1. 9/12/2011
Year 2
Lecture 1
GINGIVITIS
11-9-2011 Classification of gingivitis- lecture 1 1
GINGIVITIS
Module Introduction
In Module 1, you gained an insight into the form and function of the
periodontal tissues. The natural defence mechanisms of the gingival
tissues were described and the role of commensal bacteria explained. It
is assumed that you will carry forward this knowledge and build upon
it, as more of the Modules in periodontics are presented.
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2. 9/12/2011
Review of aspects of Module 1
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Sequence of developing gingivitis
 Increased gingival crevicular fluid flow
 Bleeding on probing
 Colour change
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 Changed gingival contours
 Retractability of the gingival tissues
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GINGIVITIS
When you have completed Module 2, you are expected to
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be able to:
♦ Describe the anatomy and physiology of the gingival tissues in detail.
♦ Understanding the microbiology, etiology and pathogenesis of chronic gingivitis
♦ Have an overview of the many different gingival diseases and conditions.
♦ Be able to recognise chronic and acute forms of gingivitis and know the
appropriate treatment for these conditions
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♦ Understand the medical conditions that can cause modified/exaggerated
gingival responses to dental biofilm.
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GINGIVITIS
Gingival health represents a
balance between biofilm and
host resistance factors.
Gingivitis most often occurs
as a CHRONIC disease and is
present over many
years/decades. It is
reversible, meaning that
gingiva can return to clinical
and histological health when
biofilm and calculus is
removed.
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GINGIVITIS
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Gingival Diseases
 These diseases may occur on a periodontium with no
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attachment loss or on a periodontium with attachment loss
that is stable and not progressing.
I. Gingivitis associated with dental plaque
only
II. Non‐plaque‐Induced Gingival Lesions
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Dental Plaque‐Induced Gingival Diseases
 Gingivitis has been previously characterized by the presence of
clinical signs of inflammation that are confined to the gingiva and
associated with teeth showing no attachment loss.
 It has been concluded that plaque‐induced gingivitis may occur on a
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periodontium with no attachment loss or on a periodontium with
previous attachment loss that is stable and not progressing.
I. Gingivitis associated with dental plaque only
II. Gingival diseases modified by systemic factors
III. Gingival diseases modified by medications
IV. Gingival diseases modified by malnutrition
IV Gingival diseases modified by malnutrition
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Gingivitis
Non‐specific Inflammation
Response
of the gingival tissues towards a
Non‐specific Plaque Challenge
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The most common type
of gingivitis is
 Plaque induced gingivitis
caused by biofilm.
 Chronic’ means that
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gingivitis is present
for a long time… usually
years or decades.
 Plaque induced gingivitis
caused by biofilm
 Plaque induced gingivitis is
the most common
periodontal disease you will
be treating.
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I. Gingivitis associated with dental plaque only:
I Gingivitis associated with dental plaque only:
A. Without local contributing factors
B. With local contributing factors
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B. With local contributing factors
 Local factors that may contribute to gingivitis, in addition to
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plaque‐retentive calculus formation on crown and root
surfaces.
 Localized tooth‐Related Factors That can differ or
Predispose to Plaque‐Induced Gingival Diseases
1. Tooth anatomic factors
2. Dental restorations or appliances
3. Root fractures
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4. Cervical root resorption and cemental tears
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II. Gingival diseases modified by systemic factors
A. Associated with endocrine system
1. Puberty‐associated gingivitis
2. Menstrual cycle–associated gingivitis
3. Pregnancy associated
a. Gingivitis
b. Pyogenic granuloma
4. Diabetes mellitus–associated gingivitis
B. Associated with blood dyscrasias
B Associated ith blood d scrasias
1. Leukemia‐associated gingivitis
2. Other
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 Plaque‐induced gingival
disease is the result of an
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inter‐action between the
microorganisms found in
the dental plaque biofilm
and the tissues and
inflarnmatory cells of the
host.
 Modified by factors which
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can influence the severity
and duration of the
response:
 Systemic factors.
 Medications
 Malnutrition.
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 Systemic factors contributing to gingivitis, such as the
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endocrine changes associated with puberty, the menstrual
cycle, pregnancy, and diabetes, may be exacerbated
because of alterations in the gingival inflammatory response
to plaque.
• This altered response appears to result from the effects of
systemic conditions on the host's cellular and immunologic
functions.
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Puberty‐associated gingivitis
 The incidence of marginal gingivitis
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peaks at 11 to 13 years of age, then
decreases slightly after puberty.
 The most frequent manifestations in
adolescents is bleeding and
inflammation in the interproximal
areas. This is usually the result of
hormonal changes that magnify the
tissue inflammatory response to
dental plaque.
 It occurs in both males and females
and reduces in severity after puberty,
it resolves as the person matures.
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Gingival Disease in Pregnancy
 Pronounced ease of
bleeding is the most
striking clinical feature.
 The gingiva is inflamed
and varies in color from a
bright red to bluish
 The marginal and
interdental i i
i t d t l gingiva are
edematous, pit on
pressure, appear smooth ,
shiny and are soft.
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 The extreme redness results
from marked vascularity, and
there is an increased tendency to
bleed.
 Gingivitis in pregnancy is caused
by bacterial plaque, just as it is
in nonpregnant women.
 Pregnancy accentuates the
gingival response to plaque and
modifies the resultant clinical
picture .
 Pregnancy affects the severity of
previously inflamed areas; it
does not alter healthy gingiva.
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10. 9/12/2011
Tumor‐like Gingival Enlargement
 The so‐called pregnancy
tumor is not a neoplasm; it
is an inflammatory response
to bacterial plaque and is
modified by the patient's
condition.
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Diabetes mellitus–associated gingivitis
Gingivitis caused by biofilm, modified by poorly
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controlled diabetes
Diabetes may be first picked up by the oral health
practitioner because of the unusual response of the
gingival tissues to plaque.
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 The most striking
changes in
uncontrolled diabetes
are the reduction in
defense mechanisms
and the increased
susceptibility to
infections, leading to
destructive periodontal
disease.
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Diabetes: What to look for?
 Severe gingival
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inflammation
 Deep periodontal
pockets,
 Rapid bone loss,
 Frequent periodontal
abscesses.
 Slow resolution of
gingivitis after
conventional
treatment.
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 Blood dyscrasias such as leukemia may alter immune function
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by disturbing the normal balance of immunologically
competent white blood cells supplying the periodontium.
Gingival enlargement and bleeding are common findings and
may be associated with swollen, spongy gingival tissues caused
by excessive infiltration of blood cells.
Classification of gingivitis- lecture 1 slide 23
III. Gingival Diseases Modified by
Medications
A. Drug influenced gingival diseases
A. Drug‐influenced gingival diseases
1. Drug‐influenced gingival enlargements
2. Drug‐influenced gingivitis
a. Oral contraceptive–associated gingivitis
b. Other.
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 Gingival diseases modified by medications are increasingly
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prevalent because of the increased use of anti‐convulsant
drugs known to induce gingival enlargement, such as phenytoin,
immunosuppressive drugs such as cyclosporine , and calcium
channel blockers such as nifedipine.
 The development and severity of gingival enlargement in
response to medications are patient specific and may be
influenced by uncontrolled plaque accumulation.
 The increased use of oral contraceptives by premenopausal
women has been associated with a higher incidence of gingival
inflammation and development of gingival enlargement, which
may be reversed by discontinuation of the oral contraceptive
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Phenytoin
 Anticonvulsant drug used in
the treatment of epilepsy.
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14. 9/12/2011
Cyclosporine
 Potent immunosuppresive
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drug used to prevent organ
rejection following
transplantation.
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Nifedipine
 Are drugs developed to treat
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several cardiac diseases such as
hypertension, angina pectoris,
coronary artery spasms.
 In patients of Kidney transplant it
is used in combination of both
Cyclosporin and nifedipine
leading to larger enlargements of
the gingiva.
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IV. Gingival diseases modified by
malnutrition
A. Ascorbic acid deficiency gingivitis
B. Others.
 Gingival diseases modified by malnutrition have
received attention because of clinical
descriptions of bright‐red, swollen, and bleeding
gingiva associated with severe ascorbic acid (
vitamin C) deficiency or scurvy.
 Nutritional deficiencies are known to affect
immune function and may affect the host s ability
immune function and may affect the host's ability
to protect itself against some of the detrimental
effects of cellular products, such as oxygen
radicals.
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Non—Plaque‐Induced Gingival Lesions
I. Gingival diseases of specific bacterial origin
II. Gingival diseases of viral origin
III. Gingival diseases of fungal origin
IV. Gingival lesions of genetic origin
V. Gingival manifestations of systemic conditions
VI. Traumatic lesions (factitious, iatrogenic, or
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accidental)
VII. Foreign body reactions
VIII. Not otherwise specified Gingival Diseases
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I. Gingival Diseases of Specific Bacterial
Origin
A. Neisseria gonorrhoeae
B. Treponema pallidum
B Treponema pallidum
C. Streptococcus species
D. Other
 Gingival diseases of specific bacterial origin are increasing in prevalence,
especially as a result of sexually transmitted diseases such as gonorrhea
(Neisseria gonarrhoeae) and to a lesser degree, syphilis (Treponenra
pallidum).’
 Oral lesions may be secondary to systemic infection or may occur
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through direct infection. Streptococcal gingivitis or gingivostomatitis is
a rare condition that may present as an acute condition with fever,
malaise, and pain associated with acutely inflamed, diffuse, red, and
swollen gingiva with increased bleeding and occasional gingival abscess
formation.
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II. Gingival diseases of viral origin
A. Herpesvirus infections
1. Primary herpetic gingivostomatitis
2. Recurrent oralherpes
2 Recurrent oralherpes
3. Varicella zoster
B. Other.
Gingival diseases of viral origin may be caused by a
variety of deoxyribonucleic acid (DNA) and
ribonucleic acid (RNA) viruses, the most common
being the herpesviruses. Lesions are frequently
b i h h i L i f l
related to reactivation of latent viruses, especially as
a result of reduced immune function.
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Types of gingivitis
Acute gingivitis Acute
 Viral gingivitis
• Viral
Herpes virus-induced gingivitis
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III. Gingival diseases of fungal origin
A. Candida species infections: generalized gingival
A Candida species infections: generalized gingival
candidiasis
B. Linear gingival erythema
C. Histoplasmosis
D. Other
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Types of gingivitis
•Auto-
immune
•not
biofilm-
biofilm
related
Lichen Planus
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IV. Gingival lesions of genetic origin
A. Hereditary gingival fibromatosis
A Hereditary gingival fibromatosis
B. Other.
 Gingival diseases of genetic origin may involve the tissues of the
periodontium. One of the most clinically evident conditions is hereditary
gingival fibromatosis, which exhibits autosomal dominant or (rarely)
autosomal recessive modes of inheritance. The gingival enlargement may
completely cover the teeth, delay eruption, and present as an isolated finding
or may be associated with several more generalized syndromes.
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V. Gingival manifestations of systemic conditions
A. Mucocutaneous lesions B. Allergic reactions
1. Lichen planus
1 Lichen planus 1. Dental restorative materials
1 Dental restorative materials
2. Pemphigoid a. Mercury
3. Pemphigus vulgaris b. Nickel
4. Erythema multiforme c. Acrylic
5. Lupus erythematosus d. Other
6. Drug induced 2. Reactions attributable to:
7. Other a. Toothpastes or dentifrices
b. Mouth rinses or mouthwashes
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c. Chewing gum additives
d. Foods and additives
3. Other.
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 Gingival manifestations of systemic conditions may appear
as desquamative lesions, ulceration of the gingiva, or both.
 Allergic reactions that manifest with gingival changes
are uncommon but have been observed in association with
several restorative materials, tooth‐pastes, mouthwashes,
chewing gum, and foods .
Classification of gingivitis- lecture 1 slide 39
Non plaque‐induced gingival lesions
VI. Traumatic lesions (factitious, iatrogenic, or accidental)
A. Chemical injury
B. Physical injury
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C. Thermal injury
 Traumatic lesions may be factitious (produced by artificial
means; unintentionally produced), as in the case of
toothbrush trauma resulting in gingival ulceration, recession,
or both; iatrogenic (trauma to the gingiva induced by
the dentist or health professional), as in the case of
preventive or restorative care that may lead to traumatic
injury of the gingiva; or accidental, as in the case of
damage to the gingiva through minor burns from hot foods
And drinks.
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VII. Foreign body reactions
 Foreign body reactions lead to localized inflammatory conditions of
the gingiva and are caused by the introduction of foreign material
into the gingival connective tissues through breaks in the epithelium.
 Common examples are the introduction of amalgam into the gingiva
during the placement of a restoration or extraction of a tooth, leaving
an amalgam tattoo, or the introduction of abrasives during polishing
procedures.
VIII. Not otherwise specified
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