29. treatment
o Draining the abscess
o Excising sinus tract with
high doses of antibiotics
to accelerate healing
o Penicillin
o Tetracycline
o Erythromycin
31. Acute infection of nervous
system
Intense activity of motor
neurons
Severe muscle spasms
Gram positive bacillus
Clostridium tetani
Acts at synapse of
interneurons of inhibitary
pathways & motor neurons
to produce blockade of
spinal inhibition
35. *General measures:
*Remove spores at site of wound
*Cardiopulmovary monitoring
*Sedation,airway & nutrition to be maintained
*Penicillin 10-12million units IV for 10days
*Metronidazole 1gm every 12hrs
*Antitoxin injected to neutralise circulating toxin & unbound toxin with
wound.
*Prophylaxis : wound debridement & TT booster doses
*Unimmunized individuals : anti tetanus serum(ATS)
1500units or TIG 250units.
treatment
37. o Veneral disease
o Male & female genitourinary
Tract
o Neisseria gonorrhoeae
o Gram negative
o Nonmotile, nonspore forming
o Grows in pairsage : 15-29yrs
oIncubation pd : 1-5 days
o Oropharyngeal gonorrhoea in
20% women
Clinical features
41. Treponema pallidium
Episodes of active
disease interrupted by
Period of latency
Gram positive, motile
Microaerophillic
Darkfield microscope
Route of transmission:
Sexual contact
Mother to child in utero
42. ACQUIRED SYPHILLIS
PRIMARY STAGE
Chancre : at site of innoculation
3-90 days after infection
Solitary
m/c site males: penis
females: cervix or
vulva
95% occur in genitalia
Extragenital syphillis : increase in
altered sexual activity & contact
among
Infected homosexuals.
44. SECONDARY STAGE
Skin: macules or papules,
painless
Oral lesions: MUCOUS
PATCHES, multiple, painless
Gray white plaques overlying
ulcerated surface.
Tongue, gingiva, buccal
mucosa
HIGHLY INFECTIOUS
,contain vast number of
micro-organisms
Serologic reaction is always
+ve
Explosive, widespread form :
LUES MAILGNA
MUCOUS PATCHES
Leão JC, Gueiros LA, Porter SR. Oral manifestations of syphilis. Clinics
(Sao Paulo). 2006 Apr;61(2):161-6. Epub 2006 Apr 25.
45. *Late syphilis
*Do not appear for years
*CVS & CNS
*Noninfectious
*Gumma: result of hypersensitivity
*Focal, granulomatous inflammatory
*Process with central necrosis
*i/o gumma : tongue & palate
*Firm nodular mass in tissue
*May ulcerate to deep painless ulcer
*Palate: perforation by sloughing
*Herxheimer reaction
TERTIARY SYPHILIS
46. Atrophic or interstitial glossitis is most characteristic &
important lesion of syphilis & is due to endarteritis obliterans
SYPHILITIC GLOSSITIS
Tongue surface gets broken up by fissures.
Atrophy & fibrosis of tongue musculature.
Hyperkeratosis
May undergo carcinomatous transformation
47. Transmitted to offspring by
Mother
Frontal bossae
Short maxilla
High palatal arch
Saddle nose
Mulberry molars
Higoumenakis sign
Relative protuberance of mandible
Rhagades
Saber shin
CONGENITAL
SYPHILIS
RHAGADES
FRONTAL
BOSSAE
INTERSTITIAL
KERATITIS
HIGOUMENAKIS SIGNSADDLE NOSE
SABER SHIN
48. Diagnosis & treatment
Penicillin: DOC
Surgical correction
of facial defects
gives good esthetic
51. Clinical features
Hypopigmented
patches
Total loss of
cutaneous sensation
light touch to be
affected first
Thickening of nerves
Presence of acid fast
bacilli in skin or nasal
smear
GENERAL
FEATURES
Single/ multiple
macular
erythematous
eruptions
Dermal &
peripheral nerve
trunk involvement
Loss of sensation
Loss of sweating
of affected skin
Tuberculoid Leprosy
Early erythematous
macules or papules
Thickening of skin
Characteristic
nodules
Severe disfigurement
Lepromatous Leprosy
60. PAIN
INTERDEN
TAL
ULCERATI
ON
ANUG
GINGIVAL
BLEEDING
Involves free gingival margin,
crest of gingiva, interdental
papillae
May spread to soft palate &
tonsillar areas : vincents angina
Necrotizing ulcerative
periodontitis
Associated with HIV
Common in young & adults
etiology
• Fusiform bacillus & borrelia
vincentii
• Vibrio & coccal forms
• Acc to mc donald , Bacteroides
melaninogenicus : main causative
agent
• Stress , immunosupression
,smoking
• Upper resp tract infection , local
trauma
• Poor nutritional status , poor oral
Predisposingfactors
61. *Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute
necrotizing ulcerative gingivitis. J Periodontol. 1982 Apr;53(4):223-
30.
*Treponema and Selenomonas sp., 32 and 6%, respectively, of the
microscopic count;
*B. melaninogenicus ssp. intermedius and Fusobacterium sp., which
averaged 24 and 3%, respectively, of the viable count.
*Plaque samples from 22 ulcerated sites in 8 patients with ANUG.
*
62. Clinical features
Painful, hyperemic gingiva, sharply
punched out crater like erosions
of interdental paillae
Grayish green necrotic
pseudomembrane
Fetid odour
Inability to eat
Gingival bleeding
Incubation zone
63. Diagnosis based on clinical finding :
gingival pain, ulceration & bleeding
Bacterial smear from gingiva
Fusiform bacillus: elongated rod with
Tapered ends 5-14microns in length
0.5-1.0microns diameter.
Weakly gram+ve
Borrellia vincentii: gram-ve
10-15microns length
Diagnosis
A- spirochete; B- bacillus fusiformis; C-
filamentous organism; D- streptococcus;
E- vibrio; F- treponema microdentinum
64. treatmentFIRST VISIT:
Medical history,
diet
background,smoking,
rest , risk factors
for HIV, stress
Examination of
general appearance,
halitosis, fever
Topical anesthetic6,
area swabbed with
moist cotton
Pseudomembrane &
non attached debris
removed
Superficial calculus
removed by
ultrasonic scaling
Antibiotics:
Amox 500mg 6hrs for
10days
Metronidazole 500mg
twice daily for 7days
Tooth xtraction or pdl
surgery
Postponed until 4weeks
Rinse with equal
amount of 3% h2o2 &
warm water every
2hrs or twice daily
with CHX
Adequate rest
Ultrasoft brush
NSAID for pain relief
SECOND VISIT
1,2 days after 1st
visit
Diminished pain
Gingival margins
erythematous but
without
Pseudomembrane
Scaling if needed
THIRD VISIT
5 DAYS after
Resolution of
symptoms
Plaque control
procedures
Counselling on
nutrition, smoking
cessation
CHX rinses for 2-4
weeks
Reevaluation after 1
month
Gingival contouring :
gingivoplasty
Nutritional
supplements
66. small ulcer of gingiva spreads
involve surrounding tissues of jaw,lip
& cheeks by gangrenous necrosis.
rapidly spreading
Gangrenous stomatitis
m/c in children
seen in persons who are
undernourished or debilated
from infection
diptheria,dysentry,tb,syphilli
s,anemia…
Secondary complication of
systemic disease rather than
a primary disease.
Specific infection by
vincents organisms,
ANUG…soon complicated by
secondary invasion of
streptococci, staphylococci &
Clinical features
67. Area of
stagnation
Around fixed
bridge or crown
Overlying skin
inflammed,edem
atous & necrotic
Large mass of
tissue slough out.
Blackening of
skin.
Subcutaneous fat
undergoes
necrosis.
Foul odour
High
temperature,sec
ondary infection,
death from
toxemia
73. * : inflammatory lesion occuring around the
impacted or partially erupted tooth.
Mixed infection(anaerobes)
*Mand 3rd molar
*Pain & swelling
*Difficulty in opening & chewing
Mildly ill, fever & regional lymphadenopathy
Sixou JL, Magaud C, Jolivet-Gougeon A, Cormier M, Bonnaure-Mallet M. Microbiology of
mandibular third molar pericoronitis: incidence of beta-lactamase-producing bacteria. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Jun;95(6):655-9
PERICORONITIS
Clinicalfeatures
alpha-hemolytic streptococci (26/26)
Prevotella (15/26), Veillonella (15/26),
Bacteroides (9/26), and
Capnocytophaga (9/26)
74. *Gently flushing area with warm water
*Entrapped food debris must be removed
*Swabbing with antiseptic after elevating flap
Gently from tooth with a scaler
*Upper tooth when involved should be
ground or extracted
*Radiograph help in assessing position of tooth
*Surgical removal after acute symptoms subside
*Antibiotics to relieve symptoms & to prevent spread of
infection.
treatment
76. *Originate as a response of tissue
*To a nonspecific infection.
*Tumor like growth : exaggerated
*Conditioned response to minor
* trauma
Infection staphylococci or streptococci
Arise as a result of minor trauma to
tissues
Pathway for invasion of nonspecific
type of micro-organism.
Surface of pyogenic granuloma in cases
of ulceration abounds with typical
colonies of saprophytic organisms.
Sulfhydryl radical
etiology
80. *Multifactorial disease affecting commissure of lips
*m/c in denture wearers
*Associated with infection
*Reduced vertical dimension of mouth
*60% : candida albicans & staphylococcus
*20%: staphylococcus
*20%: candida albicans
*Nutritional deficiencies: fe, vit B, folic acid
*Ariboflavinosis: circumoral lesions
*Seen in diabetes, neutropenia, AIDS
81. *Occur in both young children & adults
*Dryness, burning sensation at corners
*Wrinkled skin at commissure
*Deep fissures & cracks
*Fissures stop at mucocutaneous
junction
Clinical features
82. Depending on the specific cause, the following treatments may
be useful:
*Lip balm or thick emollient ointment, applied frequently.
*Topical antiseptics.
*Topical or oral antistaphylococcal antibiotic.
*Topical antifungal cream.
*Oral antifungal medication
*.ketoconazole tab 200-400mg twice daily with food for 2weeks
* Fluconazole cap 50-100mg once daily for 2-3weeks
*Nutritional supplements.
treatment
84. *:
*Cellulitis is a diffuse inflammation of soft tissues which is
not circumscribed or confined to one area, but which, in
contrary to the abscess, tends to spread through tissue
spaces and along fascial planes.
*Common causative agent : streptococci viridans
*Produce : streptokinase, hyaluronidase, fibrinolysins
*Prevotella & porphyromonas : destroy collagen
*As result of apical abscess, osteomyelitis, following pdl
infection
*Pericoronitis
*Injection with infected needle
CELLULITIS
86. *Moderately ill
*Elevated temperature
*Leukocytosis
*Firm & brawny, painful swelling of soft tissues
*Inflammatory edema
*Inflammed , orange peel appearance
*Regional lymphadenitis
*Infections in maxilla perforate outer cortical layer
Of bone above buccinator attachment : swelling of upper half
of face
*Eye: cavernous sinus thrombosis
*Infection in mandible perforate outer
cortical plate below buccinator :
*diffuse swelling of lower half of face
*Spread to cervical tissue : respiratory discomfort
Clinical features
87. histology
Diffusion exudation
of
Polymorphonuclear
Leukocytes,
lymphocytes
Separation of
connective tissue or
muscle fibers
treatment
Treatment for cellulitis depends on what
caused the infection, the severity of
symptoms and the general state of health.
Hospital treatment may be necessary if
symptoms such as fever, nausea and
vomiting suggesting infection has spread
from skin to bloodstream or other parts of
the body.
Antibiotics:
flucloxacillin, 25mg/kg(max 500mg) 6hr for
7days
Flucloxacillin 50mg/kg iv 6hr
Ceftriaxone 50mg/kg/dose iv 12 hr
Drink plenty of fluids to avoid dehydration.
NSAIDS : pain control
89. *
*Ludwig's angina, otherwise known as angina ludovici, is a
serious, potentially life-threatening cellulitis, or
connective tissue infection, of the floor of the mouth,
usually occurring in adults with concomitant dental
infections and if left untreated, may obstruct the
airways, necessitating tracheotomy.
Acute, toxic begin in
submandibular space
* secondarily involve sublingual &
submental spaces spaces.
* dental origin
* mandibular molar : chief
source of infection
* other causes :
LUDWIG’S
ANGINA
90. 2nd & 3rd molars: m/c
Unusual speech(hot potato in mouth)
Bilateral sublingual space infection
Bilateral submandibular space infection
Brawny edema
Elevated tongue
Airway obstruction
Paucity of pus
CLINICALFEATURES
HALLMARK SIGNS
3’F’ :
FEARED
FATAL(often)
FLUCTUANT(rarely)
94. * ETIOLOGY:
*microbial overgrowth in association with a reduction in salivary flow
*subsequent to dehydration and debilitation
*trauma to the duct system and hematogenous spread of infection from other
areas.
*The most commonly isolated organisms in parotitis : penicillin-resistant
Staphylococcus aureus, Streptococcus viridans, and Streptococcus pneumoniae
* presence of a painful swelling,
*low-grade fever
*malaise headache
*gland is extremely tender Trismus
*purulence at the duct orifice may be produced by gentle pressure on the
involved gland or duct.
* If infection is not eliminated early, suppuration may extend beyond the
limiting capsule of the parotid gland.
*Extension into surrounding tissues along fascial planes in the neck or
extension posteriorly into the external auditory canal may follow.
CLINICAL FEATURES
96. *Laboratory studies :
*elevated erythrocyte sedimentation rale(ESR)
*leukocytosis, often with a characteristic shift to the left,
indicating acute infection.
* elimination of the causative organism
*rehydration of the patient
*drainage of purulence, if present.
*Culture and sensitivity testing of the exudate at the orifice of
the duct is the first step in antibiotic management.
*After a culture is obtained, patients empirically be placed on
regimen of a penicillinase-resistant antibiotic such as
semisynthetic penicillin. Along with rehydration and attempts
at establishing and encouraging salivary flow, moist
compresses, analgesics, and rest are in order.
*Medications containing parasympathomimetic agents, which
reduce salivary flow, should be reduced or eliminated.
Treatment & prognosis
97. *A biopsy and retrograde sialography should be avoided.
* may cause sinus tract formation, may allow infection to proceed beyond the
boundaries of the gland into surrounding" soft tissues.
* With prompt and effective treatment, recurrence is generally avoided.
* recurrent parotitis, considerable destructive glandular changes can be seen.
* juvenile, variant, of parotitis, intermittent unilateral or bilateral painful
swelling is accompanied by fever and malaise.
*initial attack : ages 2 and 6 years,
* neonatal form of suppurative parotitis may develop, with S. aureus being
the most common causative pathogen.
* Gross destruction of the parenchymal and ductal elements may be noted on
sialographic examination.
*Absence of secretory acinar components and a damaged ductal system with
numerous punctate globular spaces.
*Spontaneous regeneration of parotid salivary tissue.
99. *Sarcoidosis a multisystem granulomatous disease of unknown origin
characterized by the formation of uniform ,discrete, compact, non-caseating
epithelioid granulomas. I
*blacks >>whites.
* infectious etiology : Mycobacterium and Propionibacterium
* young adults
*lesions most common in the lungs, skin, lymph nodes, salivary glands,
spleen, bones,& the mouth.
*characterized by depression of delayed-type hypersensitivity
suggesting an impaired cell-mediated immunity, and raised or
abnormal serum immunoglobulins suggesting lymphoproliferation
*interferon gamma (IFN-J) and cytokines such as TNF-D, IL-12 and
IL-18 play an important role in the formation of granulomatous
lesions
103. Oral manifestations
Small papular nodular
plaques, resemble
herpetic lesions or fever
blisters
Bleblike, containing
clear yellowish
fluid, or as solid
nodules
LIPS
HARD PALATE
BUCCAL MUCOSA
104. Intracutaneous test: kveim siltzbach test
A lip biopsy may occasionally provide evidence of sarcoid involvement of minor
salivary glands in support of a clinical impression of pulmonary disease.
* Lab assay for angiotensin I—converting enzyme
* Elevation of this enzyme in conjunction with a positive chest radiograph has a
high diagnostic reliability
* Spontaneous resolution
* Corticosteroids: doc for symptomating pulmonary sarcoidosis
* Chloroquine anti TNF agents
* Immunosuppresive drugs to those not responding to steroids
* Levamisole for arthritic symptoms
* Good prognosis
diagnosis
TREATMENT
105. HISTOLOGY
Nests of epitheloid cells with
multinucleated giant cells
Non caesating
Solid, amorphous,eosinophillic,
hyaline mass
106. *a form of sarcoidosis in which characteristically there is
firm, painless, usually bilateral enlargement of the parotid
glands, accompanied by inflammation of the uveal tracts of
the eye and cranial nerve involvement.
*The submandibular and sublingual glands may be involved
* chronic, low-grade fever lassitude, malaise and vague
gastrointestinal disturbances nausea, and vomiting.
*Xerostomia is common.
* patchy erythema of the skin
*Enlargement of the cervical lymph nodes
earliest symptom : uveitis
*
*most common nerve involvement is unilateral or bilateral
seventh nerve paralysis,in one-third to one-half of all cases
UVEOPAROTID FEVER (HEERFORDT SYNDROME)
108. *Tuberculosis (TB) is a specific infectious granulomatous disease
caused by Mycobacterium tuberculosis
*M. tuberculosis is a rod-shaped, nonspore forming, and thin
aerobic bacteria called acid-fast bacilli,
*once stained, it cannot be decolorized by acid alcohol.
*Its acid-fastness is due to the high content of mycolic acids,
long chain cross-linked fatty acids and other cell wall lipids.
*Males are more affected than females in India though it
affects all ages, from an average of 1% in the under-five age
group.
M. tuberculosis is a facultative intracellular
atypical or opportunistic mycobacteria: pulmonary or
generalized infection in immunocompromised individuals
etiology
109. *M. tuberculosis is most commonly transmitted from a
person with infectious pulmonary TB by droplet nuclei,
which are aerosolized by coughing, sneezing, or speaking.
The tiny droplets dry rapidly; the smallest (<5–10 μm in
diameter) may remain suspended in the air for several
hours and may reach the terminal air passages when
inhaled. There may be as many as 3000 infectious nuclei
per cough
112. Exposure to TB
No infection(70-90%) Infection (10-30%)
Latent TB (90%) well
Never develop TB
Not infectious
Active TB (10%) ill
5% develop TB within 2
yr
5% develop TB many yrs
later
untreated treated
50% die
within 5
years
25% remain
sick
25% recover
cured
121. *Demonstration of organism by microbial stains
*Culture of sputum or infected tissue : lj medium middle brook media
*Presence of acid fast bacilli in sputum : gold standard
*Radiograph
*Tuberculin test
*CT scan: mediastinal or hilar lymphadenopathy
*MRI : extrapulmonary TB
*Ziehl Nielsen stain, Kinyouns stain , rhodamine staining for fluorescent
microsopy
*Minimum of 5 acidfast bacilli on fluorescent microscopy positive
*3 on ZN staining
*Rapid slide culture technique
*Radiometric culture method
*Radioimmunoassay
*ELISA
*PCR
DIAGNOSIS
126. *Global TB statistics
*In 2014 1.5 million people died of TB. Of these people 0.4 million people
were HIV positive.
*TB now annually causes more deaths worldwide than HIV.
*In 2014 1.2 million people died of HIV and this includes the 0.4 million TB
deaths among HIV positive people. People who have both TB and
HIV when they die, are internationally classified as having died from HIV.
*There were an estimated 9.6 million new cases of TB in 2014.There were
an estimated 3.2 million cases and 480,000 TB deaths among women.
*There were also an estimated 1.0 million cases of TB in children and
140,000 deaths.
130. * The World Health Organisation (WHO) current estimates in 2015 are that 1 million children
currently suffer from TB worldwide (<15 years), and that more than 136,000 die each year.
* 70-80% of children with TB have the disease in their lungs (pulmonary TB). The rest are
affected by TB disease in other parts of their body (extra pulmonary TB) –
* Some children are at greater risk of getting TB than others and these include: A child that
lives in the same household as a person who has been recently diagnosed with smear
positive TB
* A child less than 5 years old
* A child with HIV infection
* A child with severe malnutrition
* in children with pulmonary TB the commonest chronic symptoms are a chronic cough that
has been present for more than 21 days, a fever, and weight loss or failure to thrive.
TB & CHILDREN
131. *The 2010 WHO TB drug dosage guidance for children
*The major recommendations of the WHO drug dosage guidance
for children were that:
*1) The dosages of the following four TB drugs should be:
• Isoniazid(H) 10mg/kg (range 10-15 mg/kg); maximum dose 300
mg/day
• Rifampicin(R) 15mg/kg (range 10-20 mg/kg); maximum dose 600
mg/day
• Pyrazinamide(Z) 35mg/kg (30-40) mg/kg)
• Ethambutol(E) 20mg/kg (15-25 mg/kg)
*As children approach a body weight of 25kg, adult dosages can
be used.
134. *Osteomyelitis is defined as the inflammation of bone and its
marrow contents.
* trauma and road traffic accidents;
*gunshot wounds, radiation damage, Paget’s disease, and osteopetrosis.
*Systemic conditions like malnutrition, acute leukemia, uncontrolled diabetes
mellitus, sickle cell anemia, and chronic alcoholism.
CLASSIFICATION
SUPPURATIVE NONSUPPURATIVE
ACUTE CHRONIC CHRONIC
SCLEROSI
NG
FOCAL DIFFUSEGARRE
PREDISPOSING FACTORS:
136. *
*serious sequela of periapical infection that often results in a diffuse spread
of infection throughout the medullary spaces, with subsequent necrosis of a
variable amount of bone.
*MAXILLA : well localised MANDIBLE : diffuse & widespread
* neonatal maxillitis in infants and young children
*severe pain, trismus, and paresthesia of the lips : mandibular involvement
*elevation of temperature regional lymphadenopathy.
*WBC elevated.
teeth loose and sore eating is difficult,
Pus may exude from the gingival margin.
Until periostitis develops, there is no swelling or reddening of the skin or
mucosa.
ACUTE SUPPURATIVEOSTEOMYELITIS
CLINICAL FEATURES
138. Chronic
osteomyelitis
Most infectious
(bacterial)
Varaiable pain,
swelling,
drainage
Radiolucent or
mottled
pattern
Appropriate
antibiotic,
sequestromy
Chronic
osteomyelitis
with
proliferative
periostitis
Sequelae of
tooth abscess,
extraction
Usually
associated
with lower
molar,perioste
um involved
children
Radiolucent or
mottled with
concentric
periosteal
opacities
Tooth removal,
antibiotics
Diffuse
sclerosing
osteomyelitis
Probably low
grade
infection,
pulpitis,period
ontal disease
Ocassional
pain, swelling,
drainage
mandible
Opacification
throughout jaw
Antibiotics,
find cause &
treat if
possible
Focal
sclerosing
osteitis
Low grade
focal bone
irritation
Asymptomatic,
Found on
routine
examination
Opaque mass
usually at root
apex
Treat offending
tooth
Etiology Clinical
features
Radiographs Treatment
139. * a reaction to mild bacterial infection entering the bone through a carious
tooth in persons who have a high degree of tissue resistance and tissue
reactivity.
the tissues react to the infection by proliferation rather than destruction,
since infection acts as a stimulus rather than an irritant. .
MOST COMMON : CHILDREN
mandibular first molar with a large carious lesion. Endodontic treatment
or extraction
mild pain associated with an infected pulp.
CONDENSINGOSTEITIS
treatment
140. Medical management:
1.Systemic antibiotics- penicillin(empirical) 2-4 months
Metronidazle
Clindamycin
Cephalosporins
Vancomycin
2.Local application of antibiotics
PMMA beads- antibiotic impregnated beads
Surgical management:
Removal of necrotic foci
a) sequestrectomy- dead necrotic bone(avascular, antibiotics donot penetrate)
b) Saucerisation
c) Decortication- lateral & inferior cortical bone is removed
d) Ressection & reconstruction
MANAGEMENT
HBO THERAPY
142. *1) Harrison’s principles of internal medicine.19th edition
*2)Scott C Kachlany. Deadly diseases and epidemics. Infectious diseases of the
mouth.2007
*3) Shafer.Hine.Levy. Textbook of OralPathology.7th edition
*4)Greenberg. Glick. Ship. Burket’s OralMedicine.11th edition
*5) Regezi.Sciubba.Jordan. OralPathologyClinical pathological correlations.4th
edition
6)Philip D Marsh. Michael V Martin. Oral Microbiology.5th edition
*7)Michael Miloro. Peterson’s Principles of Oral And Maxillofacial Surgery.2nd
edition
references