who will develop chronic period o n t i t i s .52 Nevertheless, it may eventually be possible to develop a risk profile that would incorporate several factors to determine who has a predisposition to develop periodontitis.

HIV
Patients with HIV may be at greater risk of developing periodontitis than individuals who are HIV seronegative.32,53,54 However, less than 5% of HIV patients with periodontitis manifest necrotizing ulcerative periodontitis, a rapidly progressive lesion.54 In general, individuals with HIV have clinical and radiographic signs of disease that are indistinguishable from patients with periodontitis who are HIV seronegative.32 Therefore, it should not be assumed that HIV patients will usually manifest pathognomic signs of an HIV infection (eg, linear gingival erythema and necrotizing ulcerative periodontitis).

Osteoporosis
Currently, it cannot be categorically stated that osteoporosis is a risk factor for periodontitis. However, it appears that there is a clear association between these 2 disease entities.46 There are data to suggest that women with osteoporosis manifest more clinical attachment loss than women without osteoporosis.47 In addition, estrogen-deficient women have more bleeding on probing and less bone mass than estrogen-sufficient women.48 It also has been reported that women on hormone replacement therapy have better tooth retention and less clinical attachment loss than women not receiving hormone replacement therapy.49 The strength of these associations suggests that patients with osteoporosis may be predisposed to periodontitis and they should be monitored carefully.

Systemic Effects of Periodontal Diseases

Emerging data suggest that periodontitis may be a risk factor for systemic diseases. However, this information is derived mostly from association studies, and conclusions need to be based on longitudinal and intervention studies. Current information should be interpreted judiciously and treatment recommendations should be in accord with substantiated findings.

Cardiovascular Disease Genetics

Several lines of evidence support the contention that genetically determined susceptibility is important in the clinical expression of periodontal diseases: familial aggregation, formal genetic studies, twin studies, and the finding that certain genetic polymorphisms are associated with an abnormal host response.33 A recent study conducted in twins indicated that 50% of the clinical manifestation of periodontitis can be attributed to genetic factors.50 Other investigators have suggested that specific genetic polymorphisms associated with the interleukin 1A and 1B
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A 2001 review article55 indicated that 5 longitudinal investigations noted an increased risk of developing cardiovascular disease among individuals with periodontitis,56-60 but 3 studies did not support this conclusion.61-63 It has been suggested that oral bacteria and inflammatory reactions to antigens may be associated with the development of atherosclerotic lesions that precede thromboembolitic events, which can cause coronary thrombosis, ischemic heart disease, or stroke.55 However, the actual biologic basis for this relationship is unclear.55 An association between disease entities (eg, cardiovascular disease and periodontitis) should not be interpreted
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as being a causal relationship. Intervention studies are needed to determine if prevention or reduction of periodontitis leads to a decrease in the incidence of cardiovascular disease.

Periodontal Therapy
Conventional scaling and root planing or ultrasonic debridement have both been proven to be very effective for early to moderate periodontitis.80,81 Single episodes of subgingival irrigation as an adjunct to scaling and root planing do not usually enhance mechanical instrumentation.82 However, daily supragingival irrigation does help reduce gingival inflammation beyond normal hygiene in individuals who do not practice good home care.82 Controlled local drug delivery devices83-87 and systemic antibiotics88-90 may aid in the treatment of patients with periodontitis. However, local and systemic delivery of antibiotics are often reserved for patients and/or locations that do not respond to conventional therapy (Table 3).4,5 Host modulation also may be an adjunct to conventional therapy.23,24,91 In general, subsequent to treatment, supportive therapy is recommended to keep the bacterial challenge below the threshold needed to initiate disease.7 Surgical intervention is dictated by the magnitude of the lesion being treated, the actual or potential response to nonsurgical therapy, and the desired clinical outcome (such as regeneration of lost periodontal support).92-94 Typical results that can be achieved with different clinical procedures are listed in Table 3. Ultimately, selection of a treatment should be based on a careful inspection and interpretation of the available data. When choosing a treatment method, consider the magnitude of reported changes associated with a therapy, the severity of the defect to be treated, the desired treatment outcome, and the medical and dental histories of the patient.

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Pregnancy Complications
Several investigations have indicated that there is an association between periodontitis and the incidence of adverse pregnancy outcomes (low birthweight infants, spontaneous preterm births).64-69 This may be the result of subclinical infections or increased levels of biologically active molecules such as prostaglandins, which may stimulate premature labor. Studies indicated that periodontal therapy reduced the risk of preterm births, thereby supporting the contention that periodontal diseases may be a nidus of infection resulting in adverse pregnancy outcomes.68,69 Additional data are needed to verify a causeand-effect relationship and large investigations are needed to determine if periodontal treatment can decrease the incidence of adverse pregnancy outcomes.70

Diabetes
A few studies have demonstrated that periodontal therapy improved metabolic control among diabetics.71-75 As a consequence of periodontal treatment, patients had reduced glycolated hemoglobin levels and required less insulin.71-73 If this is verified, physicians may consider periodontal therapy a needed adjunctive therapy in the treatment of certain diabetic patients who are having difficulty with glycemic control.

Respiratory Diseases
There is relatively weak epidemiological evidence for an association between periodontal diseases and respiratory diseases.76-78 After adjusting for confounding variables, several studies suggested that if a patient had periodontitis there were increased odds of between 1.45 and 1.77 of developing chronic obstructive pulmonary disease (emphysema, chronic bronchitis). The biological mechanism for the dissemination of oral bacteria into the lungs is biologically plausible, but the connection between periodontitis and respiratory diseases remains speculative. 79 Large, randomized clinical trials are needed to evaluate this relationship.
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Conclusion
Periodontal diseases are infections that can be modified by risk factors. Conversely, they may have systemic consequences. In this regard, periodontal paradigms are changing and enlarging the scope of periodontal therapy. The ultimate goal of periodontal treatment has been the retention of healthy teeth. Attaining this objective is maximized if therapies are biologically based and integrate changed periodontal concepts. Furthermore, it may be proven that achieving periodontal health will diminish the risk of certain systemic diseases, thereby enhancing the quality of life for many patients, reducing medical costs, and decreasing the burden on the health care system.
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Update
Since acceptance of this paper, the 2003 Workshop on Contemporary Science in Clinical P e r i od ontics was conducted.95-104 Systematic reviews were developed for this workshop with respect to the relationship between periodontal disease and some systemic diseases and the efficacy of specific therapies. The data were reviewed by sections of the workshop, and consensus reports were developed. Important data and remarks from the consensus statements that addressed the applicability of the information to patient management are briefly described to bring the reader current information.

ease and adverse pregnancy outcomes in certain patient populations.97 There also is preliminary evidence that suggests that periodontal therapy may reduce the incidence of adverse pregnancy outcomes. The group assessing the data suggested that additional studies be conducted in high-risk populations of different ethnic and racial origins and geographic environments to determine the generalizability of the observed association between periodontal disease and adverse pregnancy outcomes. Nevertheless, it was concluded that there was enough data to suggest that patients and clinicians should be notified that periodontal therapy might prevent adverse pregnancy outcomes.

Associations Between Periodontal Disease and Systemic Diseases Cardiovascular Disease

The consensus report indicated an association between cardiovascular disease and periodontal disease. 95 This also was true for periodontal disease and ischemic stroke; however, causality was unclear. Furthermore, the committee indicated that there is insufficient data to demonstrate that periodontal therapy can decrease the incidence of heart disease. In this regard, intervention studies are needed to validate this hypothesis. Nevertheless, the section recommended that patients and clinicians should be aware that periodontal therapy might reduce the incidence of atherosclerotic diseases.

Consensus Reports on the Efficacy of Certain Therapies Host Modulation

The section that addressed host modulation concluded that there was evidence to support the use of SDD [subantimicrobial dose doxycycline] as an adjunct to mechanical instrumentation in the treatment of chronic periodontitis and the clinicians decision to use SDD therapy remains a matter of individual clinical judgment, based on the phase of treatment and the patients status and prefere n c e s . 98 A meta-analysis indicated that mechanical instrumentation with adjunctive SDD provided statistically significant benefits concerning probing depth reduction and gains of clinical attachment when compared with mechanical instrumentation alone. In- creased probing depth reductions associated with SDD use at sites initially 4 mm to 6 mm and 7 mm deep were 0.448 mm and 0.481 mm, respectively. Increased gains of clinical attachment with SDD at pockets initially 4 mm to 6 mm and 7 mm deep were 0.442 and 0.452 mm, respectively. It should be noted that data provided by a meta-analysis has been adjusted for variability of studies included in the analysis and therefore reflect relative, not actual improvements. Furthermore, mean numbers do not necessarily reflect the results that will be attained at any individual site; the results can be better or worse.

Nosocomial Pneumonia and Chronic Obstructive Pulmonary Disease

It was concluded that there is an association between nosocomial pneumonia and poor oral health of individuals who are institutionalized (patients in nursing homes, intensive care units).96 However, the data were inconclusive with regard to the role of periodontal disease as a cause of pneumonia. The section also noted that there was insufficient evidence to substantiate that there is an association between periodontal disease and chronic obstructive pulmonary disease. It was suggested that improved oral hygiene among individuals in institutions might reduce the incidence of pneumonia.

Adverse Pregnancy Outcomes

The consensus report indicated that there is a positive association between periodontal dis-

Anti-Infective Therapies
Another paper that assessed the use of anti-infective agents concluded that chlorhex-

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idine chips, doxycycline gel, minocycline gel, and minocycline microspheres could be useful as adjuncts in the treatment of chronic period o ntitis.99 The meta-analysis indicated that when scaling and root planing plus an adjunctive anti-infective agent were compared with scaling and root planing alone, combined therapy resulted in a statistically significantly better mean probing depth reduction by 0.338 mm and an insignificant improvement with regard to gain of clinical attachment (0.058 mm). It was determined that both manual and mechanical instrumentation are effective and that there is insufficient evidence to compare the time used by these treatment methods in improving periodontal status among patients with chronic periodontitis. 100 It also was noted that subgingival irrigation does not improve the efficacy of mechanical or manual instrum e n t a t i o n . 100 With regard to systemic antibiotics, the consensus report reached the following conclus i o n s : 101 1. Adjunctive antibiotics enhanced the gain of clinical attachment for at least 6 months in patients with chronic or aggressive periodontitis. 2. Adjunctive antibiotics provide better results at sites initially 6 mm deep. 3. Antibiotics that demonstrated statistically significant improvements included tetracyclines, metronidazole, and a combination of metronidazole and amoxicillin. They also noted that there is insufficient information to determine the best dosage or duration of therapy to maximize results.

Tissue Engineering
It was concluded that the data in the literature does not support the use of ethylenediaminetetracetic acid, tetracycline, or citric acid on root surfaces to enhance probing depth reduction or gain of clinical attachment.102 However, root surface modification is beneficial as an adjunct to root preparation (eg, smear layer removal or root detoxification). With respect to bone replacement grafts, the consensus report indicated that a variety of materials could be placed in an osseous defect to enhance healing. Evidence was noted that supported the use of demineralized freeze dried bone allograft (DFDBA) as a periodontal regenerative material.103 Other data indicated that porous hydroxyapatite and bone allografts achieved similar results in the treatment of intrabony defects.103 Limited evidence supported the use of autogenous bone, DFDBA in combination with an absorbable polylactide barrier, anorganic bovine bone, and anorganic bovine bonecollagen. There also was limited evidence to indicate that a combination of bone grafts and barrier material provided better results than bone grafts alone.103 It was concluded that barrier membranes provide a superior result when compared with open flap debridement with respect to reducing probing depths and gaining clinical attachment in furcations and intrabony defects.104 Evidence indicated that bone and a physical barrier enhanced clinical outcomes in furcation defects. However, in intrabony defects, the use of a barrier attained similar results to bone plus a barrier.104 It was also noted that there may be increased recession after the use of a barrier.
New York: Plenum; 1991:3-58. The American Academy of Periodontology. Supportive periodontal therapy (SPT) (position paper). Chicago: The American Academy of Periodontology, 1997. Lamont RJ, Yilmaz O. In or out: the invasiveness of oral bacteria. Periodontol 2000. 2002;30:61-69. Slots J, Ting M. Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in human periodontal disease: occurrence and treatment. Periodontol 2000. 1999;20:82-121. van Winkelhoff AJ, Rams TE, Slots J. Systemic antibiotic therapy in periodontics. Periodontol 2000. 1996;10:45-78. Socransky S, Haffajee AD. Dental biofilms: difficult therapeutic targets. Periodontol 2000. 2002;28:12-55. Costerton JW, Lewandowski Z, Caldwell DE, et al. Microbial biofilms. Annu Rev Microbiol. 1995;49:711-745. Ali RW, Martin L, Haffajee AD, et al. Detection of identical ribotypes of Porphyromonas gingivalis in patients residing in the United States, Sudan, Romania and Norway. Oral Microbiol Immunol. 1997;12:106-111.

References
1. Moore WE, Moore LH, Ranney RR, et al. The microflora of periodontal sites showing active destructive progression. J Clin Periodontol. 1991;18:729-739. Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol 2000. 1994;5:78-111. Socransky SS, Haffajee AD, Cugini M, et al. Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25:134-144. American Academy of Periodontology. Systemic antibiotics in periodontics (position paper). J Periodontol. 1996;67:831-838. Greenstein G, Tonetti M. The role of controlled drug delivery for periodontitis. The Research, Science, and Therapy Committee of the American Academy of Periodontology. J Periodontol. 2000;71:125-140. Evans AS. Epidemiological concepts. In: Evans AS, Brachmen PS, eds. Bacterial Infections of Humans: Epidemiology and Control.

7.

8. 9.

2.

3.

10. 11. 12. 13.

4. 5.

6.

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15. 16.

17.

18.

19.

20.

21. 22.

23.

24.

25.

26. 27. 28. 29. 30. 31. 32.

33. 34.

35. 36. 37.

38.

He T, Hayashi J, Yamamoto M, et al. Genotypic characterization of Actinobacillus actinomycetemcomitans from periodontitis patients by arbitrarily primed polymerase chain reaction. J Periodontol. 1998;69:69-75. Greenstein G, Lamster I. Bacterial transmission in periodontal diseases: a critical review. J Periodontol. 1997;68:421-431. Asikainen S, Chen C. Oral ecology and person-to-person transmission of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Periodontol 2000. 1999;20:65-81. Preus HR, Zambon JJ, Dunford RG, et al. The distribution and transmission of Actinobacillus actinomycetemcomitans in families with established adult periodontitis. J Periodontol. 1994;65:2-7. Kononen E, Saarela M, Karjalainen J, et al. Transmission of oral Prevotella melaninogenica between a mother and her young child. Oral Microbiol Immunol. 1994;9:310-314. van Steenbergen TJ, Petit MD, Scholte LH, et al. Transmission of Porphyromonas gingivalis between spouses. J Clin Periodontol. 1993;20:340-345. Petit MD, van Steenbergen TJ, de Graaff J, et al. Transmission of Actinobacillus actinomycetemcomitans in families of adult periodontitis patients. J Periodontal Res. 1993;28:335-345. Socransky SS, Haffajee AD. Evidence of bacterial etiology: a historical perspective. Periodontol 2000. 1994;2:7-25. Page RC, Offenbacher S, Schroeder HE, et al. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000. 1997;14:216-248. Caton JG, Ciancio SG, Bleiden TM, et al. Treatment with subantimicrobial dose doxycycline improves the efficacy of scaling and root planing in patients with adult periodontitis. J Periodontol. 2000;71:521-532. Novak MJ, Johns LP, Miller RC, et al. Adjunctive benefits of subantimicrobial dose doxycycline in the management of severe, generalized, chronic period o n t i t i s . J Periodontol. 2002;73:762-769. Socransky SS, Haffajee AD, Goodson JM, et al. New concepts of destructive periodontal disease. J Clin Periodontol. 1984;11:21-32. Reddy MS, Geurs NC, Jeffcoat RL, et al. Periodontal disease progression. J Periodontol. 2000;71:1583-1590. Clark WB, Loe H. Mechanisms of initiation and progression of periodontal disease. Periodontol 2000. 1993;2:72-82. Ralls SA, Cohen ME. Problems in identifying bursts of periodontal attachment loss. J Periodontol. 1986;57:746-752. Greenstein G, Caton J. Periodontal disease activity: a critical assessment. J Periodontol. 1990;61:543-552. Loe H. Periodontal diseases: a brief historical perspective. Periodontol 2000. 1993;2:7-12. Armitage GC. Periodontal diseases: diagnosis. A n n Periodontol. 1996;1:37-215. Salvi GE, Lawrence HP, Offenbacher S, et al. Influence of risk factors on the pathogenesis of periodontitis. Periodontol 2000. 1997;14:173-201. Hart TC, Kornman KS. Genetic factors in the pathogenesis of periodontitis. Periodontol 2000. 1997;14:202-215. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1-6. Oliver RC, Brown LJ, Loe H. Periodontal diseases in the United States population. J Periodontol. 1998;69:269-278. Albandar JM. Periodontal diseases in North America. Periodontol 2000. 2002;29:31-69. Persson GR. The effects of line-angle versus midproximal periodontal probing measurements on prevalence estimates of periodontal diseases. J Periodontal Res. 1991;26:527-529. Kornman KS. Patients are not equally susceptible to periodontitis: does this change dental practice and the dental curriculum? J Dent Educ. 2001;65:777-784.

39.

Schenkein HA. Finding genetic risk factors for periodontal diseases: is the climb worth the view? Periodontol 2000. 2002;30:79-90. 40. Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: an overview. Ann Periodontol. 2001;6:91-98. 41. Scannapieco FA. Position paper of the American Academy of P e r i odontology: periodontal diseases as a potential risk factor for systemic diseases. J Periodontol. 1998;69:841-850. 42. Mealey BL. Periodontal implications: medically compromised patients. Ann Periodontol. 1996;1:256-321. 43. Papapanou PN. Periodontal diseases: epidemiology. Ann Periodontol. 1996;1:1-36. 44. Martinez-Canut P, Lorca A, Magan R. Smoking and periodontal disease severity. J Clin Periodontol. 1995;22:743-749. 45. Zambon JJ, Grossi SG, Machtei EE, et al. Cigarette smoking increases the risk for subgingival infection with periodontal pathogens. J Periodontol. 1996;67(suppl 10):1050-1054. 46. Reddy MS. Osteoporosis and periodontitis: discussion, conclusions, and recommendations. Ann Periodontol. 2001;6:214-217. 47. von Wowern N, Klausen B, Kollerup G. Osteoporosis: a risk factor in periodontal disease. J Periodontol. 1994;65:1134-1138. 48. Genco RJ, Grossi SG. Is estrogen deficiency a risk factor for p e r i odontal disease? Compend Contin Educ Dent. 1998;(suppl 22):S23-29. 49. G r odstein F, Colditz GA, Stampher MJ, et al. Tooth loss and hormone use in postmenopausal women. Compend Contin Educ Dent. 1998;(suppl 22):S9-16. 50. Michalowicz BS, Diehl SR, Gunsolley JC, et al. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol. 2000;71:1699-1707. 51. Kornman KS, Crane A, Wang HY, et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol. 1997;24:72-77. 52. Greenstein G, Hart TC. A critical assessment of interleukin-1 (IL-1) genotyping when used in a genetic susceptibility test for severe chronic periodontitis. J Periodontol. 2002;73:231-247. 53. Ryder MI. An update on HIV and periodontal disease. J Periodontol. 2002;73:1071-1078. 54. Lamster IB, Grbic JT, Mitchell-Lewis DA, et al A. New concepts regarding the pathogenesis of periodontal disease in HIV infection. Ann Periodontol. 1998;3:62-75. 55. Beck JD, Offenbacher S. The association between periodontal diseases and cardiovascular diseases: a state-of-the-science review. Ann Periodontol. 2001;6:9-15. 56. DeStefano F, Anda RF, Kahn HS, et al. Dental disease and risk of coronary heart disease and mortality. BMJ. 1993;306:688-691. 57. Joshipura KJ, Rimm EB, Douglass CW, et al. Poor oral health and coronary heart disease. J Dent Res. 1996;75:1631-1636. 58. Beck J, Garcia R, Heiss G, et al. Periodontal disease and cardiovascular disease. J Periodontol. 1996;67(suppl 10):11231137. 59. Wu T, Trevisan M, Genco RJ, et al. Periodontal disease and risk of cerebrovascular disease: the first national health and nutrition examination survey and its follow-up study. Arch Intern Med. 2000;160:2749-2755. 60. Morrison HI, Ellison LF, Taylor GW. Periodontal disease and risk of fatal coronary heart and cerebrovascular diseases. J Cardiovasc Risk. 1999;6:7-11. 61. Mattila KJ, Asikainen S, Wolf, et al. Age, dental infections, and coronary heart disease. J Dent Res. 2000;79:756-760. 62. Hujoel PP, Drangsholt M, Spiekerman C, et al. Periodontal disease and coronary heart disease risk. JAMA. 2000;284:1406-1410. 63. Howell TH, Ridker PM, Ajani UA, et al. Periodontal disease

90

Compendium / February 2005

Vol. 26, No. 2

64.

65.

66.

67.

68.

69.

70.

71.

72. 73.

74.

75.

76.

77.

78.

79.

80. 81.

82.

83. 84.

and risk of subsequent cardiovascular disease in US male physicians. J Am Coll Cardiol. 2001;37:445-450. Offenbacher S, Katz V, Fertik G, et al. Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol. 1996;67(suppl 10):1103-1113. Offenbacher S, Lieff S, Boggess KA, et al. Maternal periodontitis and prematurity. Part I: Obstetric outcome of prematurity and growth restriction. Ann Periodontol. 2001; 6:164-174. Dasanayake AP. Poor periodontal health of the pregnant women as a risk factor for preterm low birth weight. Ann Periodontol. 1998;3:206-212. Jeffcoat MK, Geurs NC, Reddy MS, et al. Periodontal infection and preterm birth: results of a prospective study. J Am Dent Assoc. 2001;132:875-880. Mitchell-Lewis D, Engebretson SP, Chen J, et al. Periodontal infections and pre-term birth: early findings from a cohort of young minority women in New York. Eur J Oral Sci. 2001;109:34-39. Lopez NJ, Smith PC, Gutierrez J. Periodontal therapy may reduce the risk of preterm low birth weight in women with periodontal disease: a randomized controlled trial. J Periodontol. 2002;73:911-924. Armtiage GC. Periodontal disease and pregnancy: discussion, conclusions, and recommendations. Ann Periodontol. 2001;6:189-192. Grossi SG, Skrepcinski FB, DeCaro T, et al. Response to periodontal therapy in diabetics and smokers. J Periodontol. 1996;67(suppl 10):1094-1102. Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: a two-way relationship. Ann Periodontol. 1998;3:51-61. Grossi SG. Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research. Ann Periodontol. 2001;6:138-145. Taylor G. Bi-directional interrelationships between diabetes and periodontal diseases: an epidemiologic perspective. Ann Periodontol. 2001;6:99-112. Lamster IB, Lalla E. Periodontal disease and diabetes mellitus: discussion, conclusions, and recommendations. A n n Periodontol. 2001;6:146-149. Hayes C, Sparrow D, Cohen M. The association between alveolar bone loss and pulmonary infection:. The VA Dental Longitudinal Study. Ann Periodontol. 1998;3:257-261. Scannapieco FA, Papandonatos GD, Dunford RG. Associations between oral conditions and respiratory disease in a national sample survey population. Ann Periodontol. 1998;3:251-256. Scannapieco FA, Ho AW. Potential associations between chronic respiratory disease and periodontal disease: analysis of National Health and Nutrition Examination Survey III. J Periodontol. 2001;72:50-56. Scannapieco FA, Wang B, Shiau HJ. Oral bacteria and respiratory infection: effects on respiratory pathogen adhesion and epithelial cell proinflammatory cytokine production. Ann Periodontol. 2001;6:78-86. Cobb CM. Non-surgical pocket therapy: mechanical. Ann Periodontol. 1996;1:443-490. Drisko CL, Cochran DL, Blieden T, et al. Position paper: sonic and ultrasonic scalers in periodontics. Research, Science, and Therapy Committee of the American Academy of Periodontology. J Periodontol. 2000;71:1792-1801. American Academy of Periodontology. The role of supra and subgingival irrigation in the treatment of periodontal diseases (position paper). Chicago: American Academy of Periodontology, 1995. Drisko CH. Non-surgical pocket therapy: pharmacotherapeutics. Ann Periodontol. 1996;1:491-566. Drisko CL, Cobb CM, Killoy WJ, et al. Evaluation of periodontal treatments using controlled-release tetracycline fibers: clinical response. J Periodontol. 1995;66:692-699.

85.

86.

87.

88.

89.

90.

91.

92. 93.

94.

95.

96.

97.

98.

99.

100.

101.

102.

103.

104.

Jeffcoat MK, Bray KS, Ciancio SG, et al. Adjunctive use of a subgingival controlled-release chlorhexidine chip reduces probing depth and improves attachment level compared with scaling and root planing alone. J Periodontol. 1998;69:989-997. Garrett S, Johnson L, Drisko CH, et al. Two multi-center studies evaluating locally delivered doxycycline hyclate, placebo control, oral hygiene, and scaling and root planing in the treatment of periodontitis. J Periodontol. 1999;70:490-503. Williams RC, Paquette DW, Offenbacher S, et al. Treatment of periodontitis by local administration of minocycline microspheres: a controlled trial. J Periodontol. 2001;72:1535-1544. Loesche WJ, Giordano JR, Hujoel P, et al. Metronidazole in periodontitis: reduced need for surgery. J Clin Periodontol. 1992;19:103-112. Loesche WJ, Schmidt E, Smith BA, et al. Effects of metronidazole on periodontal treatment needs. J Periodontol. 1991;62:247-257. Magnusson I, Clark WB, Low SB, et al. Effect of non-surgical periodontal therapy combined with adjunctive antibiotics in subjects with refractory periodontal disease. (I). Clinical results. J Clin Periodontol. 1989;16:647-653. Oringer RJ; Research, Science, and Therapy Committee of the American Academy of Periodontology. Modulation of the host response in periodontal therapy. J Periodontol. 2002;73:460-470. Erratum in J Periodontol. 2002;73:684. Palcanis KG. Surgical pocket therapy. Ann Periodontol. 1996;1:589-617. Laurell L, Gottlow J, Zybutz M, et al. Treatment of intrabony defects by different surgical procedures. A literature review. J Periodontol. 1998;69:303-313. Kalpidis CD, Ruben MP. Treatment of intrabony periodontal defects with enamel matrix derivative: a literature review. J Periodontol. 2002;73:1360-1376. Scannapieco FA, Bush RB, Paju S. Association between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann Periodontol. 2003;8:38-53. Scannapieco, FA, Bush RB, Paju S. Association between periodontal disease and risk for nosocomial bacterial pneumonia and chronic obstructive pulmonary disease. A systematic review. Ann Periodontol 2003;8:54-69. Scannapieco, FA, Bush RB, Paju S. Periodontal disease as a risk factor for adverse pregnancy outcomes. A systematic review. Ann Periodontol. 2003;8:70-78. Reddy MS, Gears NC, Gunsolley JC. Periodontal host modulation with antiproteinases, anti-inflammatory, and bone sparing agents. A systematic review. Ann Periodontol. 2003;8:12-37. Hanes P, Purvis JP. Local anti-infective therapy: Pharmacological agents. A systematic review. Ann Periodontol. 2003;8:79-98. Hallmon WW, Rees TD. Local anti-infective therapy: Mechanical and physical approaches. A systematic review. Ann Periodontol. 2003;8:99-114. Haffajee AD, Socransky SS, Gunsolley JC. Systemic antiinfective periodontal therapy. A systematic review. Ann Periodontol. 2003;8:115-181. Mariotti A. Efficacy of chemical root surface modifiers in the treatment of periodontal disease. A systematic review. Ann Periodontol. 2003;8:205-226. Reynolds MA, Aichelman-Reidy ME, Branch Mays GL, Gunsolley JC. The efficacy of bone replacement grafts in the treatment of osseous defects. A systematic review. Ann Periodontol. 2003;8:227-265. Murphy KG, Gunsolley J. Guided tissue regeneration for the treatment of periodontal intrabony and furcations defects. A systematic review. Ann Periodontol. 2003;8:266-30. Compendium / February 2005

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Quiz1
1. Of the over 500 types of bacteria found within the oral cavity, about how many are commonly associated with bacterial infections? a. 10 b. 100 c. 250 d. 450 2. By definition, an infection occurs when there is a bacterial etiology and: a. increased saliva. b. decreased saliva. c. an immune response. d. anaphylaxis. 3. Genetically different subspecies of bacteria that exist within a species are called: a. mutations. b. alterations. c. clonal types. d. morphogenic colonies. 4. What are associated with bone destruction? a. osteoblasts b. chondroclasts c. OPG d. prostaglandins 5. What are involved in the destruction of collagen? a. kallikrein b. matrix metalloproteinase c. rank-L d. cDNA 6. For a disease to be initiated, the: a. host must be susceptible. b. bacteria must be virulent. c. bacteria must overwhelm the host response. d. all of the above 7. When periodontal infections may be risk factors for certain systemic diseases, this concept reflects an emerging area of interest referred to as: a. risk assessment. b. periodontal medicine. c. cohort analysis. d. confounding factors. 8. Smokers have how much greater a chance of developing periodontitis compared with nonsmokers? a. 1.4 b. 2.8 c. 4.2 d. 5.6 9. An association between disease entities (eg, cardiovascular disease and periodontitis) should not be interpreted as being: a. factual. b. a causal relationship. c. statistically significant. d. meaningful. 10. Surgical intervention is dictated by the: a. magnitude of the lesion being treated. b. actual or potential response to nonsurgical therapy. c. desired clinical outcome. d. all of the above.

This article provides 1 hour of CE credit from Dental Learning Systems, in association with the University of Southern California School of Dentistry and the University of Pennsylvania School of Dental Medicine, representatives of which have reviewed the articles in this issue for acceptance. Record your answers on the enclosed answer sheet or submit them on a separate sheet of paper. You may also phone your answers in to (888) 596-4605 or fax them to (703) 404-1801. Be sure to include your name, address, telephone number, and social security number.

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