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THE NORMAL PERIODONTIUM
 Consists of investing and supporting tissues of the
tooth
 Gingiva
 Periodontal ligament
 Alveolar Bone
 Cementum
 It is divided into two parts:
 The gingiva whose main function is protection of the
underlying tissues
 The attachment apparatus, composed of the periodontal
ligament , cementum and alveolar bone
Normal Periodontium
Types of gingivitis
Depending on course and duration
 Acute gingivitis: is of sudden onset and short
duration and can be painful
 Subacute: is less severe than acute
 Recurrent : reappears after treatment
 Chronic gingivitis: slow in onset, long
duration, usually painless and the most
common
Depending on distribution
 Localized or generalized : a group of teeth or
entire mouth
 Marginal : limited to the marginal gingiva
 Papillary : limited to the interdental papilla
 Diffuse : when the inflammation spreads to
the attached gingiva
OTHER GINGIVALINFECTIONS
Acute lesions of sudden onset, limited duration and well-defined
clinical features.
 Traumatic lesions, both physical and chemical
 Viral infections
 Bacterial infections
 Fungal infections
 Gingival abscess
 Aphthous ulcers
 Erythema multiforme
 Drug allergy
Traumatic lesions
Physical injury
 Mechanical or thermal
 Chemical damage
Asprin burn
Silver nitrate
Hydrogen peroxide
Careless use of caustics by dentist e.g. chlorophenol, tetra
acetic acid
–Asprin burn
Traumatic injuries
 The diagnosis is easy since the patient is
usually aware of the accident and suffers from
immediate and severe pain.
 A localized area of inflammation and
ulceration may form.
 Healing of traumatic lesions is fairly quick and begins
with epithelium covering the ulcer. Does not need
active treatment
 Healing can be complicated by secondary infection.
This may be accompanied by lymph gland
enlargement and malaise, then an antibiotic may be
needed.
Viral infections
 Acute herpetic gingivostomatitis
 Herpangina
 Hand foot and mouth disease
 Measles
 Herpes varicella/zoster virus infections
 Glandular fever
 HIV infection and AIDS
Acute herpetic gingivostomatitis
 Primary infection by the herpes simplex
virus type 1.
 Usually occurs in children (1-10) but may
affect older children or even adults
 Infection in neonates can produce
encephalitis or meningitis
 In children or adults it produces a febrile
illness or subclinical infection
 Incubation period is 5 days
CONT.
 Symptoms appear abruptly with fever and
temperatures as high as 39.4 C
 Lymph gland enlargement, malaise and the mouth and
throat may be painful
 Irritability in children, refusal to eat and increase
salivation
 Small vesicles form on the gingivae, tongue, buccal
mucosa and lips
 Vesicles burst and form round or irregular ulcers with
grey membrane and surrounded by a red mucosa
 There is acute gingivitis with redness swelling and
bleeding
Herpetic gingivostomatitis
 Symptoms subside in
10-21 days
 About 30% of patients
develop recurrent
infections later in life.
 The recurrence is
usually herpes labialis
and it is a reactivation
of the latent virus in
the trigeminal ganglion
Herpes labialis
Treatment
 Symptomatic and supportive
 In infants, milk of magnesia
 Benzocaine lozenges are useful in the older child
 Aspirin or paracetamol
 Phenergan a sedative in the child
 In severe cases acyclovir tabs 200mg four times daily or
suspension 5ml four times daily
 Acyclovir cream can be used as a preventive measure
Hand, foot and mouth disease
 Acute febrile illness
 Coxsackie virus A type 16
 Sporadic outbreak affecting mainly children
 Maculopapular and vesicular lesions appear on
the skin and oral mucosa
 Skin lesions affect the hands, arms and feet
 The oral vesicles break into ulcers
 Uneventful recovery in 10-14 days
Measles
 Severe febrile illness affecting mainly children
 Presents with fever, malaise, cough, conjunctivitis,
photophobia and lacrimation
 Blotchy macular rash
 Oral lesions present as Koplik’s spots which are
bluish-white specks surrounded by a bright red
margin on the buccal mucosa mainly
 Oral lesions precede skin lesions by a few days.
 Recovery in 2-3 weeks in healthy, fit well fed
children
 Can be serious in poor and malnourished
previously unexposed children
 Vaccination is available against measles
Herpes varicella/zoster virus infections
 Varicella or chickenpox is an acute febrile illness mainly
in children
 Widespread maculopapular or vesicular eruptions on the
skin
 Small vesicles also form on the oral mucosa, tongue and
gingival
 Recovery in 2-3 weeks
 Herpes zoster or shingles is caused by
reactivation of latent varicella virus and
common in older adults.
 Affects sensory nerves and produces severe
neuralgia
 Vesicular eruptions on the skin or mucosa
innervated by the affected sensory nerve
Herpes zoster
BACTERIAL INFECTIONS
 Acute necrotizing ulcerative gingivitis
(NUG)
 Tuberculosis
 syphilis
Necrotizing Ulcerative
Gingivitis
Syphilis
Secondary syphilis occurs 6 weeks after primary
infection and produces skin rash and oral eruption. The
ulcers are either mucous patches or snail track
Acute Gingival Abscess
GINGIVALABSCESS
 Abscess formation may follow damage by toothpick
or fish bone if the foreign object is not removed.
 Gingival abscess associated with physical damage
 can also arise from wall of a gingival pocket
where drainage has been impeded
 localized shiny, painful, red swelling and
associated teeth TTP
 may drain spontaneously or require the removal
of foreign object
 hot salt water mouthwashes and antibiotics if
systemic involvement
Aphthous ulcers
 Most common type of recurrent ulcerative condition
 Possible defect of cell-mediated immune response
 painful lesions which appear without any reason, last for
several days to heal and, after sometime recur
 Cause unknown but may be auto-immunity to a
component of the oral mucosa.
 Related factors may be stress and hormonal changes
 In some patients related to the menstrual cycle
 Relationship between ulceration, iron-deficiency anaemia,
folic acid deficiency and Vitamin B12
Three types
 minor aphthous ulcers,
 major aphthous ulcers
 herpetiform ulcers
MINOR APHTHOUS ULCERS
Clinical features
 Well circumscribed white-yellow round lesion with red margin
 Usually less than 5 mm in size
 Affects non-keratinized oral mucosa
 Moderate to severe pain
 Heals without scarring within 7 to 10 days
 Affected patients report a history of aphthous ulcers usually for “as
long as they can remember”
Management
 Inquire about type of toothpaste used SLS (sodium
lauryl sulphate)-containing toothpastes may
aggravate condition)
 Discontinue any SLS-containing toothpaste for
1month.
 Discontinue use of any mouthwash
 Rx topical steroid (e.g., fluocinonide, clobetasol) to
be applied tid as soon as prodromal Symptoms occur
(may reduce duration of ulcer by half)
 Always instruct patient to come back if ulcer not
healed after 3 weeks
MAJORAPHTHOUS ULCERS
Clinical features
 Larger, more severe, less common than minor
 Ulcers 10 to 30 mm in diameter
 Extremely painful, heals with scarring within weeks or even
months
 Affected patients report a history of aphthous ulcers usually
for “as long as they can remember”
 Major “aphthous-like”ulcers occur among immunosuppressed
patients (HIV+; transplant recipients) with no prior history of
aphthous ulcers
MANAGEMENT
Topical steroids:
 Fluocinonide ointment 0.05% mixed 1/1
with orabase B(apply tid)
 Clobetasol ointment 0.05% mixed 1/1 with orabase
B(apply tid)
 Tablets of hydrocortisone
 Treatment topical anaesthetics
 Antibacterial rinses to clear secondary bacterial
infection,
 Tetracycline caps (250mg): dissolve in 1 Tbsp water,
then rinse for 1 minute + expectorate qid
Copyright © 2003, Elsevier Science (USA). All rights reserved.
56
Periodontitis
Defined as:-
“an inflammatory disease of the supporting
tissues of the teeth caused by specific micro-
organisms resulting in progressive
destruction of the periodontal ligament and
alveolar bone with pocket formation,
recession, or both”
Periodontitis
 Chronic periodontitis
 Aggressive periodontitis
 Periodontitis as a manifestation of systemic
diseases
Chronic Periodontitis
 Prevalent in adults but can occur in children
 Amount of destruction consistent with local
factors
 Associated with variable microbial pattern
 Subgingival calculus frequently found
 Slow to moderate rate of progression with
possible periods of rapid progression
 Possibly modified by: systemic factors such as
diabetes and HIV; local factors: enviromental
factors such as smoking and emotional stress
 Localized or generalized
 Slight – 1-2mm of clinical attachment loss
 Moderate – 3-4mm CAL
 Severe - ≥ 5mm CAL
Chronic periodontitis
Aggressive periodontitis
 Otherwise clinically healthy patient
 Rapid attachment loss and bone
destruction
 A/o microbial deposits inconsistent with
disease severity
 Familial aggregation of diseased individuals
Localized form
 Circumpubertal onset of disease
 Localized to first molars or incisors with
proximal attachment loss on at least two
permanent teeth one of which is a first molar
Generalized form
 Usually affecting persons under 30 years of
age (maybe older)
 Generalized proximal attachment loss
affecting at least three teeth other than first
molars and incisors
 Pronounced episodic nature of periodontal
destruction
 Poor serum antibody response to infecting
agents
Periodontitis as a manifestation of
systemic diseases
Haematological disorders
1. Acquired neutropenia
2. Leukaemias
3. Other Genetic disorders
a. Familial and cyclic neutropenia
b. Down syndrome
c. Leukocyte adhesion deficiency syndrome
d. Papillon-Lefevre syndrome
e. Chediak-Higashi syndrome
f. Histiocytosis syndromes
g. Glycogen storage disease
h. Infantile genetic agranulocytosis
i. Cohen syndrome
j. Ehlers-Danlos syndrome (types IV andVIIIAD)
k. Hypophosphatasia. etc
Necrotizing periodontal
diseases
 Necrotizing ulcerative gingivitis
 Necrotizing ulcerative periodontitis
Tissue necrosis is the primary clinical feature.
Necrotizing ulcerative
periodontitis
Abscesses of the
periodontium
A periodontal abscess is a localized purulent
infection of periodontal tissues and is
classified by its tissue of origin
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess
Periodontal abscess
DrugAllergy
 Can be provoked by:-
 Penicillin
 Diazepam
 Local anaesthetic
 Codeine
 Tetracycline
 Barbiturates
 Others
Drug allergy and contact hypersensitivity
 Two types:-
 Those following systemic
administration of a drug or chemical
 Those following direct contact with
the oral mucosa
 Manifestation depends on the type of allergic
response provoked, ranging from simple drying
of the mouth to the most severe response,
anaphylactic shock, which is potentially fatal.
 Hypersensitivity to drugs may involve type 1, II,
III and IV mechanisms.
Symptoms
 Burning sensation of oral mucosa, swelling,
redness of the tongue, lips and gingivae
 Peeling epithelium leaving very sore ulcerated
areas
 Gingivae, bright red and sensitive.
 Poor oral hygiene due to the sensitivity in
brushing
Contact hypersensitivity
Reactions of the oral mucosa have been reported to:-
 Chewing gum
 Toothpaste
 Mouthwashes
 Sweets
 Cosmetics
 Topical anaesthetic
 Topical antibiotics
 Periodontal dressings
 Flavouring agents e.g. peppermint, menthol cinnamon and
eugenol
Management
 Implicated substance immediately withdrawn.
 Antihistamine
 Injection of hydrocortisone hemisuccinate
 In anaphylactic shock, intramuscular injection
of 0.5ml of 1:1000 adrenaline is necessary
 Frequent warm saline rinses.
DEFINITION
 PERICORONITIS (From the Greek
peri, “around”, Latin corona “crown”
and itis, “inflammation”) also known
as operculitis, is the inflammation of
soft tissues surrounding the crown of a
partially erupted tooth, including the
gingiva (gums) and the dental follicles.
ANATOMIC RELATIONSHIP
 The occlusal surface of an involved
tooth may be partly covered by a flap of
tissue, the operculum, which exists
during the eruption of the tooth and
may persist afterwards.
 Varying degrees of eruption,
malposition, or impaction may further
complicate the soft tissue architecture
CONT…
 An accumulation of bacteria and debris beneath the operculum
 Mechanical trauma (e.g. biting the operculum with the
opposing tooth).
 Often associated with partially erupted and impacted
mandibular third molars.
 Periodontal pain.
 Pulpitis from dental caries (tooth decay).
 Acute myofascial pain in the temporomandibular joint
disorder.
CLINICAL FEATURES
 The symptoms vary based on whether the condition is acute
or chronic.
ACUTE
 Sever pain near the back teeth
 Swelling of gum tissue due to fluid accumulation
 Pain when swallowing
 The discharge of pus
CHRONIC
 Bad breath
 A bad taste in the mouth
 A mild or dull ache lasting for one or two days
 Swelling of the lymph nodes in the neck
 Infection
 Fever
 Loss of appetite
COMPLICATIONS
 The involvement may become localized in the form of
a pericoronitis abscess.
 It may spread posteriorly into the oropharyngeal area
and medially to the base of the tongue, making
swallowing difficult.
 Involvement of sub maxillary, cervical, deep cervical
and retropharyngeal lymph nodes.
CONT…
 The partially erupted or impacted mandibular
third molar is the most common site of
pericoronitis.
 The space between the crown of the tooth
and overlying gingival flap is an ideal area for
the accumulation of food debris and bacterial
growth.
 An influx of the inflammatory fluid and
cellular exudates results in an increase in the
bulk of the flap.
CONT…
 Swelling of the cheek in the region of the angle of
the jaw and lymphadenitis.
 Mandibular movement is limited (Trismus).
 Toxic systemic complications – fever, leucocytosis
and malaise.
 Foul taste and an inability to close the jaws.
 Radiating pain to the ear, throat, and floor of the
mouth.
RISK FACTORS
 Occur in young adults in their mid 20s who are
experiencing poorly erupting wisdom teeth.
 Poor oral hygiene.
 Excess gum tissue.
 Fatigue and emotional stress
TREATMENTS
Depending on the severity of the condition, the
treatment option may vary.
 Gently flush the area with warm water or antiseptic
to remove debris and exudates
 Pain management and resolving the pericoronal
inflammation and/or infection
 Antibiotics can be prescribed in severe cases.
 Minor oral surgery to remove the overlapping
gingival tissue
 Wisdom tooth or teeth removal
Questions?
THANKYOU FOR LISTENING

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5.GINGIVAL_INFECTIONS.ppt dental patholo

  • 1. THE NORMAL PERIODONTIUM  Consists of investing and supporting tissues of the tooth  Gingiva  Periodontal ligament  Alveolar Bone  Cementum  It is divided into two parts:  The gingiva whose main function is protection of the underlying tissues  The attachment apparatus, composed of the periodontal ligament , cementum and alveolar bone
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  • 18. Types of gingivitis Depending on course and duration  Acute gingivitis: is of sudden onset and short duration and can be painful  Subacute: is less severe than acute  Recurrent : reappears after treatment  Chronic gingivitis: slow in onset, long duration, usually painless and the most common
  • 19. Depending on distribution  Localized or generalized : a group of teeth or entire mouth  Marginal : limited to the marginal gingiva  Papillary : limited to the interdental papilla  Diffuse : when the inflammation spreads to the attached gingiva
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  • 23. OTHER GINGIVALINFECTIONS Acute lesions of sudden onset, limited duration and well-defined clinical features.  Traumatic lesions, both physical and chemical  Viral infections  Bacterial infections  Fungal infections  Gingival abscess  Aphthous ulcers  Erythema multiforme  Drug allergy
  • 24. Traumatic lesions Physical injury  Mechanical or thermal  Chemical damage Asprin burn Silver nitrate Hydrogen peroxide Careless use of caustics by dentist e.g. chlorophenol, tetra acetic acid –Asprin burn
  • 25. Traumatic injuries  The diagnosis is easy since the patient is usually aware of the accident and suffers from immediate and severe pain.  A localized area of inflammation and ulceration may form.
  • 26.  Healing of traumatic lesions is fairly quick and begins with epithelium covering the ulcer. Does not need active treatment  Healing can be complicated by secondary infection. This may be accompanied by lymph gland enlargement and malaise, then an antibiotic may be needed.
  • 27. Viral infections  Acute herpetic gingivostomatitis  Herpangina  Hand foot and mouth disease  Measles  Herpes varicella/zoster virus infections  Glandular fever  HIV infection and AIDS
  • 28. Acute herpetic gingivostomatitis  Primary infection by the herpes simplex virus type 1.  Usually occurs in children (1-10) but may affect older children or even adults  Infection in neonates can produce encephalitis or meningitis  In children or adults it produces a febrile illness or subclinical infection  Incubation period is 5 days
  • 29. CONT.  Symptoms appear abruptly with fever and temperatures as high as 39.4 C  Lymph gland enlargement, malaise and the mouth and throat may be painful  Irritability in children, refusal to eat and increase salivation  Small vesicles form on the gingivae, tongue, buccal mucosa and lips  Vesicles burst and form round or irregular ulcers with grey membrane and surrounded by a red mucosa  There is acute gingivitis with redness swelling and bleeding
  • 30. Herpetic gingivostomatitis  Symptoms subside in 10-21 days  About 30% of patients develop recurrent infections later in life.  The recurrence is usually herpes labialis and it is a reactivation of the latent virus in the trigeminal ganglion
  • 32. Treatment  Symptomatic and supportive  In infants, milk of magnesia  Benzocaine lozenges are useful in the older child  Aspirin or paracetamol  Phenergan a sedative in the child  In severe cases acyclovir tabs 200mg four times daily or suspension 5ml four times daily  Acyclovir cream can be used as a preventive measure
  • 33. Hand, foot and mouth disease  Acute febrile illness  Coxsackie virus A type 16  Sporadic outbreak affecting mainly children  Maculopapular and vesicular lesions appear on the skin and oral mucosa  Skin lesions affect the hands, arms and feet  The oral vesicles break into ulcers  Uneventful recovery in 10-14 days
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  • 35. Measles  Severe febrile illness affecting mainly children  Presents with fever, malaise, cough, conjunctivitis, photophobia and lacrimation  Blotchy macular rash  Oral lesions present as Koplik’s spots which are bluish-white specks surrounded by a bright red margin on the buccal mucosa mainly  Oral lesions precede skin lesions by a few days.  Recovery in 2-3 weeks in healthy, fit well fed children  Can be serious in poor and malnourished previously unexposed children  Vaccination is available against measles
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  • 37. Herpes varicella/zoster virus infections  Varicella or chickenpox is an acute febrile illness mainly in children  Widespread maculopapular or vesicular eruptions on the skin  Small vesicles also form on the oral mucosa, tongue and gingival  Recovery in 2-3 weeks
  • 38.  Herpes zoster or shingles is caused by reactivation of latent varicella virus and common in older adults.  Affects sensory nerves and produces severe neuralgia  Vesicular eruptions on the skin or mucosa innervated by the affected sensory nerve
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  • 42. BACTERIAL INFECTIONS  Acute necrotizing ulcerative gingivitis (NUG)  Tuberculosis  syphilis
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  • 45. Syphilis Secondary syphilis occurs 6 weeks after primary infection and produces skin rash and oral eruption. The ulcers are either mucous patches or snail track
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  • 48. GINGIVALABSCESS  Abscess formation may follow damage by toothpick or fish bone if the foreign object is not removed.  Gingival abscess associated with physical damage  can also arise from wall of a gingival pocket where drainage has been impeded  localized shiny, painful, red swelling and associated teeth TTP  may drain spontaneously or require the removal of foreign object  hot salt water mouthwashes and antibiotics if systemic involvement
  • 49. Aphthous ulcers  Most common type of recurrent ulcerative condition  Possible defect of cell-mediated immune response  painful lesions which appear without any reason, last for several days to heal and, after sometime recur  Cause unknown but may be auto-immunity to a component of the oral mucosa.  Related factors may be stress and hormonal changes  In some patients related to the menstrual cycle  Relationship between ulceration, iron-deficiency anaemia, folic acid deficiency and Vitamin B12
  • 50. Three types  minor aphthous ulcers,  major aphthous ulcers  herpetiform ulcers
  • 51. MINOR APHTHOUS ULCERS Clinical features  Well circumscribed white-yellow round lesion with red margin  Usually less than 5 mm in size  Affects non-keratinized oral mucosa  Moderate to severe pain  Heals without scarring within 7 to 10 days  Affected patients report a history of aphthous ulcers usually for “as long as they can remember”
  • 52. Management  Inquire about type of toothpaste used SLS (sodium lauryl sulphate)-containing toothpastes may aggravate condition)  Discontinue any SLS-containing toothpaste for 1month.  Discontinue use of any mouthwash  Rx topical steroid (e.g., fluocinonide, clobetasol) to be applied tid as soon as prodromal Symptoms occur (may reduce duration of ulcer by half)  Always instruct patient to come back if ulcer not healed after 3 weeks
  • 53. MAJORAPHTHOUS ULCERS Clinical features  Larger, more severe, less common than minor  Ulcers 10 to 30 mm in diameter  Extremely painful, heals with scarring within weeks or even months  Affected patients report a history of aphthous ulcers usually for “as long as they can remember”  Major “aphthous-like”ulcers occur among immunosuppressed patients (HIV+; transplant recipients) with no prior history of aphthous ulcers
  • 54. MANAGEMENT Topical steroids:  Fluocinonide ointment 0.05% mixed 1/1 with orabase B(apply tid)  Clobetasol ointment 0.05% mixed 1/1 with orabase B(apply tid)  Tablets of hydrocortisone  Treatment topical anaesthetics  Antibacterial rinses to clear secondary bacterial infection,  Tetracycline caps (250mg): dissolve in 1 Tbsp water, then rinse for 1 minute + expectorate qid
  • 55. Copyright © 2003, Elsevier Science (USA). All rights reserved.
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  • 58. Periodontitis Defined as:- “an inflammatory disease of the supporting tissues of the teeth caused by specific micro- organisms resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both”
  • 59. Periodontitis  Chronic periodontitis  Aggressive periodontitis  Periodontitis as a manifestation of systemic diseases
  • 60.
  • 61. Chronic Periodontitis  Prevalent in adults but can occur in children  Amount of destruction consistent with local factors  Associated with variable microbial pattern  Subgingival calculus frequently found  Slow to moderate rate of progression with possible periods of rapid progression  Possibly modified by: systemic factors such as diabetes and HIV; local factors: enviromental factors such as smoking and emotional stress
  • 62.  Localized or generalized  Slight – 1-2mm of clinical attachment loss  Moderate – 3-4mm CAL  Severe - ≥ 5mm CAL
  • 64. Aggressive periodontitis  Otherwise clinically healthy patient  Rapid attachment loss and bone destruction  A/o microbial deposits inconsistent with disease severity  Familial aggregation of diseased individuals
  • 65. Localized form  Circumpubertal onset of disease  Localized to first molars or incisors with proximal attachment loss on at least two permanent teeth one of which is a first molar
  • 66. Generalized form  Usually affecting persons under 30 years of age (maybe older)  Generalized proximal attachment loss affecting at least three teeth other than first molars and incisors  Pronounced episodic nature of periodontal destruction  Poor serum antibody response to infecting agents
  • 67. Periodontitis as a manifestation of systemic diseases Haematological disorders 1. Acquired neutropenia 2. Leukaemias 3. Other Genetic disorders a. Familial and cyclic neutropenia b. Down syndrome c. Leukocyte adhesion deficiency syndrome d. Papillon-Lefevre syndrome e. Chediak-Higashi syndrome f. Histiocytosis syndromes g. Glycogen storage disease h. Infantile genetic agranulocytosis i. Cohen syndrome j. Ehlers-Danlos syndrome (types IV andVIIIAD) k. Hypophosphatasia. etc
  • 68. Necrotizing periodontal diseases  Necrotizing ulcerative gingivitis  Necrotizing ulcerative periodontitis Tissue necrosis is the primary clinical feature.
  • 70. Abscesses of the periodontium A periodontal abscess is a localized purulent infection of periodontal tissues and is classified by its tissue of origin  Gingival abscess  Periodontal abscess  Pericoronal abscess
  • 72. DrugAllergy  Can be provoked by:-  Penicillin  Diazepam  Local anaesthetic  Codeine  Tetracycline  Barbiturates  Others
  • 73. Drug allergy and contact hypersensitivity  Two types:-  Those following systemic administration of a drug or chemical  Those following direct contact with the oral mucosa
  • 74.  Manifestation depends on the type of allergic response provoked, ranging from simple drying of the mouth to the most severe response, anaphylactic shock, which is potentially fatal.  Hypersensitivity to drugs may involve type 1, II, III and IV mechanisms.
  • 75. Symptoms  Burning sensation of oral mucosa, swelling, redness of the tongue, lips and gingivae  Peeling epithelium leaving very sore ulcerated areas  Gingivae, bright red and sensitive.  Poor oral hygiene due to the sensitivity in brushing
  • 76. Contact hypersensitivity Reactions of the oral mucosa have been reported to:-  Chewing gum  Toothpaste  Mouthwashes  Sweets  Cosmetics  Topical anaesthetic  Topical antibiotics  Periodontal dressings  Flavouring agents e.g. peppermint, menthol cinnamon and eugenol
  • 77. Management  Implicated substance immediately withdrawn.  Antihistamine  Injection of hydrocortisone hemisuccinate  In anaphylactic shock, intramuscular injection of 0.5ml of 1:1000 adrenaline is necessary  Frequent warm saline rinses.
  • 78.
  • 79. DEFINITION  PERICORONITIS (From the Greek peri, “around”, Latin corona “crown” and itis, “inflammation”) also known as operculitis, is the inflammation of soft tissues surrounding the crown of a partially erupted tooth, including the gingiva (gums) and the dental follicles.
  • 80. ANATOMIC RELATIONSHIP  The occlusal surface of an involved tooth may be partly covered by a flap of tissue, the operculum, which exists during the eruption of the tooth and may persist afterwards.  Varying degrees of eruption, malposition, or impaction may further complicate the soft tissue architecture
  • 81.
  • 82. CONT…  An accumulation of bacteria and debris beneath the operculum  Mechanical trauma (e.g. biting the operculum with the opposing tooth).  Often associated with partially erupted and impacted mandibular third molars.  Periodontal pain.  Pulpitis from dental caries (tooth decay).  Acute myofascial pain in the temporomandibular joint disorder.
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  • 85. CLINICAL FEATURES  The symptoms vary based on whether the condition is acute or chronic. ACUTE  Sever pain near the back teeth  Swelling of gum tissue due to fluid accumulation  Pain when swallowing  The discharge of pus
  • 86. CHRONIC  Bad breath  A bad taste in the mouth  A mild or dull ache lasting for one or two days  Swelling of the lymph nodes in the neck  Infection  Fever  Loss of appetite
  • 87. COMPLICATIONS  The involvement may become localized in the form of a pericoronitis abscess.  It may spread posteriorly into the oropharyngeal area and medially to the base of the tongue, making swallowing difficult.  Involvement of sub maxillary, cervical, deep cervical and retropharyngeal lymph nodes.
  • 88. CONT…  The partially erupted or impacted mandibular third molar is the most common site of pericoronitis.  The space between the crown of the tooth and overlying gingival flap is an ideal area for the accumulation of food debris and bacterial growth.  An influx of the inflammatory fluid and cellular exudates results in an increase in the bulk of the flap.
  • 89. CONT…  Swelling of the cheek in the region of the angle of the jaw and lymphadenitis.  Mandibular movement is limited (Trismus).  Toxic systemic complications – fever, leucocytosis and malaise.  Foul taste and an inability to close the jaws.  Radiating pain to the ear, throat, and floor of the mouth.
  • 90. RISK FACTORS  Occur in young adults in their mid 20s who are experiencing poorly erupting wisdom teeth.  Poor oral hygiene.  Excess gum tissue.  Fatigue and emotional stress
  • 91. TREATMENTS Depending on the severity of the condition, the treatment option may vary.  Gently flush the area with warm water or antiseptic to remove debris and exudates  Pain management and resolving the pericoronal inflammation and/or infection  Antibiotics can be prescribed in severe cases.  Minor oral surgery to remove the overlapping gingival tissue  Wisdom tooth or teeth removal