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Deborah A. Termeie, DDS
Clinical Lecturer
Department of Periodontics
School of Dentistry
University of California, Los Angeles
Los Angeles, California

[DNLM: 1. Periodontal Diseases--Examination Questions. 2. Periodontics--Examination Questions. 3. Periodontium--Examination Questions. WU 18.2]

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Becoming certified by the American Board of Periodontology (ABP) is an immense honor and an outward sign of a dedication to the specialty of periodontics and a drive to excel within the profession. According to the American Academy of Periodontology, the ABP “evaluates standards of periodontic practice by examining the qualifications and competence of periodontists who voluntarily apply to the board for certification as diplomates.” After successful completion of a written qualifying examination, a candidate is considered board eligible and must then complete an oral examination in a defined period of time.The ABP defines a diplomate as “a periodontist who has made significant achievements beyond the mandatory educational requirements of the specialty and who is certified by the ABP.” This reinforces board certification as a sign of dedication to the specialty and of committment to become the best periodontist possible.

To be educationally qualified for board certification, a candidate must be a certified dentist who has completed an accredited 3-year educational program in periodontology. The written and oral board examinations are comprehensive, covering all phases of periodontal health and disease and its diagnosis, treatment, and evaluation. In fact, the mission of the ABP is to “advance the art and science of periodontics and elevate the quality of periodontal care through the examination, certification, and recertification of periodontists and by encouraging the achievement and maintenance of diplomate status.” Thus, one can appreciate that mastery of the body of knowledge required to complete the written and oral examinations is intimidating and overwhelming! Periodontal Review by Dr Deborah Termeie is an organized, detailed, and well-documented compilation of information designed to help candidates navigate the board certification examinations.

There are many periodontal specialty programs across the United States, and while each covers the components mandated by the Commission on Dental Accreditation of the American Dental Association, variation exists between programs because of different faculties and diverse patient experiences. Therefore, a comprehensive well-documented study guide can help standardize the information provided in the various educational programs. More important, the body of knowledge that one must know to become board certified is overwhelming, and as more publications in the peer-reviewed literature become available every year, this body of knowledge grows exponentially. Learning the necessary material seems impossible. These are just two reasons why this study guide is helpful.

In the past, study to become board certified would require months of preparation just to figure out how to organize the literature to understand the critical information. Dr Termeie has done this task for you. Chapters cover diverse topics of periodontolgy, including health and disease conditions and therapeutic options, and the information is presented in an easy-to-understand question and answer format. The detail for treatment options alone is impressive; it includes nonsurgical and surgical therapy, chemotherapeutics, lasers, occlusal therapy, and bone and implant therapy for replacing missing teeth. Dr Termeie includes other material relevant to the board candidate, such as evidence-based medicine and dentistry, related human physiology and pathology, pharmacology, and oral medicine and pathology.

Another helpful aspect to this study guide is that Dr Termeie often provides data for and against a question in a concise and understandable format. Additionally, simple diagrams, tables, and charts are used throughout, which makes the text easy to understand even when discussing difficult topics. Dr Termeie also provides clinical examples that demonstrate how patient cases are documented and presented during the board examinations.

Collectively this study guide provides a comprehensive and well-organized review of major concepts in the field of periodontology and can be used either to start the studying process or as a self-examination review prior to taking the examinations. I believe that this study guide will be an essential tool for anyone who is going through the periodontal certifying board examinations or the board recertification examination or who would like to have a comprehensive reference guide in periodontology. I would like to thank Dr Termeie for the time and effort that she expended to compile this information and for making it comprehensive, organized, and easy to understand. Present and future periodontal diplomates will be much better prepared due to this effort by Dr Termeie.

As periodontal residency graduates embark on their journey to board certification, many of them come face to face with a plethora of study materials and information but no comprehensive study resource designed to help them prepare for their examinations. Periodontal Review was specifically written to address this void.

The material in this book is presented in a question and answer format for ease of study.The classic literature is cited as well as more recent and practical literature on topics such as diagnosis, nonsurgical therapy, surgical therapy, regeneration, and implants. Literature evidence for opposing viewpoints is also presented throughout the book. Additionally, each chapter contains clear and relevant tables, illustrations, and pictures. This comprehensive and yet concise approach to periodontics is aimed at preparing the candidate for periodontal examinations and clinical practice.

Periodontal Review is a useful resource for residents, practicing periodontists preparing for board certification, dental students, and dental hygiene students seeking a broader appreciation and in-depth understanding of periodontics. Topics chosen are those emphasized in periodontal residency graduation examinations as well as the oral examintation of the American Board of Periodontology.

I would like to acknowledge my mentors—Philip R. Melnick, DDS; Thomas N. Sims, DDS; Paulo M. Camargo, DDS; and Thomas Han, DDS—for their guidance and advice. I would also like to thank my program director at UCLA, Perry R. Klokkevold, DDS. Lastly, I would like to thank my loving husband, David, and my children, Gabriella and Elliot. Without their love and support, this book would not have been possible.

About the Author

Deborah A. Termeie, dds, is a clinical instructor in the Department of Periodontics at UCLA in Los Angeles, California. She is a diplomate of the American Board of Periodontology (ABP), and it was her experience preparing for the ABP qualifying exams that inspired her to write this book. Dr Termeie has published on the topic of evidence-based dentistry and is the recipient of several awards, including the Excellence in Implantology Research award from the California Society of Periodontics. She maintains a private practice in Beverly Hills, California.

Evidence-based dentistry is the merging of clinically pertinent scientific evidence to the patient’s oral and medical condition and history. The dentist uses the evidence to make sound decisions about diagnosis, prognosis, and treatment.

The PICO question is a question that includes a population to be examined, the nature of the intervention to be inspected, a comparison statement, and the type of outcome to be evaluated. It should be problem-focused and concise.

Example: In patients with periodontitis (population), what is the effect of osseous surgery (intervention) compared with controls (comparison) on clinical and patient-centered outcomes (outcome)?

Q: What is the step-by-step process for making an evidence-based decision in a dental practice?

The steps involved in evidence-based decision making in a dental practice are shown in Fig 1-1.

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Fig 1-1 Evidence-based decision making. (Based on data in Chiappelli et al.¹)

Q: What are the different study types (ranked from highest level of evidence to lowest)?

The different types of studies are shown, ranked in order of highest to lowest level of evidence, in Fig 1-2.

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Fig 1-2 Different studies ranked from highest level of evidence to lowest. (Based on Chiappelli et al.²)

Q: Describe the difference between a cross-sectional study and a longitudinal study.

A cross-sectional study is done at one time point, whereas a longitudinal study ranges over a period of time, allowing temporal relationships to be investigated.

The P value is the probability of obtaining a test statistic at least as extreme as the one observed, assuming that the null hypothesis is true. The smaller the P value, the less likely the effect was due to chance.

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Fig 1-3 Internal and external validity.

1. Chiappelli F, Brant XMC, Oluwadara OO, Neagos N, Ramchandani MH. Introduction: Research synthesis in evidence-based clinical decision-making. In: Chiappelli F, Brant XMC, Neagos N, Oluwadara OO, Ramchandani MH (eds). Evidence-Based Practice: Toward Optimizing Clinical Outcomes. London: Springer, 2010:5.

2. Nocini PF, Verlato G, De Santis D, et al. Strengths and limitations of the evidence-based movement aimed to improve clinical outcomes in dentistry and oral surgery. In: Chiappelli F, Brant XMC, Neagos N, Oluwadara OO, Ramchandani MH (eds). Evidence-Based Practice: Toward Optimizing Clinical Outcomes. London: Springer, 2010:151.

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Fig 2-1a Illustration of the periodontium. (Reprinted from Fan and Berry¹ with permission.)

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Fig 2-1b Labeled anatomy of the periodontium. (Reprinted from Fan and Berry¹ with permission.)

The external carotid artery and its main branches, which include the lingual, facial, and maxillary arteries, are the vascular supply for the periodontium. Locally, the blood supply comes from the supraperiosteal vessels and vessels from the periodontal ligament (PDL) and bone.²

The trigeminal nerve and its branches provide the main innervation for the periodontium.

The attached gingiva is the area from the base of the sulcus to the mucogingival junction. It prevents the free gingiva from being separated from the tooth. Its height is determined by subtracting the sulcus probing depth from the total width of the keratinized tissue. It consists of thick lamina propria and deep rete pegs. Goaslind et al³ reported that the attached gingival thickness is 1.25 ± 0.42 mm.

The keratinized attached gingiva is that found from the gingival margin to the mucogingival junction.

Alveolar mucosa is the covering of the alveolar process that is nonkeratinized, unstippled, and movable. It extends from the mucogingival junction to the floor of the mouth and vestibular epithelium.

Ante’s law states that the root surface area of the abutment teeth must be equal to or greater than that of teeth being replaced with pontics.This helps determine the number of abutments needed for a fixed partial denture.

Healthy gingiva is coral pink, firm, follows the CEJ of the teeth, and may be stippled. The color of the gingiva is associated with the pigmentation of the patient. In dark-haired individuals, the gingiva can be darker than that in blond patients.

• Fibers extending horizontally beyond the alveolar crest height and then apically along the alveolar bone cortex

2. Alveologingival group: Fibers in this group run coronally into the lamina propria from the periosteum at the alveolar crest.

3. Dentoperiosteal fibers: These fibers insert into the periosteum of the alveolar crest and fan out to the adjacent cementum.

4. Circular group: These are the only fibers that are confined to the gingiva and do not attach to the teeth.

5. Transseptal group: These fibers bridge the interproximal tissue between adjacent teeth and insert into the cementum.

Q: What is the composition of the oral mucosa (the tissue lining the oral cavity)?

The oral mucosa is composed of masticatory, lining, and specialized tissues (Fig 2-2).

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Fig 2-2 Composition of the oral mucosa. (Based on Avery.⁴)

The gingival epithelium consists of oral (masticatory), oral sulcular, and junctional epithelia (Fig 2-3).

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Fig 2-3 Composition of the gingival epithelium. (Based on Clerehugh et al.⁵)

1. Stratum basale: Cuboidal cells found at the basement membrane; epithelial cell replication takes place in this location. This layer contains melanocytes and Merkel cells.

2. Stratum spinosum: The “spines” are desmosomes allowing intracellular contacts. It is the thickest layer and contains Langerhans cells, which are derived from bone marrow and take part in immune surveillance.

3. Stratum granulosum: Cells in this layer appear flat. Keratinocytes migrating from the underlying stratum spinosum become known as granular cells in this layer. These cells contain keratohyalin granules, protein structures that promote hydration and cross-linking of keratin.

4. Stratum corneum: Outermost layer containing dead cells and consisting of ortho- and parakeratinization. It is composed of compactly packed tonofilaments.

The average thickness of the gingiva is 1.25 mm.³ The widest zone of gingiva is in the maxillary anterior region; the narrowest zone is at the facial aspect of the mandibular first premolar.²

Connective tissue is fibrous, consisting of mostly type I collagen, ground substances, and mucopolysaccharides. It also contains white blood cells, blood vessels, lymphatics, and nerves.²

The underlying connective tissue determines whether the epithelium is keratinized.⁶

Older individuals have thicker fiber bundles in the PDL than younger individuals. The average width of the PDL is 0.2 mm.

Superior and inferior alveolar arteries provide the blood supply to the PDL, which is a vascular tissue.

The fibers of the PDL include the alveolar crest, horizontal, oblique (most numerous), interradicular, and apical fibers.

Ankylosis is the fusion of the cementum and alveolar bone with obliteration of the PDL. It develops after chronic periapical inflammation, tooth reimplantation, and occlusal trauma.

Acellular cementum is located on the enamel at the CEJ. It does not contain cementocytes and forms slowly.

Cellular cementum is located at the apical third of the root. It is more irregular and forms rapidly. With age, there is an increase in width of the cellular cementum.

Extrinsic fibers are made of Sharpey fibers from the PDL, whereas intrinsic fibers are cementum fibers produced by cementoblasts (Fig 2-4).

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Fig 2-4 Characteristics of extrinsic and intrinsic cementum.

The junctional epithelium attaches to the cementum via hemidesmosomes and replicates every 5 days.

The meniscus divides the joint into two compartments. The upper compartment has translational movement, and the lower compartment has rotational movement.

• With reduction: The disc as well as the posterior band of the meniscus is anteriorly displaced in front of the condyle upon opening. This causes a popping or clicking sound.

• Without reduction: In some patients, the meniscus remains anteriorly displaced at full opening. This is a much more serious condition.

• Type I: Skin, tendon, vascular ligature, organs, bone (main component of the organic part of bone)

• Type III: Comprised of reticular fibers, commonly found alongside type I collagen, found mostly in smooth muscle

The biologic width is defined as the physiologic dimension of the junctional epithelium and connective tissue attachment. It is measured from the most coronal part of the junctional epithelium to the crest of the alveolar bone. In studies on cadavers, Gargiulo⁷ found a connective tissue attachment of 1.07 mm and a junctional epithelium attachment of 0.97 mm. Therefore, the biologic width is about 2 mm. He also found the sulcus, which is not part of the biologic width, to be 0.69 mm.

If subgingival restorations violate the biologic width, periodontal bone loss and inflammation may occur. The body will try to make room between the margin of the restoration and the alveolar bone to allow for reestablishment of the biologic width.

The mesial aspect of the maxillary first premolars and first molars are the most common areas of recurrent pockets.

1. Fan PP, Berry TG. Cast-gold restorations. In: Summitt JB, Robbins JW, Hilton TJ, Schwartz RS (eds). Fundamentals of Operative Dentistry: A Contemporary Approach, ed 3. Chicago: Quintessence, 2006:543.

2. Serio FG, Hawley C. Manual of Clinical Periodontics. Hudson, OH: Lexi-Comp, 2002.

3. Goaslind GD, Robertson PB, Mahan CJ, Morrison WW, Olson JV. Thickness of facial gingiva. J Periodontol 1977;48:768–771.

4. Avery J. Oral Development and Histology, ed 3. Stuttgart, Germany: Thieme Medical, 2002:250.

5. Clerehugh V, Tugnait A, Genco R.J. Periodontology at a Glance. Oxford: Wiley-Blackwell, 2009:3.

6. Karring T, Lang NP, Löe H. The role of gingival connective tissue in determining epithelial differentiation. J Periodontal Res 1975;10:1–11.

7. Gargiulo AW. Dimensions and relations of the dentogingival junction in humans. J Periodontol 1961;32:261–267.

In a study on periodontal patients, Svärdström and Wennström¹ found a greater prevalence of furcation involvement in maxillary molars than in mandibular molars. The narrowest furcation entrance was found on the buccal aspect of maxillary and mandibular molars, and the highest frequency of involvement was the distal aspect of the maxillary first molar. The mesial aspect of the second molar had the least frequency of furcation involvement.

Q: Is the Nabers probe a valid and efficient tool for detecting furcation invasion?

Eickholz and Kim² found that the Nabers Probe, marked in 3-mm increments, is a valid method of diagnosing furcation lesions.

• F2: The furcation can be probed greater than 3 mm, but it is not a through and through furcation involvement.

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Fig 3-1 Glickman classification.

The classification by Tarnow and Fletcher⁵ is a subclassification of the Glickman furcation classification that measures the vertical probing depth from the roof of the furca:

• Regeneration (guided tissue regeneration [GTR] and enamel matrix derivative [EMD])

A review by Cobb⁶ demonstrated a less favorable response to scaling and root planing by molars with furcation involvement compared with those without furcation lesions and single-rooted teeth. He surmised that this was related to the inability to remove all pathogenic microbial flora due to the furcal anatomy restricting access for mechanical therapy.

Bower⁷ found that 81% of the time the furcation entrance is 1 mm or less. The study also found that 58% of the time the furcation entrance is 0.7 mm or less. The blade width of commonly used periodontal curettes is 0.75 mm. The ultrasonic (smaller) tip would fit better than the tip of a Gracey curette in a grade II or III furcation.

Wylam et al⁸ found no significant difference between open and closed flap root planing. The study further concluded that root planing is inefficient in the debridement of furcation lesions and does not allow for periodontal regeneration.

Q: Can a grade II furcation be treated successfully? Which treatment is the most effective?

Evans et al⁹ reviewed 50 papers that studied 1,016 grade II furcations. The teeth had received various treatments such as bone grafts, open flap debridement, and GTR. The study found complete closure of the furcation in 20% of the grade II furcations and an improvement of a grade II to a grade I furcation in 33% of the cases. In general, there was a 50% improvement for grade II furcations. The most effective treatment was a bone graft with GTR, and the least effective treatment was open flap debridement (2% of the grade II furcations had complete closure).

Bowers et al¹⁰ discovered complete closure of grade II mandibular furcations in 50% of patients. There was a 68% improvement of a grade II to a grade I furcation.

Murphy and Gunsolley¹¹ performed a systematic review and discovered that GTR is more effective than open flap debridement in the treatment of furcation defects. The study also found that in furcation lesions vertical probing depth, vertical probing attachment levels, and horizontal open probing attachment levels—but no intrabony outcomes—were improved by augmentation with a particulate graft in conjunction with the GTR barrier.

Bowers et al¹⁰ found poorer results in the treatment of furcation lesions in smokers. Smokers had a 62.5% chance of having a class II residual defect compared with nonsmokers, who had a 14.3% chance. Furcation fill decreases at an increased horizontal and vertical presurgical probing attachment level (greater than 5 mm). The following were found to reduce the frequency of clinical closure:

• Increased distance between the roof of the furcation and the base of the defect

Q: Are teeth that undergo the tunnel preparation in the furcation area prone to caries?

Hellden et al¹² studied 156 teeth with advanced periodontal furcation defects that were treated by tunnel preparations. The study found that 25% of the teeth developed caries.

A retrospective study by Feres et al¹³ demonstrated that a history of root caries was the only factor with a positive association with caries incidence in tunnels.

• EMD: A study by Araújo and Lindhe¹⁴ used EMD and a barrier in the test defects and just a barrier in control defects. The test defect was found to have acellular cementum in the apical portion, while in the coronal portion a thick cellular cementum, similar to the cementum found in the control group, was detected. Both the test and control group furcation defects were found to be clinically closed and to contain bone and periodontal ligament tissue that appeared structurally similar to newly formed root cementum.

• Recombinant human osteogenic protein-1 (OP-1): Giannobile et al¹⁵ found distinct stimulation of osteogenesis, regenerative cementum, and new attachment formation in sites treated with three different concentrations of OP-1.

• Platelet-rich plasma (PRP): Pradeep et al¹⁶ reported that although the degree II status of the studied furcation defects was unchanged, sites treated with PRP showed a statistically significant difference in all clinical and radiographic parameters compared with those receiving open flap debridement.

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Fig 3-2 Anatomical factors associated with furcation lesions.

Gutmann¹⁷ studied 102 molars and found that 28.4% (29.4% of mandibular molars and 27.4% of maxillary molars) have accessory canals in the furcation.

Swan and Hurt¹⁹ discovered that mandibular second molars had the highest incidence of cervical enamel projections (51.0%), while the lowest incidence was found in the maxillary first molars (13.6%). The most frequently encountered enamel projections in the study were grade 1, and the buccal surfaces were the most common location of cervical enamel projections.

Roussa²⁰ observed 60 teeth and discovered cervical enamel projections in 30% of the teeth examined.

It is believed that the existence of cervical enamel projections inhibits connective tissue attachment and makes management of the furcation difficult.

Swan and Hurt¹⁹ showed a positive correlation between grade 2 and grade 3 cervical enamel projections and periodontally involved furcations. However, the study did not find a relationship between grade 1 projections and furcation involvements.

A review by Lima and Hebling²¹ found an association between cervical enamel projection, inflammatory periodontal disease, and molar furcation involvement.

Q: Describe how root concavities can affect prognosis of a tooth. Where are the concavities located on the first molars?

It is much more difficult to perform scaling and root planing on teeth with concavities, and as a result they can have a deleterious effect on the prognosis of a tooth. It is also challenging for the patient to maintain oral hygiene.

The root concavities for the first molars, as described by Bower,²² are presented in Fig 3-3.

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Fig 3-3 Anatomy of root concavities.

• Mandibular molars: Buccal furcation entrance width is greater than lingual furcation entrance width.

• Maxillary molars: Mesial entrance width is greater than distal entrance width, which is greater than buccal entrance width.

Q: Where are enamel pearls found most often? How can they contribute to furcation lesions?

According to Moskow and Canut,²³ enamel pearls have a tendency to originate in the furcation areas of molars, especially the maxillary second and third molars.The study found an incidence of 1.1% to 9.7%.

As with cervical enamel projections, the existence of enamel pearls inhibits connective tissue attachment and makes management of the furcation difficult.

Q: How much attachment loss occurs for a furcation entrance to be observed in a maxillary molar?

According to Gher and Dunlap,²⁴ the mean distances from the CEJ to the mesial, facial, and distal furcation entrances are 3.6, 4.2, and 4.8 mm, respectively. Attachment loss of 6 mm is associated with a class III furcation.

According to Hermann et al,²⁵ the roots comprise the following surface areas:

Q: What is an intermediate bifurcation ridge? How can it contribute to a furcation lesion?

Everett et al²⁶ first described the ridges. He studied 328 mandibular teeth and found that 73% had an intermediate bifurcation ridge, which is cementum extending from the mesial to the distal of a furcation opening on a mandibular molar. Its existence can hamper effective plaque control by the patient and the dentist.

Cementicles are calcified masses adherent to or separated from the tooth’s root. Similar to intermediate bifurcation ridges, they compromise effective scaling and root planing by the dentist and oral hygiene by the patient.

Q: Do restored molars have a higher percentage of furcation lesions than teeth without restorations?

Wang et al²⁷ demonstrated a higher percentage of furcation involvement but no greater mobility in molars with a crown or proximal restoration when compared with nonrestored molars. Restored molars also showed a greater mean probing periodontal attachment loss than nonrestored molars, but the difference was only marginally significant.

1. Svärdström G,Wennström JL. Prevalence of furcation involvements in patients referred for periodontal treatment. J Clin Periodontol 1996;23:1093–1099.

2. Eickholz P, Kim TS. Reproducibility and validity of the assessment of clinical furcation parameters as related to different probes. J Periodontol 1998;69:328–336.

3. Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted teeth. Results after 5 years. J Clin Periodontol 1975;2:126–135.

4. Glickman I. Clinical Periodontology: The Periodontium in Health and Disease; Recognition, Diagnosis and Treatment of Periodontal Disease in the Practice of General Dentistry. Philadelphia: Saunders, 1953.

5. Tarnow D, Fletcher P. Classification of the vertical component of furcation involvement. J Periodontol 1984;55:283–284.

6. Cobb CM. Non-surgical pocket therapy: Mechanical. Ann Periodontol 1996;1:443–490.

7. Bower RC. Furcation morphology relative to periodontal treatment. Furcation entrance architecture. J Periodontol 1979;50:23–27.

8. Wylam JM, Mealey BL, Mills MP, Waldrop TC, Moskowicz DC. The clinical effectiveness of open versus closed scaling and root planing on multi-rooted teeth. J Periodontol 1993;64:1023–1028.

9. Evans GH, Yukna RA, Gardiner DL, Cambre KM. Frequency of furcation closure with regenerative periodontal therapy. J West Soc Periodontol Periodontal Abstr 1996;44(4): 101–109.

10. Bowers GM, Schallhorn RG, McClain PK, Morrison GM, Morgan R, Reynolds MA. Factors influencing the outcome of regenerative therapy in mandibular Class II furcations: Part I. J Periodontol 2003;74:1255–1268.

11. Murphy KG, Gunsolley JC. Guided tissue regeneration for the treatment of periodontal intrabony and furcation defects. A systematic review. Ann Periodontol 2003;8:266–302.

12. Hellden LB, Elliot A, Steffensen B, Steffensen JE. The prognosis of tunnel preparations in treatment of class III furcations. A follow-up study. J Periodontol 1989;60:182–187.

13. Feres M, Araujo MW, Figueiredo LC, Oppermann RV. Clinical evaluation of tunneled molars: A retrospective study. J Int Acad Periodontol 2006;8(3):96–103.

14. Araújo MG, Lindhe J. GTR treatment of degree III furcation defects following application of enamel matrix proteins. An experimental study in dogs. J Clin Periodontol 1998;25: 524–530.

15. Giannobile WV, Ryan S, Shih MS, Su DL, Kaplan PL, Chan TC. Recombinant human osteogenic protein-1 (OP-1) stimulates periodontal wound healing in class III furcation defects. J Periodontol 1998;69:129–137.

16. Pradeep AR, Pai S, Garg G, Devi P, Shetty SK. A randomized clinical trial of autologous platelet-rich plasma in the treatment of mandibular degree II furcation defects. J Clin Periodontol 2009;36:581–588.

17. Gutmann JL. Prevalence, location, and patency of accessory canals in the furcation region of permanent molars. J Periodontol 1978;49:21–26.

18. Masters DH, Hoskins SW. Projection of cervical enamel into molar furcations. J Periodontol 1964;35:49–53.

19. Swan RH, Hurt WC. Cervical enamel projections as an etiologic factor in furcation involvement. J Am Dent Assoc 1976;93:342–345.

20. Roussa E. Anatomic characteristics of the furcation and root surfaces of molar teeth and their significance in the clinical management of marginal periodontitis. Clin Anat 1998;11:177–186.

21. Lima AF, Hebling E. Cervical enamel projection related to furcation involvement. Braz Dent J 1994;5:121–127.

22. Bower RC. Furcation morphology relative to periodontal treatment. Furcation root surface anatomy. J Periodontol 1979;50:366–374.

23. Moskow BS, Canut PM. Studies on root enamel (2). Enamel pearls. A review of their morphology, localization, nomenclature, occurrence, classification, histogenesis and incidence. J Clin Periodontol 1990;17:275–281.

24. Gher MW Jr, Dunlap RW. Linear variation of the root surface area of the maxillary first molar. J Periodontol 1985;56:39–43.

25. Hermann DW, Gher ME Jr, Dunlap RM, Pelleu GB Jr.The potential attachment area of the maxillary first molar. J Periodontol 1983;54:431–434.

26. Everett FG, Jump EB, Holder TD, Williams GC. The intermediate bifurcational ridge: A study of the morphology of the bifurcation of the lower first molar. J Dent Res 1958;37:162–169.

27. Wang HL, Burgett FG, Shyr Y. The relationship between restoration and furcation involvement on molar teeth. J Periodontol 1993;64:302–305.

A risk factor is a characteristic that places an individual at increased risk of contracting a disease. A risk indicator is a probable or putative risk factor that has been identified in cross-sectional correlation studies but not confirmed through longitudinal studies.

• According to Grossi,¹ smokers are 2.7 times more likely to have periodontal disease than nonsmokers.

• Listgarten² suggested increased plaque mass or reduced host defense may precipitate episodes of periodontal destruction.

• Löe et al³ observed 480 tea plantation workers that were not exposed to preventive care for 15 years. They found that 8% of the population had rapid progression to periodontal disease, 11% had no progression, and 81% had moderate progression.

• Three times more bone loss and attachment loss has been found in patients with diabetes.

• After treatment of periodontal disease, there is a 10% drop in sugar levels.⁴

• In a study by Kornman et al,⁵ 86.0% of the severe periodontitis patients were either smokers or had the interleukin 1 genotype.

• According to Michalowicz et al,⁶ 50% of enhanced risk for periodontitis can be accounted for by genetics alone.

• Age: Increased age is associated with increased extent and severity of chronic periodontitis.

• Socioeconomic status: Those with lower socioeconomic status have less education and limited access to care.

• Race: There is a greater incidence of periodontitis in black and Hispanic populations. Blacks were found to be at much greater risk of aggressive periodontitis than whites.⁷

• Obesity: Adipose tissue can produce cytokines, which can lead to a hyperinflamed state. Gorman et al⁸ found that overall obesity and central adiposity are associated with an increased hazard of periodontal disease progression in men.

• Alcohol: Shepherd⁹ found evidence suggesting that alcohol consumption is a risk indicator for periodontitis. Longitudinal studies on the association of alcohol dependence and consumption with periodontitis are needed to confirm the association.

• Stress: Genco et al¹⁰ found that financial stress and the coping mechanism of the patient were related to periodontal disease. They found that the effects of stress on periodontal disease can be moderated by adequate coping behaviors.

• Contraceptives: There is a possible association between injectable progesterone contraceptives and poor periodontal health, as indicated by a study that found an increased likelihood of indicators of poor periodontal health, including gingivitis and periodontitis, in women who had taken or were currently taking depot medroxyprogesterone acetate (DMPA) injectable contraceptives.¹¹

An odds ratio is the probability that a person with an adverse outcome was exposed to risk. An odds ratio that is greater than 1 has a positive association.

Sensitivity is the proportion of subjects with a disease who test positive, and specificity is the proportion of subjects without the disease who test negative.

Prevalence is defined as the total number of cases (or cases of the risk factor) in the population at a given time, divided by the number of individuals in the population. Incidence is a measure of the risk of developing a new condition within a specified period of time.

The Gingival Index (Löe¹²) incorporates bleeding on probing and color change:

• 1: Mild inflammation, slight color change, slight edema, and no bleeding on probing

• 3: Severe inflammation, marked redness, edema, ulceration, and spontaneous bleeding

• 1: Mild inflammation, slight color change, and slight edema but not involving the entire marginal or papillary unit and no bleeding on probing

• 2: Mild inflammation, slight color change, and slight edema involving the entire marginal or papillary unit and no bleeding on probing

• 3: Moderate inflammation, redness, edema, glazing, bleeding on probing, and hypertrophy of the entire marginal unit

In the Periodontal Index (Russell¹³), the supporting tissues around the tooth are scored. Periodontal probing is not recommended.