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TABLE OF CONTENTS
About the Authors
Chapter 1:Problem-Based Periodontal Diagnosis and Disease Management. ...........5
Ηealth and Disease ... ....... 5
Disease Categories ... ....... 5
Diagnosis and Classification ... ... ... 5
Evidence-Based Thinking ......... .. . I
Equivalence Testing ...... 8
Superiority Testing ....... 8
Parameters of Care ... ....... I
Chapter 2: Anatomy, Ηistology, and Physiology of the Periodontium. ............ 9
Functions of the Periodontium.. ......9
Surface Characteristics of the Periodontium. ......... 9
Histology of the Periodontium .. . 10
Clinically Healthy Gingiva .... . 10
Supporting Structures Beneath the Gingiva .... ..... 11
Blood Supply ........ 12
AttachmentΑpparatus . . 13
Gingival Crevicular Fluid... ..........13
Chapter 3: Etiology and Classification of the Periodontal Diseases 15
Concepts of Etiology . . 15
Biofilms. .... . 15
Features of Periodontal Pathogens. ......... 16
Dental Calculus .... .. .......17
Risk Factors - Local and Systemic ...... .. . 18
Classification of Periodontal Diseases. ......22
1999 Classification System. .........23
Distinguishing Characteristics of Gingivitis, Periodontitis, and Other Periodontal Diseases
and Conditions...... ......29
Chapter 4: Clinical Αssessment, Diagnosis, and τreatment Pιanning . . '.. 31
Components of the Clinical Periodontal Examination .. . . 31
lnstruments and Materials for Periodontal Assessment ..... 34
Radiographic Examination. ..........34
Periodontal Screening and RecordingτΜ Examination....... . ''.'' 34
Adjunctive DiagnosticTechniques ...........35
Periodontal Treatment Planning . .. . . 36
SamplePeriodontal ΤreatmentPlans. ..'...36
Periodontal Prognosis ....... 39
chapter5: Prevention of Disease and Maintenance of Ηealth ''''.''''' 41
Toothbrushing Methods ..... 41
lnterproximal Cleaning ...... 41
Antimicrobial Agents ........ 42
Dentifrices . . ..43
Therapeutic Endpoints . .. 43
Clinical Parameters of Success .43
Maintenance of Periodontal Health. ......... 44
Components of the Maintenance Visit. ..........45
Chapter 6: Nonsurgical Treatment: Scaling and Root Planing, occlusal Therapy, and Αntibiotic
Scaling and Root Planing ......... .. 47
occlusal Τrauma ...'..' '.. ' ' 52
occlusal τherapy. . '''''52
Force Control ...... .... .. 55
Antibiotic τherapy ..... ...... 58
Suggested Systemic Αntibiotic Regimens ........... 59
Local AntibioticΤherapy. ............60
Chapter 7: Surgical Treatment: Principles .... 61
Basic Principles...... ....61
Categories of Surgery ...... ..... 61
When ls Surgery Necessary? .. .... . 61
Flap Surgery ... .... . 63
Basic Approaches .... ...... .... . 63
Types of Flaps .. .... . 63
Anatomic Landmarks ... ..... 66
Wound Closure. ..... 68
Wound Healing . .70
Chapter8: Surgical τreatment: Repair, Resection, and Regeneration .... '.'''.73
Electrosurgery ...... .74
Apically-Positioned Flap . . .,. 75
Classification of Osseous Defects ...........77
Crown Lengthening . ........ 82
Periodontal Regeneration ........... 83
Meοhanisms for Bone Grovvth ....... 83
Materials for Regenerative Therapy . ........ 87
Techniques Used in Regenerative τherapy ..... .... 88
Chapter 9: Surgical Treatment: Periodontal Plastic Surgery ..... 91
Defects Treated by Periodontal Plastic Surgery Procedures ........ 91
Aesthetic Εvaluation. .....91
Gingival Recession .. ........ 92
Alveolar Ridge Defects ...... 93
Εxcessive Gingival Display- DiagnosisandTreatment...... '''.''.94
Procedures Used in Periodontal Plastic Surgery . .. .... 94
Chapter 10: Periodontal Emergencies . . .. 1ο5
Diagnosis of Periodontal Emergencies . .. 105
Signs, Symptoms, and Treatment of Periodontal Emergencies. ... 105
Periodontal Abscess ... 106
Pericoronitis .... 106
Αcute Herpetic Gingivostomatitis ... . .. 106
Necrotizing Ulcerative Gingivitis . ....... 1O7
Differential Diagnosis of an Endodonticand Periodontal Abscess. .......107
Chapter 11: Considerations in lmplant Dentistry . . . 109
Biomechanics of Modern lmplants . . 109
Signs of a Healthy and Αiling lmρlant ...... 109
Protocol for lmplant Maintenance .......... 110
Medical Considerations in the Periodontal Patient ......... 114
Calcium Channel Blockers and Gingival Ηyperplasia ....'. 115
Dental Drug lnteractions: Update on Drug Combinations Requiring Special Considerations........ 116
Occupationsl Exposure to Bloodborne Pathogens (Universal Precautions) ......... 121
Predominant Cultivable Microorganisms of the Oral Cavity . . . .. . . . 124
Reference Values for Adults .. . . . 125
Dentifrice Products . .. ...... 128
Oral Rinse Products. .......133
Prescription Writing ......134
Safe Writing Practices. .....'136
lnsurance Coding for the Periodontal Patient .. . . .. 137
Selected Readings - General .......141
Selected Readings - Specific .......142
ABoUτ τHE AUτHoRs
ABOUT THE AUTHORS
FRANCIS G. SERIO, DMD, MS
Dr. Francis G. Serio is Professor and Chairman of the Department of Periodontics at the University of Mississippi
School of Dentistry. He is a Diplomate of the Αmerican Board of PeriodontoΙogy. He received his B.A. from The
Johns Ηopkins University, D.M.D. from the University of Pennsylvania, and M.S. and Certifiοate in Periodontics from
the University of Maryland. Dr. Serio has been involved in education, research, and international volunteer activities
since 1981 . He has published 30 articles, 3 books, several book chapters, and numerous abstracts. He has lectured
throughout the United States and in six other countries on various aspects of Periodontics.
Dr. Serio is the founder of the Dominican Dental Mission Project, a volunteer program that provides dental care to
the rural poor in the Dominican Republic. ln 1991 , the project received the President's Volunteer Action Award from
President George H.W. Bush, and was named one of the Points of Light in 2001 by President George W. Bush. ln
addition to his academic responsibilities, Dr. Serio maintains a private practice limited to Periodontics and lmplant
CHARLES E. HAνVLΕY, DDs, PhD
Dr. Hawley was Professor in the Department of Periodontics, Dental School, University of Maryland from 1982-
2001. During that time period, Dr. Haw|ey directed, at one time or another, every eduοational program the
department offered to predoctoral and postdoctoral students. He was Director of the Αdvanced Dental Education
Program in Periodontics from 1996-2001. He is Professor Emeritus in the Department of Periodontiοs at Maryland
and also Visiting Professor, Department of Periodontology, Tufts University. Dr. Hawley is a consultant in periodon-
tics to the Commission on Dental Accreditation of the Αmerican Dental Association. He has published over 70
manuscripts, abstracts, and book chapters.
From 1962-1982, Dr. Hawley νvas a career dental officer in the U.S. Army Dental Corps. Dr. Hawley Λ,as the first
Director of the U.S. Army Residency Program in Periodontics at Ft. Gordon, GA. He retired from the Army at the
rank of Colonel, and at that time, Dr. Hawley was awarded the Legion of Merit.
Dr. Hawley received a Bachelors degree from The Johns Hopkins University, a DDS from the University of
Pennsylvania, a Certificate in Periodontics and a Masters degree in Histology from the University of lllinois, and a
PhD in Microbiology and lmmunology from the University of Maryland. He is a Diplomate of the American Board of
Periodontology. During his professional life, Dr. Ηawley was elected to the lnternational College of Dentists, the
American College of Dentists, and the Pierre Fauchard Αcademy.
students, and dental hygiene students. Both basic and clinical science topics.are arranged in a tabular form to
allow for easy access to each chapιer.
Each chapter is presented in a "Question & Answer'' format, providing a stepwise approach to thal particular area.
This book has been written in a straighforward manner, making it a practical resource both in clinical practice and in
an educational setting. Chapters are arranged by basic principles, disease entities, diagnosis, treatment planning,
and then various treatment options.
The authors intend that this book be a quick and easy reference to many of the clinical problems that challenge all
practitioners and students of periodontics.
CHAPτEB 1 -
CHAPTER 1: PROBLEM-BASED PERIODONTAL
DIAGNOSIS AND DISEASE MANAGEMENT
The framework of effective periodontal therapy includes a
working diagnosis and classifiοation of disease, the identifi-
cation of pertinent etiologic factors, and a treatment plan that
addresses eaοh of the etiologic agents in a logical sequence.
Τo ignore pertinent etiologic factors in the treatment plan will
translate to undertreatment and failure in therapy. Treaι
ment of etiologic factors that either do not exist, or that have
been incorrect|y identified, wiΙl produce overtreatment and
unnecessary financial or physical hardships for the patient.
Problem-based periodontal therapy begins wiih an under-
standing ot health and knowing what it means to diagnose
and classify a disease.
What ls Health? Mhat ls a Normal Periodontium?
What ls Meant by the Term "Disease"?
Health is the absence of disease or abnormality. Periodontal
health then is defined by the absence of marginal periodontal
inflammation, the absence of inflammation in the periodontal
ligament, or evidence of periodontal deformities. Success-
fully treated and maintained gingivitis patients may be both
free of disease and have a normal periodontium.
Periodontitis patients who have received successful perio-
dontal and maintenance therapy (ie, patients who are appar-
ently free of periodontal inflammation with no ongoing injury
in the periodontal ligament) may, by definition, be considered
healthy as well. However, these patients may not have a
DiSeaSe is defined aS a ρrocess that is οharacterized by a
series of morbid pathobiologic events that produce cliniοal
signs and symptoms in the affected host. The process
ocοurs in response to known or unknown etioΙogic factors.
What Are the Fundamental Periodontal Disease
Categories? Do These Periodontal Diseases
Conform to the Definition of Disease?
The basiο categories of periodontal diseases are:
. Gingivitis. The gingival diseases are periodontal
diseases in which the process is gingival inflammation,
the primary etiologic factors may be microbiologic,
systemic diseases, or physical injury, and the signs and
symptoms are gingival bleeding, increases in probing
depths, and pain. Loss of periodontal attachment, tooth
mobility and/or fremitus of teeth, and tooth migration,are
not ordinary features of gingivitis. As it is with all inflam-
matory diseases, the pattern and severity of gingival
inflammation in a given patient is affected qualitatively
and quantitatively by local and/or systemic contributing
. Periodontitis. The types of periodontitis are periodontal
diseases in which the process is periodontal inflamma-
tion, the primary etiologic factor may be microbiologiο,
systemic diseases, or physical injury, and the signs and
symptoms are gingival bleeding, increases in periodontal
probing depths, destruction of periodontal attachment,
pain, and tooth loss. Mobility and/or fremitus and migra-
tion of teeth are consequences of forces on teeth with
reduced/lost periodontal attachment (see occlusal trau-
matism below). The pattern and severity of periodontal
inflammation in a given patient is affected qualitatively
and quantitatively by local and systemic contributing
. Occlusal traumatism. Occlusal traumatism is a perio-
dontal disease in which the process is inflammation
ιΛ/ithin the periodontal Ιigament and the alveolar bone
(the lesion of trauma from occlusion), the primary etio-
logic factor is force acting on teeth, and the signs and
symptoms are pain, tooth mobility and/or fremitus, and
pathologic migration of teeth. The pattern and severity of
the lesion of trauma from occlusion in a given patient is
affected quantitativeΙy and qualitatively by local and
systemic contributing factors.
Each one of these categories conforms to the definition of
disease. ln each disease, there is a process, there is a series
of morbid pathobiologic events that are outcomes of the
process, and there is a reΙated set of clinica| signs and symp-
What ls Meant by the Expressions "Diagnosis"
F|GURE 1. Photomicrograph of the ρrocess of inflammation in the marginal
periodontium. τhe morbid outcome of the process is histologically repre-
sented as evidence of resorbed alveolar bone and the level of attachment
Diagnosis is the aιt of identifying the disease process. lt is
the product of a careful evaluation of the patient's history, the
array of symptoms presented by the patient, and the clinical
signs revealed during a clinical examination. For instance,
the diagnosis of periodontitis is ordinarily achieved by
detecting gingival bleeding with a periodontal probe, destruο-
tion of periodontal attachment using radiographs and/or a
probe, mobility and/or fremitus digitally, determining any
pathologic migration and/or loss of teeth. Figure 1 represents
histologically the process of marginal periodontal inflamma-
tion and the morbid outcomes (ie, loss of both alveolar bone
and periodontal attachment) of periodontitis.
PRoBLEM-BASED PERloDoNτAL D|AGNoSΙs AND D|SEASE MANAGEMENτ
CΙassification is the art of categorizing individual clinical
cases of disease according to treatment requirements. Clas-
sification systems are frequently used by third pafty prov-
iders to help understand treatment needs. For over 20 years,
dentists have been using a classification system developed
by the Αmerican Αcademy of Periodontology (AΑP) to facili-
tate dialogue among dentists and between third party individ-
uals concerning the severity of periodontal diseases, and by
direct extension, treatment needs. This classification system
. Type l. Gingivitis where gingival inflammation νas
present without radiographic evidence of intΘrproΧimaΙ
FIGURE 2. An artistic represenιation ot gingivitis" There is gingival erythema
and edema. τhe clinical attachment levels are at the cementoenamel
iunction. The alveolar bone height wilh respect to the cementoenamel
iunction is normal. Restoraιion of a healthy periodontium without further
loss of attachment may be predictably achieved with nonsurgical
therapy. (Couftesy of Kala Addess, MS, RDH)
. Type ll. Early periodontitis where gingival inflammation
was superimposed over clinical evidence of mild bone
loss without furοation invasions.
FIGURE 3. An artistic representation of earιy periodon lfis. τherΘ is gingival
erythema and edema. τhere is early loss of clinical attachment and
reduclion of alveolar bone height. Furοation invasions wilι probably not
be clinically or radiographically apparent. Periodontal health and func-
tion may usually be restored by nonsurgical and/or surgicaΙ therapy.
(cour1esy of Kala AddeSS' ΜS' RDH)
. Type lll. Moderate periodontitis where gingival inflam-
mation was superimposed over clinical evidence of
moderate bone loss with early furcation invasions and
possible tooth mobility.
FiGURΕ 4. An artistic representation ot moderate periodontitis. τhere is
gingival erythema and edema. τhere is moderate lοss of clinical atιach-
ment and reduction of alveolar bone height. Furcation invasions are
evident both cιinicaΙly and radiographically. Affected teeth may show
degrees of mobility. Shaded area on the adiacent tooth indicates that
regeneration ot Ιost periodontal tissues may be one outcome of
successful periodontal theraρΥ. (courtesy of Karla AddeSS' Ms' RDH)
. Type lV. Αdvanced periodontitis where gingival inflam-
mation was superimposed over severe bone loss with
extensive furcation invasions and tooth mobility. Cases
of this type could display tooth loss due to periodontitis,
pathologic migration of teeth, posterior bite collapse,
and/or loss of occluding vertiοal dimension.
FΙGUBE 5. An artistic representation oΙ advanced periodontitis. τhere is
gingival erythema and edema. τhere is advanced loss of clinical attach-
ment and alveolar bone height. Furcaliοn invasions are θxtensive. τooth
mobilily and/or pathologic migration may be seen. τeeth with advanced
periodontitis frequently have a poor prognosis, and decisions abοut
therapy often include the placement of implants. (Couιlesy of Κarla
Addess, MS, RDH)
While the terms that defined each type were intentionally
vague, the system did provide the framework for dialogue
among therapists, allied personnel, and third party payers
over treatment needs for each case. For instance, a treat-
ment plan for a Τype lll moderate periodontitis case
dispΙaying the osseous defects and furcation invasions
shown in Figure 6 would be expected to include resective
and/or regenerative surgical therapy. Τhe treatment plan for
a Type ll early periodontitis οase, such as that shown in
Figure 7, would probably not include resective or regenera-
FIGURE 6. A dried human mandible showing periodontaΙ osseous defects and
furcation invasions that are οonsistent with a type lll moderate periodon-
FIGURE 7. A dried human mandible showing minor periodontal osseous
deformities that are consistent with a type ll early periodontitis case.
As the knowledge base about the patterns of periodontal
diseases improved, this system of classification became
inadequate. Models of periodontitis had emerged sug-
gesting that not all cases of periodontitis behaved the
same clinically, that small (<1 mm) changes in attachment
level were difficult to detect clinically, and that there was
evidence that all cases of periodontitis did not respond the
same to therapy.
An attempt to overcome many of these shortcomings
occurred during the 1999 lnternational Workshop for a Clas-
sification of Periodontal Diseases and Conditions. Here,
scientists and clinicians agreed upon a reclassification
system to improve the understanding of periodontal diseases
among scientists, clinicians, and allied dental healthcare
agencies. Each new or revised category of disease was
based, in part, upon its etiology and the particular healthcare
requirements to control etiology.
The new System includes eight major οategories of perio-
dontal diseases or conditions, and each of the categories is
subdivided into specific etiology-based diseases or condi-
tions. This new Classification System for Periodontal
Diseases and Conditions was adopted by the AAP in 2000.
Τo facilitate its use in every-day periodontiοs, the new
system would be modified over time.
How Are Scientifically-Based Decisions Made in
Successful Periodontics? What ls Meant by the
Expression "Art of Decision-Making in
Successful periodontal therapy is based upon scientifically-
based decisions involving: the disease process, the identifi-
cation of aΙl etiologic factors, a correct diagnosis, controlling
the etiologic factors, and correcting deformities produced by
The arl of decision-making in periodontal therapy involves
the synthesis of:
1. Clinical experience of the therapist
2. Τechnical ability of the therapist
4. Experiences of others (type lll information) as
reported and presented at professional forums
5. Evidence-based thinking
F|GURE 8. οlinical decision_making in periodontics can be multifaceted.
Evidence-based thinking b.ings the outcomes of sοientificalιy sound
cΙinicaΙ trials into the process.
While the traditional components of a deοision process
remain impoftant ingredients (ie, a clinician will not ordinarily
make a treatment decision that will involve a technique that
is beyond the scope of his/her abilities), the fact remains that
the knowledge base in a|l aspects of periodontiοs is rapidly
expanding. lt is incumbent that clinicians keep current with
new science and technology, evaluate reports in the litera-
ture criticalΙy, and utilize new information in their practices
PRoBLEM-BASED PERloDoNτAL DlAGNosls AND DlsEAsE MANAGEMENτ
What ls Meant by the Expressions "Evidence-
Based Thinking", "Equivalence Testing", and
Εvidence-based thinking occurs when the therapist logically
and systematically utilizes scientifically-based clinical
evidence in the process of making decisions about diag-
nosis, prognosis, and treatment.
Εquivalence testing in c|inical trials may show that a method
is at least as effective as a commonly employed "gold stan-
dard". Superiority testing may show that a given method will
produce outcomes that will be more beneficial than another
to a patient.
lf there is evidence that a technique or concept of therapy is
predictably equivalent or superior in a given clinical scenario,
then, within the scope of experience and ability, it should be
considered as a treatment option. ln doing so, the number of
options available to the patient are increased, and the poten-
tial for placebo effects, personal biases, or clinical experi-
ences of the therapist that have no controls are kept to a
The fallout of evidence-based thinking in clinical periodontics
will inevitably be an increased number of treatment options,
increased patient confidence, practice groλ/th, and improved
What Are the Parameters of Care?
The AAP took a leadership role in developing diagnostic and
therapeutic guidelines for what might be considered the stan-
dard of care for periodontal patients. The resulting Parame-
ters of Care describe the scope of possible active treatment
plans for the following clinical situations:
ο Plaque-associated gingivitis
o Chronic periodontitis with slight to moderate loss of peri-
o Chronic periodontitis with advanced loss of periodontal
. Refractory periodontitis
ο Acute periodontal diseases
. Αggressive periodontitis
. Placement and management of the dental implant
. Occlusal traumatism in patients with chronic periodontitis
o Periodontitis associated with systemic conditions
. Systemic conditions affected by periodontal diseases
o Periodontal maintenance
The emphasis of the current parameters is treatment and
what therapeutic entities might be appropriate for given peri-
odontal conditions. Each parameter is inclusive so as to give
the reader (clinician, patient, third party healthcare provider,
etc) an appreciation of the scope of acceptable care in each
category. The parameters do not prescribe the care that
every periodontal patient in a given category should receive.
The final decision over what will constitute a treatment plan
in a given case remains, as it should be, in the hands of the
clinician and the patient.
Definitions of terms and details of each of these parameters
of care may be obtained at the web site of the American
Αcademy of Periodontology, www.perio.org.
CHAPTER 2: ANATOMY, HISTOLOGY, AND PHYSIOLOGY OF THE
Α οlear understanding of the structure and function of the
periodontium is necessary in order to appreciate the disease
process and treatment. The periodontium consists primarily
of noncalcified and οalcified connective tissues covered by a
protective layer of epithelium. lt is the destruction of the
calοified conneοtive tissues due to the host response to the
exogenous and endogenous periodontal pathogens that
gives rise to a ιoss of periodontal Support and eventua| tooth
What Are the Functions of the Periodontium?
. Attach the tooth to the alveolar bone proper
. Resist and dissipate the forces generated by mastica-
tion, speech, and deglutition
. Αdjust to οhanges in functional demands through contin-
uous remodeling, regeneration, and repair
o Defend against the external pathogenic and environ-
mental influences present in the oral cavity
What Are the Surface Characteristics /
Landmarks of the Periodontium?
FlGURE 1Α. surface characteristics and Landmarks of the Periodontium.
Free gingivat margin: This is the most coronal edge of
Free gingival groove: A groove seen on the facial
gingiva that approximates the location of the base of the
sulcus. The free gingivaΙ groove is not always present
(estimated in only 30% to 40"λ ot adults), nor is it an
exact landmark for the base of the sulcus.
Keratinized tissue: The surface of the tissue that
comprises the free and attached gingiva. Τhe boundaries
are from the free gingivaΙ margin to the mucogingival
iunction on the facial and lingual surfaces. The
keratinized tissue is continuous with the rest of the
mastiοatory mucosa of the palate. The keratin is found in
the stratum corneum of the epithelium and may be
parakeratin (cell nucΙei remaining) or orthokeratin (thick
layer of keratin without remaining cell nuclei). The
epithelium covering is also referred to as the oral
Free gingiva: The gingiva from the free gingival margin
to the base of the sulοus' This tissue is continuous with
the attached gingiva but is not bound down to any
Attached gingiva: Gingiva that is firmly bound down to
underlying tooth structure, periosteum, and bone. Τhe
boundaries of the attached gingiva are from the base of
the sulcus to the mucogingival junction. The width of
facial attached gingiva ranges from 1-9 mm and is
greatest on the facial surface of the maxillary lateral
incisor and narrowest on the facial surfaces of the
mandibular canine and first premolar. On the lingual,
attached gingiva was widest near the first and second
molars and narrowest adjacent to the incisors and
canines. The thickness of attached gingiva averages
1.25 mm + O.42 mm.
Mucogingival junction: The demarcation between the
attached gingiva and the alveolar mucosa apical to the
attached gingiva. The mucogingival junction often
appears as a distinct line between the two structures. lf
the mucogingival junction is difficult to see, it may be
identified as the fold area when the alveolar mucosa is
gently pushed in a coronal direction.
Alveolar mucosa: Part of the lining muοosa. The
a|veolar muοosa is located apical to the attached gingiva
on the facial and lingual surfaces. This tissue is loosely
attached to the underlying bone, freely moveable, and
relatively fragile compared to the gingiva. There are
more elastic fibers in the alveolar mucosa. This tissue
extends into the vestibule of the mouth and is continuous
with the labial, buccal, and lingual mucosa. There is no
alveolar muοosa on the hard palate'
Masticatory mucosa: Keratinized tissue including the
gingiva and the tissue covering the hard palate.
Frenum (frenulum): The narrow band of tissue that
attaches the labial and buccal mucosa to the alveolar
mucosa. There is also a lingual frenum that attaches the
anterior part of the tongue to the lingual aspect of the
alveolar process and the floor of the mouth in the anterior
B. Surface Characteristics and Landmarks of the Periodontium.
ANAToMY, ΗtsτoLoGY, AND PHYsloLoGY oF τHE PERloDoNτlUM
. Rugae: The irregular ridges found on the anterior part of
the hard palate adjacent to the incisors, canines, and first
. Stippling: The irregular surface texture of the attached
gingiva, similar to the surface of an orange peel, found in
40% ot adults. Stippling occurs at the intersection of
epitheΙial ridges that causes the depression and the
interspersing of connective tissue papillae between
these intersections giving rise to the small bumps.
. Sulcus: This is the space bounded by the free gingival
margin, the tooth, and the most coronaΙ attachment of
the junοtional epithelium. ln health, the sulcus usually
measures from 1-3 mm deep. ln disease, this space is
referred to as a pocket.
. Col: This is the saddle-like depression in the interdental
gingiva as seen from buccal to lingual apical to the
contact of two adlacent posterior teeth.
What Are the Layers of Cetls That Comprise the
Oral Epithelium? What Are a Keratinocyte,
Langerhans Cell, and a Melanocyte?
The oral epithelium consists of four layers of cells:
1. Stratum basale: Basal layer of cuboidal cells along the
basement membrane. This is where epithelial οell rep|i-
cation occurs. Melanocytes are found in this layer.
2. Stratum spinosum: These cells appear to have cyto-
plasmic spines when viewed by Ιight microscopy.
Langerhans cells, involved in the processing of antigens,
are found in this layer. Keratin synthesis begins in the
3. Stratum granulosum: Keratohyalin granules may be
seen in this layer. Keratin synthesis is ongoing. Cells
appear to be fΙattened.
4. Stratum corneum: This is the layer where para- or
orthokeratinization are found.
Keratinocyte: A cell of the epidermis and parts of the
mouth that produce keratin. Because of their ability to
produce keratins, epithelial cells are referred to as kerati-
nocytes. Keratins are a family of approximately 30
proteins that form the intermediate filaments of the
epithelial cell cytoskeleton. Keratins may be found eΧtra-
celluΙarly in the stratum corneum and contribute to the
protective function of epithelium.
Langerhans cell: A dendritic cell in the epidermis.These
cells are found in the suprabasal layers of the epithelium,
Τhey do not have desmosomal attachments to adja-
cent cells. Τhey move in and out of the epithelium, are
derived from bone marro,v, and probablyhave an immu-
nologic function for recognizing and processing antigens.
. Melanocyte: Α celΙ of the basal layer that produces
melanin pigment granules (melanosomes) that are trans-
ferred to surrounding keratinoοytes for transpoι1' There
are similar numbers of melanocytes in the epithelium re-
gardless of the skin or gingival pigmentation present.
What Does Clinically-Healthy Gingiva Look Like?
FlGURE 2. characteristics of the Heaιthy Pefiodontium. τhe hea,thy periodon-
tium is genefally coral pink, possibly with natural pigmentation. τhe
gingival margins are scalloped to a fine edge. τhe tissue is firm, usually
with a stippled surface.
Color: The normal οolor of gingiva is often described as
coral pink. Gingiva may also have slight to significant
brown pigmentation from the melanoοytes located in the
basal layer of the epithelium.
Size: Gingival contours generally follow the cemento-
enamel junctions of the teeth. Tissue thickness is in the
0.25-0.5 mm range. Α wider zone of gingiva is normally
seen in the maxillary anterior region, with the narrowest
zone of gingiva on the buccal surface of the mandibular
first premolars. On the lingual, it is narrowest in the
mandibular region and widest in the molar area.
Contour: Gingiva has been described as being either
thin and scalloped, or thick and flatter in contour. The
contour of the gingiva depends on the οontour of the
cementoenamel junction of the teeth, the amount of em-
brasure space, and the nature of the contact between
teeth. The gingiva appears prominent over the tooth root
and may have a slightly concave appearance in the inter-
Consistency: Gingiva is generally firm to the touch and
attached to the underlying bone and/or tooth.
Surface texture: Gingiva may have either a smooth or
stippled surface. Stippling is not an indicator of health nor
is the absence of stippling an indiοator of disease. The
reappearance of stippling during therapy may be an indi-
cation of tissue returning to health.
What Supporting Structures Lie Beneath the
F|GURE 3A. τhe supporting structures Beneath the Tissue surface. side
view, A. oral epithelium, B. suιcular epithelium, c. Junctional epithelium,
D. Dentogingivaι fibers, E. circular fibers, F. Dentoalveolar fibers' G.
Acellular cementum, H. Alveolar crestal fibers of the PDL, ι. cellular
cementum, J. Horizontal fibers of the PDL, κ. Alveolar bone, L. oblique
fibers of the PDL.
FIGURE 38. lnterproximal view. A. Dentogingival fibers, B. Circular fibers, C"
τransseptal fibers, D. Alveolar crestal fibers of the PDL, E. Horizontal
fibers of the PDL, F. Oblique fibers of the PDL, G. Apical fibers of the
PDL' Η. Alveolar bone, lnterradicular fibers not shown.
. Sulcular epithelium: The epithelium that lines the
sulοus. ln health, sulcular epithelium does not have
epithelial ridge formation.
o Junctional epithelium: The epithelium that attaches the
gingiva to the surface of the tooth, or to compatible
restorative materials' Τhe special part of the junctional
epithelium that actually provides the attachment is called
the epithelial attachment. τhis attachment consists of a
lamina lucida, lamina densa, and hemidesmosomes.
Connective tissue: The predominantly collagenous
tissue found beneath the epitheΙium. The connective
tissue contains collagen fibers (60%), fibroblasts (5%),
and interfibrillar substanοe οomposed of noncollagenous
proteins and mucopolysaccharides, small numbers of
neutrophils and lymphocytes, blood vessels, lymphatics,
and nerves (the remaining 35%). Τhe overlying epithe-
lium must have intact connective tissue in order to
survive. Most of the coΙlagen found in the periodontium is
type I collagen.
Gingival fibers: These are specially oriented fibers in
the connective tissue. Also known as Ιhe supracrestal
connective tissue fibers, these fibers are designated by
their orientation: Dentogingival, dentoperiosteal, circular,
and transseptal (connecting tνvo adjacent teeth) fibers.
Some authors inοlude the transseptal fibers in the prin-
cipaΙ fibers of the periodontal ligament, although they are
actually tooth-to-tooth and not tooth-to-bone fibΘrs.
Periodontal ligament (PDL): This is the collagenous
tissue that surrounds the tooth root and attaches the
tooth to the alveolar bone proper. The principal fibers of
the periodontal ligament have been cΙassified as the
alveolar crest, horizontal, oblique, apical, and interradic-
ular (in the furcation area of multirooted teeth) fibers. Τhe
oblique fibers are the most numerous. Fibroblasts, osteo-
blasts, cementoblasts, osteoclasts, epithelium, and
nerve celΙs are also found in the periodontal ligament
space. The width of the PDL space is about 0.25 mm in
normal function. Α tooth in hypofunction may have a
narror/er PDL space and a tooth in hyperfunction may
have a considerably wider PDL space.
FlGURE 4. τhe Attachment Apparatus. From the left: Dentin, cementum, perio-
dontal ligament fibers, alveolar bone.
. AIveolar bone: Αlso known as Ιhe alveolar process, this
is the portion of the maxilla and mandibΙe that form and
support the tooth sockets. The alveolar process gives
Support to the alveoΙi and consists of coιtical bone,
cancellous trabeοulae, and the alveo|ar bone proper.
ANAToMY. HlsτoLoGY. AND PHYsloLoGY oF τHE PERloDoNTlυM
F|GURE 5A. The Alveolar Bone. τhis section shows the relationship of the
roots of this molar to the alveolar bone proper and the rest of ιhe alveolar
FlGURE 58. τhe Alveolar Bone. ln cross section, corticaι bone can be seen on
the surface of this mandible with trabecular bone within the confines of
the iawbone. τhe density of the trabeculaιions can vary markedly from
one area of the iaw to another and among individuaΙs.
. Alveolar bone proper: That part of the alveolar bone
that lines the tooth socket. lt is a perforated cribiform
plate through which vessels and nerves pass between
the PDL and marrow.
. Basal bone: That part of the maxilla and mandible that
supports the alveolar process. Basal bone is all that
remains once all of the alveolar process is resorbed after
the teeth are lost from the arch.
. Cementum: The thin, calcif ied tissue of ectomesen-
chymal origin covering the roots of teeth in which
embedded collagen fibers attach the teeth to the alveo-
lus. There are tivo types of cementum: Αcellular and
cellular cementum. Acellular cementum does not con-
tain cementocytes and is found on the οoronal half of the
the tooth rooΙ. Cellular cΘmentum contains cementocytes
and is found primarily on the apical third of the root. lt is
continuously deposited throughout life.
What ls the Blood Supply to the Periodontium?
FlGURΕ 6Α. Local Blood supply to the Periodontium. supraperiosteal blood
vessels and PDL vessels coalesce into the gingival plexus.
F|GURΕ 68. Loοal Blood supply to the Periodontium. lnterseptal vessels
supply the alveolar bone, PDL, and gingiva.
The blood supply to the periodontium arises from the
terminal branches of the internal maxillary aftery. Locally, the
blood supply to the gingiva consists of supraperiosteal
vessels. Vessels from the alveolar bone and periodontal liga-
ment also contribute to the coalescence of vessels in the
gingival papillae, known as Ιhe gingivaΙ plexus. The alveolar
bone is supplied by branches of the anterior, middle, and
posterior superior arteries to the maxilla and branches of the
inferior alveolar artery in the mandible. lntra-alveolar or inteμ
dental vessels supply the interdental bone. Arterial blood
generally flows in an apical-to-coronal direction. Large
numbers of capillary loops that resemble renal glomeruli are
found beneath the iunctional epithelium and sulcular epithe-
lium near the surface of the gingiva.
What ls the Innervation of the Periodontium?
Nerve supply to the periodontium is derived from terminal
branches of the maxillary and mandibular branches of the
trigeminal nerve. The periodontium contains sensory recep-
tors for pain, touch, and pressure as well as proprioceptors in
the periodontal ligament but not in the gingiva. The sensory
nerves have their center in the semilunar ganglion and the
proprioceptive nerves are centered in the mesencephaliο
What ls the BioIogic ι,vidth?
FtGURE 7. Biologic νlridth. Junctional epithelium and supracrestal connective
tissue fibers (dentogingival, dentoalveolar, circular, transseptal) must be
maintained in health.
The biologic width is the apicocoronal distance that the junc-
tional epithelium and supracrestal connective tissue
(gingival) fibers are attached to the tooth. This distance is
measured histologically from the most coronal part of the
junctional epithelium (base of the sulcus) to the crest of the
alveolar bone. The average measurement of the biologic
width is 2.04 mm, approximately 1 mm for the junctional
epithelium and 1 mm for the supracrestal connective tissue
fibers. The sulcus depth is nof part of the biologic width.
ΨVhy Is the BioIogic Vvidth lmportant?
The body maintains the biologic width as a stable dimension.
When the biologic width is encroached upon and iniured by
extension of restorative preparations and materials into this
area, uncontrolled inflammation may result as the body tries
to reestablish this dimension. ln areas of thin gingiva, this
may result in recession or bleeding upon gentle probing even
when the patient has good plaque control and recession.
What ls the Attachment Apparatus?
The attachment apparatus is the alveolar bone proper, perio-
dontal ligament fibers, and cementum that attach the root to
the alveolar bone. Regeneration of the attachment apparatus
is one of the surgical goals in periodontal therapy. Regenera-
tion of the attachment apparatus is the only treatment proce-
dure in dentistry where new tissue is histologically identical
to that which has been lost due to the disease process.
ΨVhat ls Gingival Crevicular Fluid?
ln health, gingival crevicular fluid (GCF) is a transudate that
emerges from the gingival sulcus. The gingival crevicular
fluid may contain a variety of enzymes and cells, particularly
desquamating epithelium and neutrophils, that are being
shed through the sulcus. An increase in gingival crevicular
fluid flow is the first detectable sign of inflammation. Once
inflammation has ocοurred, the GCF is referred to aS an
inflammatory exudate. This exudate contains higher levels of
serum proteins and leukocytes.
CHAPTER 3: ETIOLOGY AND CLASSIFICATION OF THE
The etiology of the periodontal diseases is multifactorial, but
bacterial plaque is necessary for the initiation and progres-
sion of infΙammatory periodontal disease. Αs indicated by the
neνι Ctassification System for Periodontal Diseases and
Conditions, etiologic faοtors have become the framework for
periodontal diagnosis and classification
What ls lnflammation?
lnflammation is a soft tissue cellular and vascular response to
local iniury of physical, thermal, chemical, or microbial origin.
lnflammatory periodontal diseases are no exception to this
paradigm as local periodontal etiologic factors may be phys-
ical (factitial habits such as toothbrush abrasion or occlusal
trauma), thermal, chemical (epithelial disorders associated
With some mouthivashes, smokeless tobaοco, aspirin, and
coοaine), and microbial (dental plaque induced gingival
diseases). The most common inflammatory periodontal
diseases are caused by a locaΙ accumulation of baοteria.
What ls Meant by EtiologY?
ΕtioΙogy is "the study or theory of the causation of any
disease; the sum of knowledge regarding causes." Therefore,
etiology is a noun that defines the science of disease causa-
tion, but in common usage, etiology is a cluster of faοtors that
contribute to disease (ie, the etiology of periodontal
What Are the Microbiologiο Etiologic Factors in
Τhe microbiologic etiologic factor in periodontal diseases is
dental plaque with dental calculus as probably the most
significant local contributing factor. Food debris and the
bacteria it contains is probably a major etiologic factor in root
F|GURE 1. A photomicrograph showing severe marginaΙ inllammation and
local etiologic factors of bacteriaι origin.
There is littΙe dispute over the concept that bacteria are the
primary etiologic factors in inflammatory periodontal
diseases. ln 1965, Loe and co-workers published their classic
work that demonstrated that gingival health could be reliably
achieved with immaculate oral hygiene and that gingival
inflammation could be caused by the aοcumulation of plaque
on the teeth. Light microscopiο examination of tooth scrap-
ings revealed that plaque ivas an adherent mat of bacteria,
epithelial cells, and leukocytes encased in an amorphous
protein and polysaccharide matrix, and that cocci, filamen-
tous bacteria, spirochetes, and vibrios accumulated on teeth
in an ordered sequence. The knowledge produced in this and
later studies of plaque morphology and microbiology
emphasied that plaque was a heterogeneous community of
bacteria (see Figure 2).
Generally speaking, bacteria assoοiated with periodontal
health are characterized as Gram-positive, nonmotile faculta-
tive anaerobes. Bacteria assoοiated with disease are gener-
ally Gram-negative, motile, Strictly anaerobiο speοies. Τhe
cell wall of Gram-negative bacteria consists of a lipopolysac-
charide base, aΙso known as endotoxin, that has significant
pathogenic potential. νγhile over 350 distinct speοies of
bacteria have been isolated from the oral cavity, relatively
few are associated with gingival or periodontal inflammation.
The list of strongly associated pathogenic bacteria includes:
ο Actinobacillus actinomycetemcomitans
o Prevotella intermedia/nigresens
What ls Meant by the Term "Biofilm"?
FIGURE 2. A thin section eleclron photomicrograph of supragingival plaque
(biofilm) showing a heterogeneous popu|ation of resident bacteriaΙ
morphοtypes and bacterial debris. τhe interbacterial matrix permits the
exchange of nutrients between microorganisms.
ET|oLoGY AND cLASslFlcATloN oF τΗE PERloDoΝτAL DlsEAsEs
Biofilms form on inert surfaces where bacteria to bacteria
cohesive interactions or bacteria to surface adhesive interac-
tions are allowed to occur. Biofilms are heterogeneous
composites of bacterial communities within a nonbaοterial
protein, polysaccharide, and glycoprotein matrix of bacterial
and salivary origin. The matrix allows for a "circulation" of
nutrients and baοterial metabolites betνveen communities and
the environment outside the biofilm. τhere are extreme varia-
tions in oxygen levels ranging from highly aerobic areas
within fluid channels to almost completely anaerobic areas in
What ls the "Nonspecific Plaque Hypothesis"?
The basic tenets of the nonspecific plaque hypothesis state
that inflammatory periodontal diseases (and possibly caries)
are caused by composite effect of bacterial colonization and
maturation on the surfaces of teeth, not by specific bacteria
themselves. Gingival disease is the outcome from release of
bacterial metabolites (such as butyrate or other short chain
fatty acids) and immunogenic bacteriaΙ antigen components,
such as lipopolysaοcharide (endotoxin) from Gram-negative
cell walls during plaque growth. lnflammatory disease is the
outcome of a microbial mass that is in excess of the local
defense mechanisms of the host.
What ls the "Specific PIaque Hypothesis"?
The specific plaque hypothesis states that periodontitis is an
infection caused by a limited number of periodontal microor-
ganisms, and that these microorganisms characterize the
plaque biofilms associated with periodontitis but not gingivitis
or gingival health. lt appears that of the 300+ identifiable
species found in the oral cavity, only a small proportion (10-
12 species) are actually found in active periodontitis sites.
The bacteria believed to be pathogens in periodontitis do not
conform to the classic dogma for microbial pathogenicity (ie,
Koch's Postulates). The current understanding of mixed
infections, bacterial invasion, virulence factors, conducive
bacteria habitats, the role of so-called "beneficial species",
and the susceptibility of the host have rendered Koch's
Postulates obsolete when it comes to periodontitis.
What ls Meant by "Putative Periodontal
The criteria for implicating oral microorganisms as perio-
dontaΙ pathogens are:
1. The microorganism must be associated in high numbers
in active periodontitis lesions and either absent (not culti-
vable) or in low numbers in gingivitis or healthy sites. The
numbers of the microorganism should have increased to
a threshold level before the onset of disease.
2' Ιhe elimination of the microorganism, or its numerical
reduction below threshold levels, should parallel remis-
sion of active disease.
3. There should be a specific host immune response
against the organism (ie, elevated serum, salivary, and
crevicular fluid antibody titers).
4. The microorganism should evoke virulence factors that
contribute to its pathogenicity or explain disease pathobi-
5. The microorganism should produce periodontitis in
animal model systems.
What Features Do Most Periodontal Pathogens
Have in Common? What Are the Exceptions to
This smalΙ group of putative periodontal pathogens possesses
certain features in common. Most of them have a Gram-
negative cell wall. The outer membrane of the Gram-negative
cell wall contain lipopolysaccharide (LPS) Λ/hich has endo-
toΧin activity (see Figure 3). Typically, LPS οontaining Gram-
negative cell waΙl extracts are capable of promoting bone
resorption, inhibiting osteogenesis, οhemotaxis of neutrophils,
and other events associated with active periodontitis. Some
pathogens release a LPS that suppresses the innate immune
response. Many periodontal pathogens are strict or faculta-
tive anaerobes and are asaccharolytic, permitting survival in
the restricted ecosystem of the periodontal pocket. Among
the strict anaerobes is the only presumptive periodontal path-
ogen with a Gram-positive οell ν'ιall, Peptostreptococcus
F|GUHE 3- A terminaΙ outer membrane vesicle at the tip of Fusobacterium
nucιeatum. High concentrations of lipopolysaccharide (endotoxin) are
present in the outer membrane of Gram-negative cell walls,
Actinobacill us actinomycetemcomitans and Porphyromonas
gingivalis are the best studied and have been designated,
along with Bacteroides forsythus, as true etiologic agents in
periodontitis because of the host of virulence they produce
and their ability to invade gingival tissues. Prevotella inter-
media/nigrescens and Fusobacterium nucleatum have been
widely studied as well, and appear to satisfy all criteria for
periodontal pathogenicity. Because P. intermedia and strains
ot F. nucΙeatum have also been found in areas of Severe
gingival inflammation without evidence of attachment loss,
controversy exists as to their true periodontal pathogenicity.
Campylobacter rectus, Εikeneila corrodens, Εubacterium
species, SeΙenomonas species, enteric rods/Pseudomonas
speοies, and Treponema species satisfy some, but not all,
criteria with any degree of confidence. Nonetheless, they
remain among the list of periodontal pathogens, and microbi-
ology testing serviοes commonly report their presence
among cultivable flora.
Relative risk values of periodontal pathogens in periodontal
sites have emerged from archival reviews of data bases
located in commercial testing facilities. The relative risk of a
microorganism as a pathogen is often expressed as percent
of total cultivabιe bacteria in a given culture. For example, the
cultivability of A. actinomycetemcomitans at levels at or
above 0.01% indicates a periodontal site at risk for active
disease. The risk for P. gingivalis, C. rectus, P. intermedia,
and P. micros in periodontal sites is 0.1%, 2%,2.5%, and 3"/",
What ls Dental Calculus?
Dental calculus is mineraΙized, mature plaque covered on its
suface with nonmineralized plaque, material alba, desqua-
mated epithelial cells, and formed blood elements. The
bacterial components are largely branched and unbranched
filamentous microorganisms that are usually nonvital or
display minimal metabolic activity. These bacteria probably
play a role in the mineralization of calculus as inorganic crys-
tals are frequently found within and around microorganisms.
Structurally, calculus retains much of the histologic
morphology of its plaque precursor.
Calculus may be classified as supragingival or subgingival
based on location. lt may also be classified as salivary or
serumal based on the source of inorganiο salts that comprise
calculus. Root calculus is usually more strongly adherent to
tooth surfaces than that found on enamel sudaces (see
Figures 4 and 5).
The inorganic components of calculus deposits are primarily
organized into crystalline struοtures that vary according to the
age of the deposit. For instance, in mature calculus (>6
months), the major crystalline structure is hydroxyapatite
(Ca16[PO4]6(OH)r) with lesser amounts of octacalcium phos-
phate (Cas[HPOa]a), whitlockite (Ca3[POo]r), and brushite
(Ca[HPOo]2HrO). ln younger deposits (<3 months), brushite
predominates, but with progressive aging, octacalcium phos-
phate, whitlockite, and finally hydroxyapatite become more
FlGURE 4. A heavy deposit of suρragingival, salivary calculus on the buccal
and occlusal surfaces of nonfunctional maxillary premolar and molar
Calculus deposits have also been desοribed as radiographi-
cally apparent. The radiographiο detection of calculus is posi-
tively influenced by the thickness of the deposit, the amount
of surface area covered by the deposit, and the anatomy of
the tooth. Only 40% to 50% of calculus deposits will be radio-
graphicaΙly apparent. Therefore, radiographs should not
solely be used to measure the presence or absence of
How Does Calculus Attach to Teeth? Do the
Attachment Mechanisms Have Any Clinical
Calculus will attach to tooth suι'faces by several mechanisms.
The most common mechanism of supragingival calculus
attachment to smooth enamel surfaces is salivary pellicle,
and it is usually easily removed using ultrasonic or hand
instrumentation. The irregularities of unrestored caries and
defective dental restorations complicate the removal of
supragingival calculus. The attachment of subgingival
calculus is further complicated by microscopic irregularities in
cementum such as cementaι tears, cemental voids once
occupied by Sharpey's fibers, resorption bays, and other
surfaοe cemental defects. lt is for these reasons that clini-
cians will further designate calculus deposits as either
coronal or radicular to reflect the relative tenaciousness of
radicular and coronal calculus, and in the οase of radicular
calculus, the difficulty they may have in achieving total
calοulus removal during root planing.
FlGURE 5. serumnaι calculus deposits that have become supragingival due to
gingival reοession caused by advanced periodontitis. Note the more
generalized distribution of the deposits with no apparent relationship or
proximity to ma,or salivary ducts.
What ls the Pathogenic PotentiaΙ of Calculus?
The current view is that calculus exerts its pathogenic poten-
tial as a contributing factor that fosters plaque formation and
promotes its retention on teeth. Also, there is little question
that the microbiaΙ composition of calculus provides bacterial
factors that, by themseΙves, produce an inflammatory reac-
tion in tissue. Bacterial οomponents (outer membrane vesi-
cles containing LPS, cell ivall material containing lipoteichoiο
acids, periplasmic and cytopΙasmic enzymes, and bacterial
metabolic factors) are all suspect pathogenic factors in dental
calculus. The persistent inflammation in gingival tissue
predictably seen adjacent to reasonably plaque free calculus
is unequivocal evidence of the pathogenic effect of calculus.
EτloLoGY AND clAsslFlcAτloN oF τHE PEBloDoNτAL DlsEAsEs
F|GURE 6. τhe exposure of subgingival' serumnal calculus aΙter a period of
improved plaque control. Marginal inflammation has been reduced but
erythema and edema persist. τhis is the same patient as seen in Figure 1'
Aside from this, the rough surface of dental calculus is
usually covered with a layer of plaque biofilm. Αs such,
calculus tends to "present" plaque to periodontal soft tissues
and interfere vvith efforts to improve plaque control. The phys-
ical removal of dental calculus remains a critical component
of mechanical periodontal inflammatory disease control.
What Are the Risk Factors for Periodontal
Diseases? What ls Meant by "Risk"?
The expression risk in this context means that, in the pres-
ence of a given factor, injury to or loss of periodontal tissue is
a possibility. Risk factors may be local or systemic in nature.
Local contributing factors to the etiology of periodontal
diseases fall into two general categories: Anatomic or iatro-
genic. They share in common their ability to either facilitate
bacterial plaque, and therefore calculus, accumuΙation/reten-
tion or their ability to interfere with plaque/calculus removal.
Τhe loca| anatomic risk factors include:
1. Furcation anatomy. ln many instances, the entrance
of bifurcations or trifurcations is restricted enough to
limit access for mechanical root instrumentation.
once access to the intrafurcaΙ space has been
achieved, concavities in the furcal aspects of molar
roots wiΙl limit instrumentation as well (see Figure 7).
2. lntermediate bifurcation ridges extending from the
mesial furcation surfaοe of the distal root across the
roof of the bifurcation to the distal sudace of the
mesial root of mandibular molars. Τhese common
anatomic deformities interfere with a patient's ability
to effeοtively remove plaque biofilm.
3. Cervical enamel projections (CEP). CEPs are tooth
developmental deformities of the CEJ found on
molars. They are classified according to their involve-
ment in tooth furcations. Α Grade l CEP presents with
minimal projection of enamel tov/ard the entrance of
the furcation. Α Grade ll οEP approximates the
entrance of the furcation, and the tip of a Grade lll
CEP is well within the furcation (see Figure 8).
FlGURΕ 7. A maxiΙlary moΙar displaying a buccal to distal furcation invasion
with a Nabers probe in place. The narrowness of the furcation entrances
and the tortuousness of the furcation invasion mitigate against access for
scaling and root planing. (Courtesy of Dr. Jeanne Salcetti)
F|GURE 8. A human dried maxilla with a grade ll cervical enamel proiΘction
(cEP) in the buccal furcation of the maxilΙary sΘcond molar. τhe cEP
could have been partially responsible tor the furcation invasion and local-
ized severe bone loss around the tooth.
4. Palato-gingival grooves (PGG). PGGs are tooth
develοpmenta| deformities of maxilΙary central and
lateral incisors. They begin in lingual piis and extend
vertically onto root suιJaces. PGGs could, on rare
occasions, extend to the root apex. PGGs are
commonly associated with increased gingival inflam-
mation, plaque aοcumulaiion, and probing depth (see
FlGURE 9. A palatogingival groove on a maxillary lateral incisor. τhe gfoove
couΙd have been partially responsible for the sΘvere attachment loss
around the tοoth. Note that because of its loss of support, the lateral
incisοr has undergone pathologic migration.
5. Open contacts and food impaction. Open contacts
between teeth may be anatomical in origin, iatrogenic
in origin, or be due to caries and pathologic migration
of periodontally involved teeth. Food impaction is
defined as the forceful wedging of food between
teeth. Any other accumulation of food or food debris
around teeth should be categorized as food retention
and is probably less threatening to the periodontium.
Food impaction and subsequent retention may
contribute to root caries in individuals who do not
perform proper oral hygiene interdentalΙy. open
contacts by themselves probably do not contribute to
periodontal pathology, but, in the presence of food
impaction, open contacts have been associated with
periodontal destruction. This may be particularly
noticeable in periodontitis cases where the progress
of disease is in its early stages or particularly obvious
where periodontitis is isolated to sites of open
F|GURE 10. surgical exposure of an anomalous maxillary first moΙar. The
palatal root is bifurcated and the distopalatal root curues into the mesial
furcation of the second molar. on the bucca| aspect, the mesiobuccaΙ
root of the second molar is in close approximation to the distobuccal root
of the first molar. Access for effective scaling and root planing is
6. Other anatomic risk factors of potential etiologic
importance are: The width of the space between
teeth and root proximity (so-called "kissing roots").
The iatrogenic risk factors are:
1. Overhanging dental restorations. Since dental
restorations remain the mainstay of dental practice, it
is not surprising that overhanging dental restorations
are arguably the most common form of iatrogeny to
affect marginaΙ periodontal health (see Figure 11).
Overhanging and improperly placed dental restora-
tions can be physicaΙly irritating' be pΙaque retentive,
foster the growth of periodontal pathogens, alter the
morphology of the interdental space, and violate the
dentogingival junction (see 2 below). By virtue of their
roughness and overall bulk, they may also interfere
ivith interdentaι plaque control.
FIGURE 11. A maxillary first molar with a mesial amalgam overhang that
eπends into the furcation. lt is probable that the preparation Ιor this
restoration impinged upon the biologic width. Note how the attachment
level on the tooth parallels the extension of the overhang onto the
cementum and into the furcation.
Violation of the "biologic width". After overhanging
restorations, iatrogenic invasion of the biologic width
may be the next more serious insult to the periodon-
tium a dentist can make. The impact of this insult is
usually permanent as the margins of dental restora-
tions are inevitably placed in the wake of the insult.
The biologic width is one of nature's constant dimen-
sions. lt is most constant within individuals and less
constant betΛ/een individuals. lf it is injured, it will
repair. lf however, restorative materials render the
invasion of the biologic width permanent, periodontitis
wilΙ produce apical migration of the .iunctional epithe-
lium, resorption of crestal alveolar bone, loss of perio-
dontal attachment, and possible vertical osseous
defeοts (Figure 1 1). Α new bio|ogic width will repair a
few mms apical to its original position on the tooth.
This represents a net loss of attachment on the tooth.
Open contacts and food impaction related to
inadequate restorative dentistry. The impact of
food impaction through open contacts created by
EτloLoGY AND clAsslFlcAτloN oF τHE PERloDoNτAL DlsEAsEs
iatrogeny offers the same threat to the periodontium
as food impaοtion associated with open contacts that
have resulted from growth and development or
Occlusal traumatism associated with inadequate
dentistry in 1, 2, and 3 above.
Additional local iatrogenic risk factors for perio-
dontal diseases include: Removable partial 2.
dentures and overdentures, fixed bridges, removal of
third molar teeth in older adults, placement of fixed
orthodontic appliances, and orthodontic movement of
periodontally involved teeth.
Uncontrolled diabetics, poorly controlled diabetics, or
diabetics whose control is unknown should only
receive emergency periodontal therapy, and that
treatment should be performed ,vith intraprocedural
and/or postoperative antibiotic coverage. The
patient's physician may also prescribe insulin or other
antihyperglycemic agents to help limit post-operative
infections or complications in wound healing.
Ηlv/AlDs. Given the immunosuppressed state of
these individuals (decreased CD4 lymphocytes), an
expectation for severe periodontitis in patients with
HIV/AIDS is reasonable. lndeed, these individuals
suffer from other bacterial, viral, and fungal diseases
more than those νvithout HIV infection. Many
sucοumb to these infections. Early studies of the peri-
odontal status in AIDS patients indicated that these
individuals showed increased severity of periodontal
diseases. H|V-gingivitis (linear erythema) and HIV-
periodontitis (necrotizing ulcerative periodontitis)
categories of periodontal diseases were quickly
proposed to designate the unique cΙinical characteris-
tics of periodontal diseases in this group. RecentΙy,
the issue has been challenged by those who report
no increases in the prevalence or extent of perio-
dontal diseases among HlV-positive individuals.
Smoking. Due to the vasoconstrictor effect of nico-
tine and the paralysis by carbon monoxide on the
ability of hemoglobin to transport oxygen, it is under-
standable that smoking is a serious environmental
risk factor for periodontal diseases. The length of time
an individual has been smoking and the frequency of
smoking play contributory roles in the severity of peri-
odontal disease in smokers. Smokers also have a
greater accumulation of plaque and οaΙcu|us than
nonsmokers and may be more at risk to harbor perio-
While probing depth reduction following conventional
nonsurgical and surgical periodontal therapy has
been reported in smokers, the amount of reduction
has been reported as less than that achieved in
nonsmokers. A growing body of evidence suggests
strongly that the failure rate of implant therapy is
higher in patients who smoke. lt is not uncommon for
a therapist to recommend against the placement of
dental implants in smokers. Patients must be coun-
seled in this regard and supported in their attempts to
overcome their addiction.
Sex hormone imbalances. The most notable
changes in the periodontium that are affected in part
by hormonal changes occur in Λ/omen in their child-
bearing years. ln the case of pregnancy, proges-
terone and estrogen levels increase to levels that are
several orders of magnitude greater than those seen
during a normal menstrual cycle. Varying degrees of
a reversible "pregnancy gingivitis" are common
during pregnancy. The biologic impact of hormone
changes range from the release of inflammatory
mediators that increase vascular permeability (pros-
taglandins), the alterations in immunoregulation and
pro-inflammatory reguιators, the imbalances in the
fibrinolytic system, and the abundant growth of the
periodontal pathogen, P. intermedia. Because the
duration of pregnancy is relatively short, hormonal
changes associated with pregnancy have little effect
on the more irreversible progress of periodontitis.
What Are the Systemic Diseases and/or
Conditions That Are Contributing Factors for
Aside from the medications that affect the clinical presenta-
tion of plaque-induced gingival diseases (nifedipine for
control of hypertension, phenytoin for control of epileptic
seizures, and cyclosporine to control organ transplant rejec-
tion), most systemic diseases and conditions that may affeοt
periodontal diseases generally alter host barrier and host
defense mechanisms. The impact of diminished host suscep-
tibility, along with the diverse virulence mechanisms invading
microorganisms possess, help to explain the individual varia-
tions in periodontal disease patterns Λ,e See in systemically ill
periodontal patients. An assessment of systemic contribu-
tions to periodontal diseases in our patients is critical to perio-
dontal diagnosis and/or treatment planning.
The systemic diseases and conditions that commonly affect
periodontal diseases are: Uncontrolled type I and type ll
diabetes mellitus, HIV/AIDS, hormone imbalances, genetic
predisposition, medications, smoking, and malnutrition.
1. Diabeιes mellitus. Diabetes mellitus (DM) is
atfecting a growing number of Americans. The inci-
dence of the disease seems to vary according to
ethnic origin, but it is estimated that 5% to 10% of
individuals in the United States are affected with
diabetes. DM is an aberration in carbohydrate, lipid,
and protein metabolism. Most of the morbid compli-
cations of DM stem from longterm impaired glucose
metabolism. The characteristic hyperglycemia of
uncontrolled DM is the basis for most of the vascular,
cellular, and immune changes assoοiated with the
Epidemiologic data has made clear associations
between increased severity of periodontal diseases
and uncontrolled type I and type ll diabetes mellitus.
Type I and type ll uncontrolled diabetics tend to
present with more gingiva! inflammation, more loss of
periodontal attachment, and radiographic evidence of
more bone loss than controlled or nondiabetic individ-
uals. There is agreement that periodontal patients
whose DM is welΙ controlled may receive periodontal
therapy without restriοtions' incΙuding periodontal
surgery and implant placement.
Oral contraceptives mimic the hormonal levels seen
during pregnancy, and it is not uncommon to find
pregnancy-like changes in patients using birth οontrol
pills (BCP). Because gingivaΙ sex hormone concen-
trations tend to be lower during normal menstruation,
it is not unexpected that women in their childbearing
years may present with "cyclic" episodes of increased
F|GURE'12. τhis lesion is a pyogenic granuloma in a 17-year-oιd femaΙe
patient as a result in changes in sex hormone levels and plaque
The most important οoncern of the dentist in
managing patients who present with gingival disease
related to hormone imbalances is to be certain that
inflammatory disease control measures are effective
This is particularly important in women who are preg-
nant because data exists to suggest a relationship
betΛ/een periodontal infections (periodontitis) and
preterm low birth weight babies. Antibiotiοs should be
used only after a medical consultation in patients who
are pregnant. Although οontroversial, there are
reports of decreased effectiveness of oral οontracep-
tives in individuals taking certain antibiotics. lndivid-
uals who are taking BCPs should be advised that the
use of prescribed antibiotics such as tetracyclines
and some penicillins may interfere with the action of
BCPs. To avoid unwanted pregnancy, these individ-
ua|s should be so warned and use aΙternative
methods of birth control ivhile taking antibiotics.
5. Genetic predisposition for periodontal diseases.
There is general agreement that individual responses
to plaque bacteria vary. lt has been suggested that
disease pattern variations could be based, in part, on
underlying genetically based differenοes in immune
function. lndeed, the association of:
a. Neutrophil receptor defects
b' Αntibody responses (lgGr) to periodontal patho-
c. οertain histoοompatibility antigens (HLΑ)
d. Lymphocyte immune regulatory defeοts in patients
with aggressive periodontitis adds credibility to this
Studies in twins indicate that many of the clinical
variations seen in chronic periodontitis can be attrib-
uted to individual genetic differenοes. Recent reports
of genetic pleomorphism in lL-1 genes and the
elevated production of proinflammatory mediators,
such as lL-1 , add another dimension to the impact
genetic variations among individuals have on the
patterns of chronic periodontitis.
EτloLoGY AND cLAsslF|cATloN oF TΗE PERIoDoNτAL DlsEAsEs
CLASSIFICATION OF PERIODONTAL DISEASES
Concepts about the etiology, pathogenesis, and treatment of
the periodontal diseases have changed significantly over the
years. NeΛ/ levels of understanding are reflected in the clas-
sification systems for these diseases and conditions. The
tΛ/o most recent widely accepted classification Systems of
the periodontal diseases and conditions were developed in
1989 and 1999. The current system, more comprehensive
than any of its predecessors, is admittedly still a work in
Ηoνv Has the Understanding of Periodontal
Diseases Changed Over the Years?
For many years, the periodontal diseases were thought of as
degenerative diseases. Early confirmation of the role of
bacterial plaque in the initiation and progression of gingivitis
was only presented in the 1960s. Since that time, many of
the earlier tenets have fallen by the wayside. Currently, it is
clear that both gingivitis and periodontitis in their varied
forms are caused by the accumulation of a bacterial plaque
biofilms on the teeth and in the subgingival area, the host
response to that aοcumulation, and the various systemic and
local factors that may affect the host response. lt is also clear
that only a relatively few bacteria are associated with inflam-
matory periodontal disease. The exact role of these bacteria,
their relationship with each other and their interaction with
the immune system in the initiation and progression of
disease is still not clearly understood. There also appears to
be a genetic component to the initiation and progression of
disease in some patients. At this iuncture, controlling the
acοumulation of plaque is the first line of defense in
preventing disease, no matter what other factors may be
What ls the Difference BetιΛreen Gingivitis and
FlGURE '|3. Gingivitis in a 12-year-old female. τhe severe gingivitis was due to
the interaction of increased levels of progesterone and plaque.
Gingivitis is inflammation of the gingival tissues in the
absence of οlinical attachment loss (Figure 13). lt may be
οharacterized by edema, erythema, increased gingival
temperature, and oοcasionally pain. As the inflammation and
loss of connective tissue is confined to the soft tissues, teeth
are not in jeopardy of being lost. Gingivitis is ordinarily
reversible with appropriate therapy. Periodontitis is infΙam-
mation that affects and destroys the attachment apparatus
(Figure l4). The histology is marked by apical migration of
the junctional epithelium from the οementoenamel junction,
Ιoss of connective tissue attachement, loss of periodontal
Ιigament, and destruction of bone. lncreased probing depths
may occur or the gingiva may recede as attachment is lost.
Continuation of this loss of attachment will eventually lead to
the loss of the tooth. The progress of periodontitis may be
arrested Λ/ith proper therapy. ln certain Situations, lost
attachment apparatus may be surgicaΙly regenerated.
FIGURE 14. Periodontitis in a 37-year-old male. Note the significant calculus
and plaque accumulations, severe gingival inflammatiοn, and recession
associated with the mandibular anterior teeth.
What ls the "Traditional" Classification of the
The 1989 World Workshop in Clinical Periodontics recom-
mended the following categories of periodontitis. This system
iS the one most familiar to a majority of cliniοians'
l. Αdult periodontitis
ll. Early-onset periodontitis
A. Prepubertal periodontitis
B' JuveniΙe periodontitis
C. Rapidly progressive periodontitis
lll. Periodontitis associated with systemic disease
lV. Necrotizing ulcerative periodontitis
V. Refractory periodontitis
One of the generally accepted classifications for gingivitis
l. Plaque-associated gingivitis
ll. Αcute necrotizing ulcerative gingivitis (ANUG)
lll. Hormonal gingivitis
lV. Drug-induced gingival overgrowth
V. Desquamative gingivitis (associated with vesiculo-
During the ensuing decade, it Λ/as determined that this
disease classification system exοluded many of the diseases
and conditions of the periodontium that clinicians and
researοhers confront on a dai|y basis. Further work was
necessary to develop a neνv, more inclusive system.
VVhat Is the 1999 Classification of Periodontal
The American Academy of Periodontology convened the
1999 lnternational Workshop for a Classification of Perio-
dontal Diseases and Conditions to reassess the disease
classification system that ivas developed by the 19B9 νvorld
Workshop in Clinical Periodontics. Based on current knoννΙ-
edge and philosophies, a more comprehensive classification
system of diseases and conditions that affect the periodon-
tium Λ/as proposed. Major οhanges include the addition of a
section on gingivaΙ diseases, changing the names of adult
periodontitis to chronic periodontitis, early onset periodontitis
to aggressive periodontitis, and the elimination of refractory
periodontitis as a distinct disease class. Periodontitis as a
manilestation of systemic disease has been further clarified,
new categories added on periodontal absοesses, perio-
dontic-endodontiο lesions, and the developmental or
acquired deformities and conditions, and the replacement of
necrotizing ulcerative periodontitis with necrotizing perio-
l. Gingival Diseases
A. Dental Plaque-lnduced Gingival Diseases
. Gingivitis associated with dental plaque only
a. Without Ιocal contributing factors (Figure 15)
FIGURE 15. Gingivitis associated with dental plaque only. Note that the
gingival inflammation is worse on the maxillary left side than the
right side. τhis may be relatθd to the hand with which the patient
biushes his teeth. As the patient turns his hand to maneuver the
brush, the lateral incisor and canine are ofιen missed.
b. V/ith local contributing factors
2. GingivaΙ diseases modified by systemic factors
a. Αssociated with the endocrine System
1. Puberty-associated gingivitis (Figure 16)
FIGURE 16. Puberty-Associated Gingivitis. τhis is related to the patient in
2. Menstrual cycle-associated gingivitis
- Pyogenic granuloma (see Figure 12)
4. Diabetes mellitus-associated gingivitis
b. Associated with blood dyscrasias
1. Leukemia-associated gingivitis
3. Gingival diseases modified by medications
a. Drug-influenced gingival diseases
1. Drug-influenced gingival enlargements
FlGURE'17Α. Drug-lnfluenced Gingival Enlargements. Gingival enlarge-
ment due to phenytoin the,aPy.
EτloLoGY AΝD cLAsSlFlcATloN oF THE PER|oDoΝTAL DlSEASES
FIGURE 178. Drug-lnfluenced Gingivat Enlargements. Gingival enlarge-
ment due to nifedipine therapy superimposed on chronic periodon-
2. Drug-influenced gingivitis
- Oral contraceptive-associated
4. Gingival diseases modified by maιnutrition
a. Αscorbiο acid-deficiency gingivitis
B. Nonplaque-lnduced Gingival Lesions
1. Gingival diseases of specific baοterial origin
a. Νeisseria gonorrhea-associated lesions
b. Treponema pallidum-associaied lesions
c. Streptococcal species-associated lesions
2. Gingival disease of viral origin
a. Herpesvirus infections
1. Primary herpetic gingivostomatitis
2' Reοurrent oraΙ herpes (Figure 1B)
FIGURE 18A. Recurrent Oral Herpes. General herpetic outbreak on the
F|GURE 188. Recurrent oraι Herpes. Herpes outbreak localized to one
side of the hard palate several days after periodontal surgery on the
same side ot the maxilla.
- VaricelΙa-zoster infectionS
3. Gingival diseases of fungal origin
a. Candida-sρecies infections
- Generalized gingival candidiasis
b. Linear gingival erythema (Figure 19)
FIGURE '19. Linear Gingival Erythema. Seen in some HIV+ patients.
Gingival lesions of genetic origins
a. Ηereditary gingival fibromatosis
Gingival manifestations of systemic conditions
. Lichen planus (Figure 20)
F]GURΕ 20. Erosive Lichen Planus. Ιn its ulcerative form, this disease
can be quite painful for the patient.
2. Pemphigoid (Figure 21)
FlGURΕ 21Α. Benign Mucous Membrane (cicatricial) Pemphigoid. A posi-
tive Νikolsky sign is seen over the maxillary right lateral incisor.
τhis indicates that a vesiculobullous disease is present.
FlGURE 21B' Benign Mucous Membrane (cicaιricial) Pemphigoid. lmmu-
notluorescence contirms the diagnosis ot pemphigoid.
3. Pemphigus vulgaris
4. Erythema multiforme
5. Lupus erythematosus
6. Drug induced
7 " Other
b. Αllergic reactions
1. Dental restorative materials
2. Reactions attributable to
- Chewing gum additives
- Foods and additives (Figure 22)
FlGURΕ 22Α. Allergic Reactions Attributable to Food. This patient
presented With severe gingival infΙammation associated with perio-
dontal disease. The patient had no history or cΙinical findings
suggesιive of sysιemic disease.
FΙGURΕ 22B' AΙlergic Reactions Atlributable to Food' After contrοl of
local factors, there was still a signiricant amount of inflammation.
EτloLoGY AND cLAsSIFlcAT|oN oF τHE PER|oDoNTAL DlsEAsEs
FIGURE 22C. Allergic Reactions Attributable to Food. An incisional
biopsy revealed a diagnosis of plasma ceΙl gingivitis (allergic reac-
FIGURE 22D. Allergic Reactions Attributable to Food. After eliminating
curry peppers from her diet, this patient's gingiva returned to
6. Traumatic lesions (factitious, iatrogenic, acci-
- Chemiοal injury
- Physical injury
- Thermal injury
7. Foreign body reaction
8. Noi otherffise specified (NOS)
ll. Chronic Periodontitis (Figure 23)-
FlGURΕ 23Α. Generalized chronic Periodontitis. A' ln spite of significant
plaque and calculus accumulations in the mandibular arch, ιhis
palient had minimal gingival intlammation.
FiGURE 23B. Generaιized chronic Periodontitis. τhe right buccal
segment showed minimal soft tissue infΙammation buι probe depths
ranged from 7-10 mm.
FlGURE 23c. Generalized chronic Periodontitis. τhe radiographs
showed significant bone loss in this area.
F|GUΗΕ 23D. Generalized chronic Periodontitis. once a full thickness
mucoperiosteal flap was reflected, the extent of bone loss was
ll!. Aggressive Periodontitis*
A. Localized (Figure 24)
FιGURES 24A and B. Localized Αggressive Periodontitis. clinical and
radiographic evidence of localized severe periodontal destruction.
FlGURΕ 24ο. Localized Aggressive Periodontitis. Note the severe bone
loss on the mesial of the tirst molar and no bone loss on the adia-
cent distal of the second premolar.
B. Generalized (Figure 25)
FΙGURE 25. Generalized Aggressive Periodontitis. τhis 1g-year-old
patient has already lost several teeth due to periοdontal disease.
τhe entire dentition has been affected by disease.
Periodontitis as a Manifestation of Systemic Diseases
Α. Αssociated With Ηematologic Disorders
1. Acquired neutropenias
B. Αssociated With Genetic Disorders
1. Familial and οyοιic neutropenia
2. Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon-Lefevre syndrome
6. Histiocytosis syndromes
7. Glyοogen siorage disease
8. lnfantile genetic agranulocytosis
9. Cohen syndrome
10. EhΙers-Danlos syndrome (Types lV and VlΙl)
1 1. Hypophosphatasia
Necrotizing Periodontal Diseases
Α. Necrotizing Ulcerative Gingivitis (NUG) (Figure 26)
FlGURΕ 26. Νecrotizing Ulceraιive Gingivitis. These lesions are quite
painful and exude a distinctive unpleasant odor.
EτloLoGY AΝD cLAsslFιcAτloN oF THE PΕRloDoNτAL D|SEASES
B. Necrotizing Ulcerative Periodontitis (NUP) (Figure
FlGURE 27. Necrotizing Ulcerative Periodontitis' τhis lesion is often seen
in an Hlv+ patient or a patient with fully developed ΑlDs.
Vl. Abscesses of the Periodontium
A. Gingival Abscess
B. Periodontal Αbscess (Figure 28)
FiGURE 28. Periodontal Abscess. τhis lesion is associated with some
popcorn that was trapped in the subgingival area.
C. Pericoronal Abscess
Vll. Periodontitis Associated With Endodontic Lesions
Α' Combined Periodontic-Endodontic Lesions
Vlll. Developmental or Acquired Deformities and
A. Localized Tooth-Related Factors That Modify or
Predispose to Plaque-lnduοed Gingival Diseases/
1. Tooth anatomic factors
2. Dental resiorations/appliances
3. Root fraοtures
4' Cervical root resorption and οemental tears
B' Muοogingival Deformities and Conditions Around
1. GingivaΙ/soft tissue recession (Figure 29)
F|GURE 29. Gingival/soft Tissue Recession. τhe recession is related to a
lack οf attached gingiva and the buccaι frenum altachment.
a. Facial or lingual surfacΘs
b. lnterproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Αberrant frenum/muscle position
5. Gingival excess
b. lnconsistent gingival margin
c. Excessive gingival display
6. Abnormal color
C. Mucogingival Deformities and Conditions on
1. Vertical and/or horizontal ridge deficiency
2. Lack of gingival/keratinized tissue
3. Gingival/soft tissue enlargement
4. Aberrant frenum/muscle position
5. Decreased vestibular depth
6. Abnormal color (Figure 30)
FTGURE 30. Abnormal Color. This abnormal gingival color is due to retro-
grade endodontic surgery and a resultant amalgam tattoo.
D. occΙusal Trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
"Cases of chronic and aggressive periodontitis may be
generally described by the extent and severity of the
disease. Localized disease would be <30o/o of sites involved
and generalized disease as >30% of sites involved. Slight
disease would have 1-2 mm of clinical attachment loss
(CAL), moderate disease 3-4 mm CAL, and severe disease
>5 mm CAL.
What Are Some of the Distinguishing
Characteristics of the New Classifications of
Gingivitis associated νιrith dental plaque only. As the
name implies, bacterial plaque must be present to initiate the
gingival infΙammation. This inflammation may be character-
ized by changes in gingival color, contour, and possibly
consistenοy; slight elevation of intrasulcular temperature;
bleeding on gentle probing; an increase in gingival crevicular
fΙuid flow (now as an exudate); and the inflammation is
confined to the soft tissues. Local factors may include resto-
ration overhangs, open contacts, and other plaque traps and
impediments to good oral hygiene.
Gingival diseases modified by systemic factors:
Pubefiy-associated gingivitis, menstrua! cycle-associ-
ated gingivitis, and pregnancy-associated gingivitis.
These conditions are all associated with changes in steroid
hormone levels, primariΙy progesterone and estrogen. Τhey
have been associated with increased levels of Prevotella
intermedia in the infΙamed sites. ln puberty-associated gingi-
vitis, the inflammation may be exaggerated even with appar-
ently minimal amounts of plaque. Menstrual cycle-associated
gingivitis may appear in a very mild form. lncreased gingival
crevicular fluid flow has been seen in a majority of subjects
during ovulation. Pregnancy-associated gingivitis has
perhaps the most radical changes, rvith the possible appear-
ance of a pyogenic granuloma. lt is an extreme response to
gingival inflammation, characterized as a painless protuber-
ance of the gingiva that bΙeeds readily at slight provocation.
Gingival diseases modified by medications. There are
three major drugs that can induce an overgroΛ/th of gingival
tissues. Phenytoin is used as an antiseizure medication,
nifedipine and several of the other calcium channel blockers
are antihypertensive/antiarrhythmic drugs, and cyclosporine
Α is an immunosuppressant. overgrowth appears to be
related to the level of plaque accumulation. Approximately
50% of phenytoin patients are susceptible to this overgro,νth.
lt has been estimated Ιhat 2o"/" of patients on calcium_
channel blockers, and 2O/" to 30% of patients on cyclo-
sporine A are susceptible to drug-induced gingival over-
Nonplaque-induced gingival lesions. Many of these
lesions are relativeΙy rare with the exception of the herpes-
virus and Candida infections. Herpesvirus infections must be
cautiously treated due to their contagious nature Λ/hile the
lesions are shedding virus. Treatment must be deferred
νvhen the patient presents with a weeping lesion. Candida
infections may be problematic if there is no apparent cause
(reοent antibiotic use' illness) for the infeοtion. Candidaintec-
tions have a high association r/ith human immunodeficiency
virus (HlV) infection, so a thorough patient work-up may be
necessary in the face of an unexplainable Candida infection.
Gingival manifestations of systemic conditions. Muco-
cutaneous disorders: These disorders include the dermato-
logic/autoimmune diseases of lichen planus, pemphigoid,
pemphigus vulgaris, erythema multiforme, lupus erythema-
tosus, and drug-induced disorders. These disorders at one
time were classified as desquamative gingivitis, a descriptive
term signifying desquamation or falling away of the surface
epithelium of the gingiva. These disorders are actually auto-
immune in nature with no clear etiology. lt is critical that a
definitive diagnosis be obtained, for while they all may have
a similar appearanοe, pemphigus has a higher morbidity,
while the mucocutaneous disorders are difficult to manage
for patient comfort.
Gingival manifestations of systemic conditions: Linear
gingival erythema. This lesion is characterized by a bright
erythematous margin of the free gingiva. lt is associated with
immunosuppression, particularly ΗlV infection. The
erythema does not resolve with the removal of plaque.
Gingival manifestations of systemic οonditions: Aller-
gies' Αllergic reactions may take on a Variety of forms from
mild erythema and edema to severe inflammation to an
apparent lichenoid appearance. The challenge is to be sure
that the inflammation is not plaque related. A diagnosis of
plasma cell gingivitis may be made by biopsy. The allergen
must then be identified and, if possible, eliminated from the
oral cavity. Allergens incΙude amalgam, base metals used in
fixed prosthodontics, flavoring agents in dentifrices and
cheνving gum' chili peppers, and other foodstuffs. lt may be
difficult to identify the offending agent. Changes must be
made one at a time, often a time-consuming process, in
order to identify the allergen.
What Are Some of the Distinguishing
Characteristics of the New Classifications of
The new classifiοation system for periodontitis is more
descriptive and not temporal as νvas the previous system.
The terms adult, juvenile, early onset, and prepubertal have
been replaced with various forms of chronic and aggressive
disease. ln addition, many periodontal conditions that νvere
not addressed in any previous classification system have
been described. The term refractory periodontitis has been
removed as a distinct disease entity, as the current thinking is
that any type of periodontitis may be refractory.
Chronic periodontitis. As the name implies, this type of
periodontitis has a relatively long-standing history in a
patient. This disease is characterized by relatively slow
progress, loss of attachment and underlying bone with
increased pocket depth. lt may have periods of rapid attach-
ment Ιoss foΙlowed by prolonged periods of inactivity. Ιt is
related to the presence of plaque and calculus, ι/ith a variety
of associated bacteria involved. There may be modifying
local factors, such as restorative overhangs, food impaction,
or open contaοts, and systemic factors, such aS uncontrolΙed
diabetes mellitus or cigarette smoking. Most often, chronic
periodontitis is responsive to mechanical therapy. lt is no
longer referred to as adult periodontitis as this disease may,
albeit rarely, be seen in οhildren.
EτloLoGY AND clAsslFlcAτloΝ oF τHE PER|oDoNTAL DlsEASEs
Aggressive periodontitis. This category replaces what
used to be known as the early-onset periodontal diseases.
Localized aggressive periodontitis replaces the older term,
juvenile periodontitis, that is manifest by rapid and severe
attachment loss in the incisor and permanent first molar
regions. Actinobacillus actinomycetemcomitans is assoοi-
ated with a majority of cases. Τhese patients have shown
abnormalities in neutrophil function that may be related to a
hyperimmune effect of their macrophages. This type of
aggressive periodontitis has a fairly clear inheritance pattern.
Τhe loοalized ρattern affects 14 or fewer teeth, mostly
confined to the incisors and first molars. The generalized
form of aggressive periodontitis, formerly known as rapidly
progressive periodontitis, affects 15 or more teeth with
possible immunologic changes as well. lt is characterized by
episodic, rapid, and severe attachment loss. At times, this
disease may be difficult to control.
Periodontitis as a manifestation of systemic diseases.
Λ/ith the exception of Down syndrome, most of the listed
genetic disorders are relatively rare. τhe Down syndrome
patient is a challenge because of the difficulty in maintaining
good oral hygiene. The prevalence and severity of periodon-
titis is high compared to unaffected siblings, and attaοhment
loss may appear in the deciduous dentition. As the roots of
teeth are often short, these patients may lose teeth earlier
due to the early onset of disease and the root anatomy.
What Are Some of the Distinguishing
Characteristics of Some of the Other Periodontal
Diseases and Conditions?
Necrotizing periodontal diseases. Τhis οategory includes
both necrotizing ulcerative gingivitis (NUG) and necrotizing
ulcerative periodontitis (NUP). NUG and NUP have been
classified together as they may be different stages of the
same disease. NUG is characterized by necrosis of the tips
of the interdental papilla with a pseudomembrane appear-
ance, pain, foul odor, spontaneous bleeding, and possible
fever and lymphadenopathy. There is no attachment loss
associated with NUG. Fusiforms and spirochetes, as well as
Prevotella intermedia,haνe been implicated in the etiology of
NUG. Significant contributing factors include stress, fatigue,
poor oral hygiene, smoking, and poor nutrition, basically
factors associated with immunosuppression. NUG and NUP
are also associated with HIV infection. NUP shares many of
the clinical characteristics of NUG along Λ/ith attachment
Abscesses of the periodontium. Periodontal abscesses
are local infections of the gingival or periodontal tissues. The
etiology may be a foreign object such as a popcorn hull or
loose piece of calculus. This type of abscess is marked by
localized swelling and tenderness or pain. As the marginal
gingiva begins to heal ιΛ,ith treatment, the orifice to deeper
drainage of infection may be closed off. lt may be drained
either externally or through the wall of the periodontal pocket.
Periodontitis associated with endodontic lesions. Endo-
dontic and periodontal Iesions may coexist separately asso-
ciated with the same tooth or may communicate with each
other. Two separate lesions may coalesce or there may be a
root fracture or root perforation. Occasionally, an isolated
endodontic lesion may masquerade as a periodontal lesion,
such as in an isolated furcation defect on a mandibular first
molar. ln this case, proper endodontic therapy will heal the
furοation lesion as weΙl. ln a true combined lesion, the endo-
dontic therapy must be performed first in order for the even-
tual periodontal therapy to succeed as well.
Developmental or acquired deformities and conditions.
Most of the deformities and conditions classified here are
self-explanatory by name. Specific conditions such as
mucogingival deformities, edentulous ridge deficiencies, and
ocοlusal trauma are described elsewhere in Ιhis Manual.
How ls a Periodontal Case Type Formulated
Using the American Academy of Periodontology
Case Type System?
The case type refers to the level of disease sΘverity, not the
specific diagnosis. Case type may be applied to each type of
gingivitis and periodontitis (also see Chapter l).
Case Type 1: Gingivitis. lnflammation confined to the
soft gingival tissues only. All gingivitis, irrespeοtive of
the level of inflammation, is considered to be in this
Case Type 2: Mild Periodontitis. This category signifies
the beginning of attachment loss, up to approxi-
maΙely 2o"/" of the attachment apparatus on the root.
τhere may be some pocketing and initial mobility.
Furcation involvement, when present, is confined to
a Class I involvement.
Case Type 3: Moderate Periodontitis. This category
signifies further loss of the attachment apparatus, up
to approximately 40% Ιo 45"/o. There is increased
bone loss, pocket depth, mobility, and furcation
involvement. Furcas may have Class ll involvement.
Case Type 4: Severe Periodontitis. There is severe
attachment loss, deep pocketing, mobility, pathologic
migration of teeth, and Class ll and possibly Class lll
f urcation involvement.