PERIODONTITIS AS A MANIFESTATION

OF SYSTEMIC DISEASE
Presentation of periodontitis in primary dentition
due to underlying systemic disease is very rare.
Local factors account for the majority of cases
of premature bone loss. The systemic diseases
that may be associated with bony destruction
in the primary dentition in the absence of local
factors are hypophosphatasia, Papillon–Lefèvre
syndrome, histiocytosis X, agranulocytosis,
leukocyte adherence deficiency, neutropenias,
leukemias, diabetes mellitus, Down syndrome,
and Chediak–Higashi syndrome. Most of them
have a genetic origin. The defect in immune
and neutrophil cell function associated with
these diseases is thought to increase patient
susceptibility to infectious periodontitis causing
alveolar bone loss and to other infections.
PAPILLON–LEFEVRE SYNDROME
It is a rare syndrome with an identified
autosomal recessive mode of inheritance*.
Clinical Features
The oral presentation of the disease is as follows:
• The primary teeth erupt at the normal time.
• The primary teeth may show severe mobility.
• Severe horizontal bone resorption in
full-mouth radiographs is seen.
• Hyperkeratosis of the palms and soles is
present.
• Previous reports have indicated that the
permanent dentition will also be affected,
however, rarely.
Etiology
Unknown
Treatment
• Attempts at conventional therapy prove
unsuccessful in preventing tooth loss.
• Periodontal treatment for these young
children includes identification of specific
pathogens, specific antibiotic therapy against
these organisms, and full mouth extractions
early enough to provide an edentulous period
before permanent tooth eruption.
DOWN SYNDROME
Down syndrome is caused by trisomy of
chromosome no. 21*. It is characterized by
mental deficiency and mental retardation.
Prevalence of periodontal diseases in these
patients is very high (100% in patients less than
30 years of age).
Etiology
• T-cell defect and defective chemotaxis
• Poor circulation in gingival tissue
Clinical Presentation
Presents with deep periodontal pockets,
substantial plaque formation, and moderate
gingivitis.
HYPOPHOSPHATASIA
• It is caused by low levels of alkaline
phosphatase* in blood.
• Teeth are lost with no signs of gingival
inflammation.
• Cementum formation is defective.
• Primary teeth may be lost prematurely.
• It involves skeletal system as well.
LEUCOCYTE ADHESION DEFICIENCY
• Rare
• Extremely acute inflammation of gingiva and
rapid destruction of bone surrounding the
teeth
• Permanent dentition may not be affected
MUCOGINGIVAL DEFECTS IN
CHILDREN AND ADOLESCENTS
Mucogingival defects involve morphology,
position, and/or amount of gingiva supporting
the teeth. The most common mucogingival
defect in children and adolescents is gingival
Chapter 20 ◆ Gingival and Periodontal Diseases in Childhood and Adolescence 217
recession. It can be seen in children and
adolescents in any of the following conditions:
• Malocclusion: Buccal eruption patterns of
tooth may cause recession
• High frenum attachments
• Displacement of any tooth after orthodontic
treatment
• Habits such as nail picking
• Inadequate oral hygiene maintenance and
improper tooth brushing
• Also as a result of progressive periodontitis
Early treatment of gingival recession in
children and adolescents is simple with a good
prognosis. Treatment may be either conservative
(meticulous oral hygiene) or surgical. The
surgical options should however be postponed
for allowing spontaneous improvement to take
place, as dimensional changes may be seen in
the attached gingiva during normal course of
growth and development.
CHAPTER
DEFINITION
Desquamative gingivitis is a condition
which is characterized by intense erythema,
desquamation, and ulceration of free and
attached gingiva.
Prinz in 1932 coined the term “desquamative
gingivitis”*.
It is a symptom rather than a disease
condition*.
Desquamative gingivitis is not a specific
disease entity, but a gingival response associated
with a variety of conditions.
CHARACTERISTIC FEATURES
• Gingival erythema not associated with plaque
• Erosion and desquamation of gingival
epithelium
• Formation of blisters
• Presence of other intraoral/extraoral lesions
• Positive Nikolsky’s sign (not a universal
feature)
Nikolsky’s sign*:
• Epithelial desquamation after application of a
sliding or rubbing force on normal appearing
gingiva
• It is strongly associated with pemphigus vulgaris*
• Mucous membrane pemphigoid: Present
• Bullous pemphigoid: Absent
ASSOCIATED CONDITIONS
DERMATIC LESIONS
• Lichen planus
• Cicatricial pemphigoid
• Bullous pemphigoid
• Pemphigus vulgaris
• Linear immunoglobulin A (IgA) disease
• Dermatitis herpetiformis
• Chronic ulcerative stomatitis
OTHER CONDITIONS
Discussed in detail in Chapters 18 and 19.
• Chronic bacterial infections
• Chronic fungal infections

Desquamative Gingivitis
At the end of this chapter, the student will be able to:
21
Ÿ Ÿ Define desquamative gingivitis
Ÿ Ÿ Identify and describe oral mucosal diseases or disorders that are commonly associated with
desquamative gingivitis
Ÿ Ÿ Discuss diagnostic interventions necessary to identify conditions associated with desquamative
gingivitis
Ÿ Ÿ Detail treatment protocols useful in patient management of the diseases and disorders most often
associated with desquamative gingivitis
Specific Learning Objectives
Chapter 21 ◆ Desquamative Gingivitis 219
• Chronic viral infections
• Reactions to medications
• Reactions to mouthwashes
• Reactions to chewing gums
• Crohn’s disease
• Sarcoidosis
• Most leukemias
LICHEN PLANUS
Oral lichen planus is a chronic immunological
inflammatory mucocutaneous disorder that
varies in appearance from keratotic (reticular
or plaque like) to erosive (erythematous
and ulcerative). It is an immunologically
mediated mucocutaneous disorder involving T
lymphocytes*.
ORAL LESIONS
Common forms are reticular and erosive lichen
planus (Table 21.1).
GINGIVAL LESIONS
These lesions are confined only to the gingiva.
They may present in four forms (Table 21.2).
HISTOPATHOLOGY
Three main features are as follows:
• Hyperkeratosis/parakeratosis
• Hydropic degeneration of basal layer
• Dense subepithelial band of lymphocytes
(T cells)
Besides the abovementioned features other
features associated with lichen planus are as
follows:
• Sawtooth rete pegs
• Subepithelial vesicle formation
• Colloid/Civatte bodies (pyknotic nuclear
bodies) at epithelial connective tissue interface
DIFFERENTIAL DIAGNOSIS
• Lichenoid mucositis
• Lupus erythematosus
• Chronic ulcerative stomatitis
• Cicatricial pemphigoid
• Pemphigus vulgaris
PEMPHIGOID LESIONS
The lesions, their clinical features, and
histopathology are discussed in Table 21.3.
Table 21.1 Clinical features of common forms of
lichen planus
Types of
Lichen Planus
Features
Reticular • Bilateral
• Asymptomatic
• Interlacing fine white lines
(Wickham’s striae)
• Alternating periods of quiescence
and aggravation
Erosive • Painful
• Sensitive to heat and spicy foods
• Atrophic, erythematous, and
ulcerated areas
• Wickham’s striae bordering
ulcerated areas
Table 21.2 Gingival lesions seen in various forms of
lichen planus
Type of Lesions Features
Keratotic lesions Raised white lesions present as
• Groups of individual papules
• Linear or reticular lesions
• Plaque like
Erosive ulcerative
lesions
• Extensive erythematous areas
• Patchy distribution: Focal or
diffuse hemorrhagic areas
• Exacerbated by slight trauma
Vesiculobullous
lesions
• Raised, fluid-filled lesions
• Rare and short lived on gingiva
• Rupture and leave an ulcerated
area
Atrophic lesions Epithelial thinning and erythema
220 Fundamentals of Periodontology
PEMPHIGUS VULGARIS
Pemphigus is an autoimmune disease that
causes blisters and erosions of the skin and the
mucous membrane. Pemphigus vulgaris is the
most common form of pemphigus*.
The blisters result due to autoantibodies
that react with desmosomal glycoproteins
(desmoglein*) present on the cell surface of a
keratinocyte.
Desmoglein 3 (DSG3) is the gene coding
for pemphigus vulgaris and is located on
Chromosome 18*.
CLINICAL FEATURES
• The lesion starts as a small vesicle on a
noninflamed base and forms large bullae.
• The bullae rupture spontaneously to form
extensive ulceration.
• The ulceration continues to extend
peripherally over a period of weeks until it
involves large portions of the oral mucosa.
• Most common site in oral cavity is areas of
friction, i.e., along the occlusal plane*.
• Soft palate, buccal mucosa, tongue, and lower
labial mucosa are common sites.
• Lesion confinement to gingiva is rare.
HISTOPATHOLOGY
• Intraepithelial vesiculation* above the basal
cell layer. This vesiculation is fluid filled
and results in bulla formation. Bulla bursts
and superficial layers of epithelium are
lost. The ulcerated lesion is infiltrated by
polymorphonuclear neutrophils (PMN) and
may show suppuration
• Tombstone appearance of epithelial cells*
• Acantholysis*
• Underlying connective tissue presents mildto-
moderate chronic inflammatory cell infiltrate
DIFFERENTIAL DIAGNOSIS
• Erythema multiforme
• Pemphigoid lesions
• Bullous lichen planus
OTHER DERMATIC LESIONS
Dermatic lesions are discussed in Table 21.4.
DIAGNOSIS AND TREATMENT
Four phases of diagnosis and treatment (Bystryn,
1988, and Sciubba, 1996):
1. Diagnostic phase: To determine etiology
2. Control phase: To reduce or eliminate signs
and symptoms of disease
3. Consolidation phase: Reduction,
modification, or elimination of therapy with
condition progression and improvement
4. Maintenance phase: Long-term maintenance
of patient’s comfort and disease free state
Table 21.3 Pemphigoid lesions
Lesion Characteristic Clinical Features (Oral) Histopathology
Bullous pemphigoid Nonscarring and
confined to skin
• Secondary occurrence*
• Erosive or desquamative or
rarely vesiculobullous
• Subepithelial vesicle
formation
• No acantholysis*
Cicatricial pemphigoid/
mucous membrane
pemphigoid
Scarring and
confined
to mucous
membranes*
• Areas of erythema,
desquamation, ulceration, and
vesiculation
• Bullae are thick and rupture in
2–3 days; ulceration occurs
• Healing: 3 weeks or more
• Subepithelial vesicle
with intact basal layer
• Epithelium and CT
separation at the
basement membrane
Chapter 21 ◆ Desquamative Gingivitis 221
Table 21.4 Other dermatic lesions
Characteristics Linear IgA Disease (LAD) Dermatitis Herpetiformis Chronic Ulcerative
Stomatitis
Presentation Uncommon
mucocutaneous disease
Cutaneous manifestation of
celiac disease
Chronic oral ulcerations
Predilection Women (middle to late age) Men (20–30 years) Women (4th decade)
Clinical presentation • Vesicles
• Painful ulcerations
• Erosive gingivitis/ cheilitis
Vesicles or bullae rupture to
form painful ulcerations
Painful, solitary small
blisters and erosions with
surrounding erythema
Areas involved • Hard and soft palate
• Tonsillar pillars
• Buccal mucosa
• Tongue
• Gingiva
• Rare cutaneous
involvement
Bilateral and symmetric
involvement. Extraoral
areas involved with rare
oral cavity involvement
• Gingiva
• Lateral border of tongue
• Hard palate
• Cutaneous lesions rare*
Histopathology Similar to erosive lichen
planus
Apex of epithelial peg
reveals foci of neutrophils
and eosinophils
interspersed with
deposits of fibrin
Similar to erosive lichen
planus
Immunofluorescence Linear deposits of IgA at the
epithelium connective
tissue interface*
Granular pattern of IgA
and C3 deposits at the
epithelium connective
tissue interface*
Typical stratified epithelium
specific antinuclear
antibodies (SES- ANA)*.
Fibrin deposits at the
epithelium connective
tissue interface
DIAGNOSTIC PHASE
Diagnosis is based on the following:
• Past history
• Clinical appearance
• Biopsy and histopathological features
• Direct immunofluorescence
• Indirect immunofluorescence
• Culture/smear for Candida albicans
• Ancillary tools: Brush biopsy, exfoliative
cytology, fluorescence lighting
• Extraoral examination
CONTROL PHASE
The aim of this phase is:
• Intense therapy to suppress disease in days or
weeks
• To find a balance between efficacy versus
safety while administrating treatment
• Patient motivation regarding multiple daily
treatment and slow treatment results
• Prevention of side effects such as candidiasis
Treatment Protocols
• Aggressive therapy: Very high potency topical
or systemic corticosteroids
• Moderate therapy: High potency topical
corticosteroids combined with intralesional
injections where indicated
• Mild therapy: Medium or low potency
topical corticosteroids and carrier (Orabase,
denture adhesive, patches, etc.)
222 Fundamentals of Periodontology
High-potency topical corticosteroids:
0.25% Desoximetasone
0.20% Fluocinolone
0.05% Fluocinonide
0.50% Triamcinolone acetonide
Continuous monitoring required for dose not to
exceed 15 grams within 2 weeks
Specific Treatments
for Various Conditions
Oral Lichen Planus
• Plaque control
• Soft mouth guards to prevent cheek, lip, and
tongue irritation
• Replacement of faulty restorations that may
cause contact lichenoid reaction
Available options for medicinal therapy are as
follows:
• Topical corticosteroids
• Oral retinoids
• Phototherapy
• Prednisone
• Oral cyclosporin 2.5–5 mg/kg/day in 2 divided
doses
• Methotrexate 2.5–7.5 mg once weekly
• Doxycycline monohydrate 100 mg daily for
3 weeks
• Metronidazole 500 mg 2 times/day for 2 months
• Topical cyclosporine A
• Topical calcineurin inhibitors: Tacrolimus
topical (0.03% or 0.1%) two times daily
• Pimecrolimus topical 15 mg two times daily
Mucous Membrane Pemphigoid
• Plaque control
• Steroids similar to oral lichen planus
• Low dose doxycycline
• Dapsone
• Methotrexate
• Azathioprine
• Mycophenolate mofetil
• Cyclophosphamide
Pemphigus Vulgaris
• Topical corticosteroids: Rarely used
• Topical carrier trays for gingival lesions
• Intralesional steroid injections
• Short- and long-term systemic corticosteroids
• Alternative treatment: Methotrexate,
azathioprine, dapsone, mycophenolate
mofetil, IV immune globulin, rituximab
(monoclonal antibody), plasmapheresis
CONSOLIDATION PHASE
The aim of this phase is:
• Maintenance of required type and dose of
medications until the majority of lesions have
healed.
• If lesions are slow to heal, intensity of the
therapy may be inadequate and dose may
have to be modified.
• Therapeutic endpoints (Periodontology
Workshop 1996): Prevent remission of disease
and suppression of existing symptoms*.
MAINTENANCE PHASE
The aim of this phase is:
• Gradual tapering of the frequency of
medication use and/or potency of medication.
• To achieve complete remission or to
determine lowest permissible dosage
necessary to prevent the development of new
lesions.
• Sustenance of periodontal health with
frequent recall intervals, oral antimicrobials
regime, etc.
• Determination of appropriate recall intervals
to maintain health.
CHAPTER
CHRONIC PERIODONTITIS
DEFINITION
Chronic periodontitis (CP) is defined as a
slowly progressing infectious disease resulting
in inflammation within the supporting tissues
of the teeth, progressive bone loss, and
attachment loss.
According to American Academy of
Periodontology (AAP), chronic periodontitis
is defined as the inflammation of the gingiva
extending into the adjacent attachment
apparatus. The disease is characterized by loss
of clinical attachment due to destruction of the
periodontal ligament and loss of the adjacent
supporting bone.
SYNONYMS
Adult periodontitis, chronic adult periodontitis
(not used now as disease is not age related*).
CLASSIFICATION
I. On the basis of disease distribution
1. Localized*: Less than 30% sites in the mouth
exhibit attachment loss and bone loss.
2. Generalized*: 30% or more than 30% sites
in the mouth exhibit attachment loss and
bone loss.
II. On the basis of disease severity
1. Mild: Not more than 1–2 mm of clinical
attachment loss (CAL)
2. Moderate: 3–4 mm of CAL
3. Severe: 5 mm or more of CAL
DISEASE DISTRIBUTION
Chronic periodontitis is a site-specific disease*
due to plaque accumulation. One surface of a
tooth shows more attachment and bone loss
depending on the presence of local contributing
factors than the other surface on the same tooth.
Local factors are discussed in Chapter 11.

Chronic Periodontitis and

Periodontal Pocket 22
At the end of this chapter, the student will be able to:
Ÿ Ÿ Define and classify chronic periodontitis and periodontal pockets
Ÿ Ÿ Discuss disease distribution, disease progression, clinical features,
diagnosis, and treatment planning
of chronic periodontitis
Ÿ Ÿ Detail clinical features, histopathology, and pathogenesis of periodontal pockets
Ÿ Ÿ Detail contents and topography of soft tissue wall and root surface wall of periodontal pockets
Ÿ Ÿ Correlate pocket clinical features with histopathology and briefly mention disease activity and repair
in periodontal pockets
Specific Learning Objectives
224 Fundamentals of Periodontology
DISEASE PROGRESSION
• Rate of disease progression in chronic
periodontitis is slow.
• Disease progression may be modified by
systemic, environmental, and behavioral factors.
• Disease progression in chronic periodontitis
does not occur at an equal rate in all affected
sites throughout the mouth*.
• Few involved areas may remain static for long
periods while others may progress at a more
rapid rate.
• Rapid progression is seen more frequently in
interproximal areas* as they are associated
with greater plaque accumulation and are
inaccessible to plaque control measures
(overhanging margins of restorations, sites of
malposed teeth, areas of food impaction).
MODELS PROPOSED
FOR DISEASE PROGRESSION
1. Continuous model: Disease progression
occurs at a slow and continuous rate.
Affected sites have a constantly progressive
rate of destruction throughout the duration
of the disease.
2. Random/episodic-burst model: Periodontal
disease progresses in short bursts of
destruction followed with periods of no
destruction/quiescence. The disease pattern
is random in distribution for tooth sites
affected and timeline of disease process.
Some sites may show a brief active burst
of destructive periodontal disease (few
days to few months) before going into a
period of remission. Other sites may be
free of periodontal disease throughout an
individual’s life.
3. Asynchronous/multiple-burst model:
Periodontal destruction progresses around
the affected teeth with higher frequency
during certain periods of an individual’s
life. The bursts of activity are interspersed
with periods of inactivity or remission.
The timeline of these bursts of disease is
asynchronous for individual teeth or groups
of teeth.
CLINICAL FEATURES
CHARACTERISTICS OF
CHRONIC PERIODONTITIS (AAP, 1999)
• Most common in adults but can occur in
children and adolescents
• Amount of destruction consistent with the
amount of local factors present
• Subgingival calculus frequently found
• Associated with variable microbial pattern
• Rate of progression: Slow to moderate,
sometimes rapid exacerbations
• Can be associated with local predisposing
factors (tooth related or iatrogenic)
• May be associated with or modified by
systemic diseases (diabetes, etc.)
• May be associated with or modified by factors
other than systemic diseases like smoking
or stress
SYMPTOMS (WHAT THE PATIENT TELLS)
• Gingival bleeding while brushing or eating
• Spaces between teeth
• Elongated teeth
• Loose teeth
• Food impaction
• Sensitivity to hot and cold (dentinal
hypersensitivity due to root exposure)
• Usually painless but sometimes the patient
may complain of localized dull pain radiating
deep into the jaw*
• Gingival itching
• Bad breath
SIGNS (WHAT A DENTIST SEES)
• Supragingival and subgingival plaque and
calculus
• Clinical attachment loss resulting in either
pocket formation or recession
• Loss of alveolar bone: Horizontal or vertical
bone loss may be present
• Occasional suppuration or inflammatory
exudate from pockets present