GINGIVAL DISEASES
Dental Plaque-Induced Gingival Diseases

Gingivitis that is associated with dental plaque formation' is
the most common form of gingival disease characterized by
the presence of clinical signs of inflammation that are
confined to the gingiva and associated with teeth showing no
attachment loss
Gingivitis associated with Dental Plaque Only:

     is the result of an interaction between the microorganisms
     found in the dental plaque biofilm and the tissues and
     inflammatory cells of the host.
                   The plaque-host interaction can
                     be altered by the effects of

*Local factors

                 *Systemic Factors

                                     *Medications

                                                     *Malnutrition
Gingival Diseases Modified by Systemic Factors

*endocrine changes

*leukemia

 gingival enlargement

                        bleeding

                                   swollen, spongy
Gingival Diseases Modified by Medications

anticonvulsant drugs            phenytoin

 immunosuppressive              cyclosporine
      drugs
 calcium channel                 nifedipine
     blockers
Oral contraceptive pills
Gingival Diseases Modified by Malnutrition


                                    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 have an impact on the
host's ability to protect itself
against some of the detrimental
effects of cellular products such
as oxygen radicals.
Non-Plaque-Induced Gingival Lesions
They are observed in lower socioeconomic groups, developing
countries, and immunocompromised individuals
Gingival Diseases of Specific Bacterial Origin:

                            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.

preceded by tonsillitis and have been associated with group
A hemolytic streptococcal infections.
Gingival Diseases of Viral Origin:


                 the most common being the herpes
                 viruses-Primary herpetic
                 gingivostomatitis Clinically appear
                 as: Multiple tiny vesicles that
                 progress to form painful ulcers.
                 Painful erythematous swollen
                 gingival. Fever, malaise, cervical
                 lymphadenopathy.
Gingival Diseases of Fungal Origin:


       under prosthetic devices

                   in individuals using topical steroids


in individuals with decreased salivary flow


                     increased salivary glucose

              decreased salivary pH.
A generalized candidal infection may manifest as white patches on
the gingiva, tongue or oral mucous membrane that can be
removed with gauze, leaving a red, bleeding surface.



In HIV-infected individuals,
candidal infection may present
as erythema of the attached
gingiva and has been referred
to as linear gingival erythema
or HIV-associated gingivitis


Diagnosis of candidal infection can be made by culture, smear.
Gingival Diseases of Genetic Origin:


hereditary gingival fibromatosis
that 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 be
associated with several more
generalized syndromes.
Traumatic Lesions:

    factitial               iatrogenic       accidental

as in the case of        as in the case of   as in the case of
tooth brush trauma       preventive or       damage to the
resulting in gingival    restorative care    gingiva through
ulceration,              that may lead to    minor burns from hot
recession both;          traumatic injury    foods and drinks.
                         of the gingiva
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.
PERIODONTITIS

   Periodontitis is defined as "an inflammatory disease of the
supporting tissues of the teeth caused by specific
microorganisms or groups of specific microorganisms,
resulting in progressive destruction of the periodontal
ligament and alveolar bone with pocket formation, recession,
or both." The clinical feature that distinguishes periodontitis
from gingivitis is the presence of clinically detectable
attachment loss.
Chronic Periodontitis

Chronic periodontitis is the most common form of periodontitis
Chronic periodontitis is most prevalent in adults but can be
observed in children therefore the age range of >35 years
previously designated for the classification of this disease has
been discarded. Chronic periodontitis is associated with the
accumulation of plaque and calculus and generally has a slow to
moderate rate of disease progression
Local factors may influence plaque accumulation systemic diseases
such as diabetes mellitus and HIV infection may influence the host
defenses; environmental factors such as cigarette smoking and stress
also may influence the response of the host to plaque accumulation

 Chronic periodontitis may occur as a
localized disease wherein <30% of
evaluated sites demonstrate
attachment and bone loss, or as a
more generalized disease wherein
>30% of sites are affected. The disease
also may be described by the severity
of disease as slight, moderate, or
severe based on the amount of clinical
attachment loss.
Aggressive Periodontitis
   Aggressive periodontitis differs from the chronic form primarily
  by the rapid rate of disease progression seen in an otherwise
  healthy individual, an absence of large accumulations of plaque
  and calculus, and a family history of aggressive disease
  suggestive of a genetic trait.

early onset periodontitis
usually affect young individuals at
or after puberty and may be
observed during the second and
third decade of life (i.e., 10 to 30
years of age). The disease may be
localized (LJP) or generalized
(GJP)
NECROTIZING PERIODONTAL DISEASES

Necrotizing Ulcerative Gingivitis
   Clinical features of necrotizing periodontal disease may
include necrosis and/or punched out ulceration of the
interdental papillae ("punched-out papillae") or gingival
margin, pseudomembranous formation painful, bright red
marginal gingiva that bleed upon gentle manipulation,
halitosis
Treatment
*irrigation
*and debridement of necrotic areas
oral hygiene instruction and the •
uses of mouth rinses
* pain medication. •
* As these diseases are often •
associated with systemic medical
issues, proper management of
the systemic disorders is
appropriate
Necrotizing Ulcerative Periodontitis

NUP" differs from NUG in that loss of clinical attachment and
alveolar bone is a consistent feature.

Several case reports have
described extensive destruction
leading to exfoliation of teeth
within 3-6 months of onset, with
sequestration of necrotic alveolar
bone and necrotic involvement of
the adjacent mandible and
maxilla. Patients may present
with concomitant malnutrition
resulting from inability to take
food by mouth.
Treatment
*Removal of plaque and debris from the site of
infection and inflammation
* Debridement of necrotic hard and soft tissues
*Chlorhexidine gluconate rinse (0.12%) twice daily after
brushing and flossing
*Antibiotic therapy Metronidazole is the drug of choice,
500 mg for 7-10 days.
PERIODONTITIS ASSOCIATED WITH ENDODONTIC
LESIONS
Endodontic-Periodontal Lesions
In endodontic-periodontal lesions, pulpal necrosis precedes
periodontal changes. A periapical lesion originating from
pulpal infection and necrosis may drain to the oral cavity
through the periodontal ligament, resulting in destruction of
the periodontal ligament and adjacen alveolar bone. This
may present clinically as a localized deep, periodontal pocket
extending to the apex of the tooth. Pulpal infection also may
drain through accessory canals, especially in the area of the
furcation, and may lead to furcal involvement through loss of
clinical attachment and alveolar bone.
Periodontal-Endodontic Lesions

  In periodontal-endodontic lesions, bacterial infection from a
periodontal pocket associated with loss of attachment and root
exposure may spread through accessory canals to the pulp,
resulting in pulpal necrosis. In the case of advanced periodontal
disease, the infection may reach the pulp through the apical
foramen.

Scaling and root planing removes cementum and underlying
dentin and may lead to chronic pulpitis through bacterial
penetration of dentinal tubules.
Combined Lesions

   Combined lesions occur when pulpal necrosis and a
periapical lesion occur on a tooth that also is periodontally
involved. A radiographically evident infrabony defect is seen
when infection of pulpal origin merges with infection of
periodontal origin
Diagnostic Methods

*Initially a detailed medical and dental history must be obtained
from the patient.
*The clinical examination should include inspection of the
gingival and mucosal tissues, palpation, mobility testing,
percussion
*Periodontal probing is essential to identify and determine the
depth of periodontal pockets and the degree of loss of
attachment.
*Pulp testing should be carried out with both carbon dioxide (dry
ice) and an electric pulp tester
*Radiographs are an essential tool to the diagnosis of any
endodontic or periodontal condition.
Treatment

 periodontal disease
 *scaling
 *root planing
 *oral hygiene instructions follow-up
 maintenance therapy, including surgery in
 some cases.

Diseased pulp tissue or infected root canals
*cleaning
* shaping
* medicating
* filling of the root canal system
DEVELOPMENTAL OR ACQUIRED DEFORMITIES AND
CONDITIONS
 Tooth Anatomic Factors
 Anatomic factors such as
 * cervical enamel projections and
 enamel pearls have been associated with clinical attachment loss, especially in
 furcation areas.
 *Palatogingival grooves, found primarily on maxillary incisors
 * Proximal root grooves on incisors and maxillary premolars




                                                  Cervical enamel
                                                     projection
Enamel pearl
Dental Restorations or Appliances


  Dental restorations or appliances are frequently associated
with the development of gingival inflammation, especially
when they are located subgingivally. This may apply to
subgingivally placed onlays, crowns, fillings and orthodontic
bands.
Root Fractures

Root fractures caused by traumatic forces or restorative or
endodontic procedures may lead to periodontal involvement


Cervical Root Resorption and Cemental Tears
  Cervical root resorption and
cemental tears may lead to
periodontal destruction when the
lesion communicates with the oral
cavity and allows bacteria to
migrate subgingivally
Classification of disseases

Classification of disseases

  • 2.
    GINGIVAL DISEASES Dental Plaque-InducedGingival Diseases Gingivitis that is associated with dental plaque formation' is the most common form of gingival disease characterized by the presence of clinical signs of inflammation that are confined to the gingiva and associated with teeth showing no attachment loss
  • 3.
    Gingivitis associated withDental Plaque Only: is the result of an interaction between the microorganisms found in the dental plaque biofilm and the tissues and inflammatory cells of the host. The plaque-host interaction can be altered by the effects of *Local factors *Systemic Factors *Medications *Malnutrition
  • 4.
    Gingival Diseases Modifiedby Systemic Factors *endocrine changes *leukemia gingival enlargement bleeding swollen, spongy
  • 5.
    Gingival Diseases Modifiedby Medications anticonvulsant drugs phenytoin immunosuppressive cyclosporine drugs calcium channel nifedipine blockers
  • 6.
  • 7.
    Gingival Diseases Modifiedby Malnutrition 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 have an impact on the host's ability to protect itself against some of the detrimental effects of cellular products such as oxygen radicals.
  • 8.
    Non-Plaque-Induced Gingival Lesions Theyare observed in lower socioeconomic groups, developing countries, and immunocompromised individuals
  • 9.
    Gingival Diseases ofSpecific Bacterial Origin: 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. preceded by tonsillitis and have been associated with group A hemolytic streptococcal infections.
  • 10.
    Gingival Diseases ofViral Origin: the most common being the herpes viruses-Primary herpetic gingivostomatitis Clinically appear as: Multiple tiny vesicles that progress to form painful ulcers. Painful erythematous swollen gingival. Fever, malaise, cervical lymphadenopathy.
  • 11.
    Gingival Diseases ofFungal Origin: under prosthetic devices in individuals using topical steroids in individuals with decreased salivary flow increased salivary glucose decreased salivary pH.
  • 12.
    A generalized candidalinfection may manifest as white patches on the gingiva, tongue or oral mucous membrane that can be removed with gauze, leaving a red, bleeding surface. In HIV-infected individuals, candidal infection may present as erythema of the attached gingiva and has been referred to as linear gingival erythema or HIV-associated gingivitis Diagnosis of candidal infection can be made by culture, smear.
  • 13.
    Gingival Diseases ofGenetic Origin: hereditary gingival fibromatosis that 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 be associated with several more generalized syndromes.
  • 14.
    Traumatic Lesions: factitial iatrogenic accidental as in the case of as in the case of as in the case of tooth brush trauma preventive or damage to the resulting in gingival restorative care gingiva through ulceration, that may lead to minor burns from hot recession both; traumatic injury foods and drinks. of the gingiva
  • 15.
    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.
  • 16.
    PERIODONTITIS Periodontitis is defined as "an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both." The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically detectable attachment loss.
  • 17.
    Chronic Periodontitis Chronic periodontitisis the most common form of periodontitis Chronic periodontitis is most prevalent in adults but can be observed in children therefore the age range of >35 years previously designated for the classification of this disease has been discarded. Chronic periodontitis is associated with the accumulation of plaque and calculus and generally has a slow to moderate rate of disease progression
  • 18.
    Local factors mayinfluence plaque accumulation systemic diseases such as diabetes mellitus and HIV infection may influence the host defenses; environmental factors such as cigarette smoking and stress also may influence the response of the host to plaque accumulation Chronic periodontitis may occur as a localized disease wherein <30% of evaluated sites demonstrate attachment and bone loss, or as a more generalized disease wherein >30% of sites are affected. The disease also may be described by the severity of disease as slight, moderate, or severe based on the amount of clinical attachment loss.
  • 19.
    Aggressive Periodontitis Aggressive periodontitis differs from the chronic form primarily by the rapid rate of disease progression seen in an otherwise healthy individual, an absence of large accumulations of plaque and calculus, and a family history of aggressive disease suggestive of a genetic trait. early onset periodontitis usually affect young individuals at or after puberty and may be observed during the second and third decade of life (i.e., 10 to 30 years of age). The disease may be localized (LJP) or generalized (GJP)
  • 20.
    NECROTIZING PERIODONTAL DISEASES NecrotizingUlcerative Gingivitis Clinical features of necrotizing periodontal disease may include necrosis and/or punched out ulceration of the interdental papillae ("punched-out papillae") or gingival margin, pseudomembranous formation painful, bright red marginal gingiva that bleed upon gentle manipulation, halitosis
  • 21.
    Treatment *irrigation *and debridement ofnecrotic areas oral hygiene instruction and the • uses of mouth rinses * pain medication. • * As these diseases are often • associated with systemic medical issues, proper management of the systemic disorders is appropriate
  • 22.
    Necrotizing Ulcerative Periodontitis NUP"differs from NUG in that loss of clinical attachment and alveolar bone is a consistent feature. Several case reports have described extensive destruction leading to exfoliation of teeth within 3-6 months of onset, with sequestration of necrotic alveolar bone and necrotic involvement of the adjacent mandible and maxilla. Patients may present with concomitant malnutrition resulting from inability to take food by mouth.
  • 23.
    Treatment *Removal of plaqueand debris from the site of infection and inflammation * Debridement of necrotic hard and soft tissues *Chlorhexidine gluconate rinse (0.12%) twice daily after brushing and flossing *Antibiotic therapy Metronidazole is the drug of choice, 500 mg for 7-10 days.
  • 24.
    PERIODONTITIS ASSOCIATED WITHENDODONTIC LESIONS Endodontic-Periodontal Lesions In endodontic-periodontal lesions, pulpal necrosis precedes periodontal changes. A periapical lesion originating from pulpal infection and necrosis may drain to the oral cavity through the periodontal ligament, resulting in destruction of the periodontal ligament and adjacen alveolar bone. This may present clinically as a localized deep, periodontal pocket extending to the apex of the tooth. Pulpal infection also may drain through accessory canals, especially in the area of the furcation, and may lead to furcal involvement through loss of clinical attachment and alveolar bone.
  • 25.
    Periodontal-Endodontic Lesions In periodontal-endodontic lesions, bacterial infection from a periodontal pocket associated with loss of attachment and root exposure may spread through accessory canals to the pulp, resulting in pulpal necrosis. In the case of advanced periodontal disease, the infection may reach the pulp through the apical foramen. Scaling and root planing removes cementum and underlying dentin and may lead to chronic pulpitis through bacterial penetration of dentinal tubules.
  • 26.
    Combined Lesions Combined lesions occur when pulpal necrosis and a periapical lesion occur on a tooth that also is periodontally involved. A radiographically evident infrabony defect is seen when infection of pulpal origin merges with infection of periodontal origin
  • 27.
    Diagnostic Methods *Initially adetailed medical and dental history must be obtained from the patient. *The clinical examination should include inspection of the gingival and mucosal tissues, palpation, mobility testing, percussion *Periodontal probing is essential to identify and determine the depth of periodontal pockets and the degree of loss of attachment. *Pulp testing should be carried out with both carbon dioxide (dry ice) and an electric pulp tester *Radiographs are an essential tool to the diagnosis of any endodontic or periodontal condition.
  • 28.
    Treatment periodontal disease *scaling *root planing *oral hygiene instructions follow-up maintenance therapy, including surgery in some cases. Diseased pulp tissue or infected root canals *cleaning * shaping * medicating * filling of the root canal system
  • 29.
    DEVELOPMENTAL OR ACQUIREDDEFORMITIES AND CONDITIONS Tooth Anatomic Factors Anatomic factors such as * cervical enamel projections and enamel pearls have been associated with clinical attachment loss, especially in furcation areas. *Palatogingival grooves, found primarily on maxillary incisors * Proximal root grooves on incisors and maxillary premolars Cervical enamel projection Enamel pearl
  • 30.
    Dental Restorations orAppliances Dental restorations or appliances are frequently associated with the development of gingival inflammation, especially when they are located subgingivally. This may apply to subgingivally placed onlays, crowns, fillings and orthodontic bands.
  • 31.
    Root Fractures Root fracturescaused by traumatic forces or restorative or endodontic procedures may lead to periodontal involvement Cervical Root Resorption and Cemental Tears Cervical root resorption and cemental tears may lead to periodontal destruction when the lesion communicates with the oral cavity and allows bacteria to migrate subgingivally