3 periodontal diseases Flashcards
types of gingivitis
- gingivitis
- localized juvenile spongiotic
- necrotizing ulcerative gingivitis (NUG)
- plasma cell
- granulomatous
- desquamative
what is gingivitis
inflammation of soft tissues surrounding teeth
what causes gingivitis
lack of proper oral hygiene, increase in dental plaque and calculus
max or mandibular more common in puberty gingivitis
upper teeth aren’t covered so maxillary regions are affected more often
puberty gingivitis is seen in ages
9-14
do males or females have a lower frequency of gingivitis
females have a lower frequency but are susceptible during pregnancy or taking certain oral contraceptives
gingivitis mouth breathers
- unique pattern
- only affects facial gingiva as smooth, swollen, red
chronic hyperplastic gingivitis
chronic inflammation causes edema or fibrosis (gums become swollen or edematous)
where is a pyogenic granuloma seen?
chronic hyperplastic gingivitis
pyogenic granuloma
inflamed granulation tissue located in gingival sulcus
mouth breathing gingivitis
gums in interdental papilla are inflamed
puberty gingivitis
red inflamed areas
-mix of hormones + difficulty cleaning with braces
what does healthy gingiva look like?
coral pink, stippling, not bleeding
chronic hyperplastic with pyogenic granuloma
looks healthy lingually, red edema, pyogenic granulomas are not confined to the gingiva
clinical findings of gingivitis
-localized or generalized
-marginal - affects free gingival margins
papillary- affects interdental papilla
- loss of stippling, bleeding on gentle probing, light red in color
generalized gingivitis
across entire oral cavity
treatment of gingivitis
- eliminate cause
- receive proper oral hygiene instructions
gingivitis color
red instead of coral pink
localized juvenile spongiotic gingival hyperplasia =
localized juvenile spongiotic gingivitis
localized juvenile spongiotic gingival hyperplasia
- idiopathic
- not plaque related
- fail to respond to improved oral hygiene
localized juvenile spongiotic gingival hyperplasia occurs in patients under
20
clinical findings of localized juvenile spongiotic gingival hyperplasia
- small bright red velvety papillary alteration
- maxillary facial gingiva most affected
- can involve interproximal areas
- can be sessile or pedunculated
treatment of localized juvenile spongiotic gingival hyperplasia
- excise conservatively
- can recur but can resolute spontaneously
localized juvenile spongiotic gingival hyperplasia vs. puberty gingivitis
maxillary area whereas puberty gingivitis could be in the margin area
necrotizing ulcerative gingivitis =
NUG
necrotizing ulcerative gingiviti (NUG) is also called what two names
vincent’s infection or trench mouth
necrotizing ulcerative gingiviti (NUG) is caused by
- fusobacterium nucleatum
- prevotella intermedia
- porphyromonas gingivalis
- treponmea and or selenomonas
necrotizing ulcerative gingiviti (NUG) occurs in times of
psychologic stress esp military personnel
trench mouth
- during WWI or WWII, men protected themselves in trenches and couldn’t move for periods of time
- soldiers wouldn’t have time to brush their teeth
factors contributing to necrotizing ulcerative gingivitis (NUG)
- smoking
- local trauma
- immunocompromised status
- poor oral hygiene
**clinical features of necrotizing ulcerative gingivitis (NUG)
interdental papilla infected- inflamed, edematous, hemorrhagic, “punched out” appearance with gray pseudomembrane appearance, foul odor, fever, lymphadenopathy, malaise
-if extends through mucosa of skin to face known as noma (cancrum oris)
NUG–> noma if infection spreads to
face
**8interdental papilla PUNCHED OUT with gray pseudomembrane appearance
necrotizing ulcerative gingivitis (NUG) ***
treatment of necrotizing ulcerative gingivitis (NUG) ***
currettage, scaling, ultrasonic instrumentation to rid of bacterial component
NOMA starts as **
NUG
NOMA
- bacterial infection, intense + extensive, lots of destruction
- rapidly progressive, polymicrobial, opportunistic infection
What does NOMA result from
normal oral flora becoming pathogenic due to compromised immune status
what debilitating illnesses cause infection?
- measles
- herpes (simplex, varicella)
- tuberculosis
who does NOMA affect?
children (1-10 yrs old)
adults w/ debilitating disease
clinical findings of NOMA
- well-defined, unilateral w/ odor
- begins on gingiva and extend to soft tissues (necrotizing ulcerative mucositis)
- necrosis extends as blue-black discoloration with cone growth pattern
- spreads through anatomic barriers and not follow tissue planes (past gingiva to face, scalp, neck)
- affects bone creating oteomyelitis (ill defined radiolucency)
necrosis extends as blue-black discoloration with CONE SHAPED growth pattern***
NOMA
cone shaped noma
starts at the tip and then spreads
treatment of NOMA
- antibiotics
- local wound care
- correcting imbalances with nutrition, hydration, electrolytes
another name for plasma cell gingivitis
atypical gingivostomatitis
**allergic response with a distinc pattern of gingival involvement
plasma cell gingivitis= atypical gingivostomatitis
plasma cell gingivitis= atypical gingivostomatitis occurs quickly because it’s an
allergic reaction
plasma cell gingivitis= atypical gingivostomatitis rapid onset made worse by
hot/spicy foods (cinnamon) or dentrifices
plasma cell gingivitis= atypical gingivostomatitis attached and free gingiva affected
- diffuse enlargement (bright red + inflamed)
- loss of stippling
- bright erythema
histopathology of plasma cell gingivitis= atypical gingivostomatitis
plasma cells in fibrous CT
plasma cell gingivitis= atypical gingivostomatitis treatment
try to rule out causative agent
plasma cell gingivitis= atypical gingivostomatitis
allergic reaction so once you remove the allergen, the gingiva should go back to coral pink
plasma cell gingivitis= atypical gingivostomatitis
firey red appearance= bright erythema
granulomatous gingivitis
- unexplained granulomatous inflammation, diagnosis of exclusion
- may result from dental materials into CT
foreign body gingivitis **
granulomatous gingivitis
granulomatous gingivitis= FBG
damage to epithelium during dental procedures and foreign material into gingiva
what is the most common form of granulomatous inflammation?
foreign bodies
what age does granulomatous gingivitis occur?
any age
granulomatous gingivitis lesions
solitary or multifocal lesions on interdental papillae or marginal gingiva
- red or red/white machules
- FBG resembles gingival lichen planus
histopathology of granulomatous gingivitis
- collections of histiocytes with lymphocytic infiltrate
- may see well-formed granulomas with multi-nucleated giant cells
treatment of granulomatous gingivitis
- if foreign body -surgical excision of affected tissue
- rule out any granulomatous inflammatory diseases
granulomatous inflammatory diseases
- sarcoidosis
- crohn’s
- deep fungal
- bacterial
- orofacial granulomatosis
- cat-scratch disease
granulomatous gingivitis
red inflamed, localized, multinucleated giant cells
desquamative gingivitis clinical term
not giving a definitive diagnosis; biopsy will be necessary
desquamative gingivitis
superficial peeling of epithelium with formation of vesicles or bulla
nikolsky sign
desquamative gingivitis
nikolsky sign
-manipulate affected epithelium with object or compressed air that results in sloughing or vesicle formation
how to check for nikolsky sign
create a vesicle; gently blow air or use another instrument to see where the epithelium is blowing away
represents a vesiculobullous condition
desquamative gingivitis
what is not a true vesiculobullous condition (desquamative gingivitis)
lichen planus
what are true vesiculobollus conditions during desquamative gingivitis?
- linear IgA
- pemphigus vulgaris
- mucous membrane pemphigoid
- epidermolysis bullosa acquisita
- systemic lupus erythematosus
types of gingival hyperplasia
- drug-related gingival hyperplasia
- gingival fibromatosis
drug related gingival hyperplasia is also called
drug-related gingival overgrowth
What is drug related gingival hyperplasiaa
abnormal gingival growth due to systemic medications
what does drug related gingival hyperplasia result from
increased amount of extracellular matrix (collagen)
when can drug related gingival hyperplasia occur?
after taking medication for 1-3 months
medications that affect the gingiva in drug related gingival hyperplasia
cyclosporine, erythromycin, oral contraceptives
and calcium channel blockers like Nifedipine
**anticonvulsants like phenytoin (dilantin) for patients with convulsions or epilepsy can cause
drug related gingival hyperplasia
example of anticonvulsant
phenytoin (dilantin)
clinical findings for drug related gingival hyperplasia
-begins in interdental papillae and spreads across teeth surfaces
what surfaces of teeth are most affected in patients with drug related gingival hyperplasia
anterior and facial surfaces
if no inflammation in drug related gingival hyperplasia
gingiva is normal in color and firm
if inflammation in drug related gingival hyperplasia
gingiva is dark-red, edematous, friable surface
-edentulous people can have this effect as well
treatment for drug related gingival hyperplasia
discontinue medication (advice of physician) and switch to another
DISCUSS WITH PHYSICIANS
if phenytoin is stopped but gingiva is still overgrowing, consider
gingivectomy
cyclosporines can cause
extra overgrowth of inflamed tissue
what kind of patient takes nifedipine and what can it lead to?
patient with hypertension or heart problems, drug related gingival hyperplasia
gingival fibromatosis is also called
fibromatosis gingivae/elephantiasis ginigvae
gingival fibromatosis
slow progressive gingival enlargement
gingival fibromatosis is caused by
collagen overgrowth
gingival fibromatosis is genetically related to
autosomal dominant or recessive
gingival fibromatosis is seen with
- hypertrichosis
- generalized aggressive periodontitis
- epilepsy
- intellectual disability
- hypothryoidism
- growth hormone deficiency
- sensorineural deafness
hypertrichosis
abnormal amount of hair growth over the body
gingival fibromatosis clinical findings
- generalized orlocalized
- affect deciduous/ permanenet dentition
- covers crowns of teeth after erupting
- firm and normal in color
- maxilla affected more
- palatal surfaces increased in thickness
treatment of gingival fibromatosis
gingivectomy + oral hygiene instructions
types of periodontitis
- chronic
- necrotizing ulcerative periodontitis (NUP)
- periodontal abscess
- pericoronitis
- localized aggressive
- generalized aggressive
- papillon-lefevre syndrome
gingivitis
inflammation of soft tissue
what is periodontitis
inflammation of gingival tissues with loss of attachment of periodontal ligament and bone support
what creates periodontal pockets in periodontitis
apical migration of crevicular epithelium creating periodontal pockets
factors that lead to periodonttitis
- dental plaque
- shift in bacterial plaque due to changes in dentogingival environment
what changes in dentogingival environment leads to shift in bacterial plaque
facultative gram-positive organisms (actinomycetes, streptococci) to anaerobic and microaerophilic gram-negative organisms
periodontitis is associated with what diseases
CV disease, rsepiratory disease, and low birth weigh babies
systemic disorders with premature attachment loss need to be ruled out of periodontitis
- acrodynia
- leukemia
- cyclic neutropenia
- crohn disease
- diabetes mellitus
- sarcoidosis
- langehans cell disease
- papillonlefevre
- trisomy 21
bacteria associated with chronic periodontitis (organized in a biofilm)
- treponema denticola
- tannerella forsynthesis
- porphyromonas gingivalis
what is the primary cause of tooth loss in people greater than 25 yrs old
chronic periodontitis
chronic periodontitis can be seen in
- advancing age
- smoking
- diabetes mellitus
- osteoporosis
- HIV infection
- low socioeconomic level**
can chronic periodontitis be seen in people with no abnormal immune system?
yes
HIV infection can lead to chronic periodontitis
low term birth weight can lead to periodontitis so pregnant womenshould take care of their oral hygiene
chronic periodontitis clinical and radiographic findings
- loss of gingival attachment
- pocket depths more than 3–4mm with periodontal probe
- tooth mobility with singificant bone loss
chronic periodontitis clinical and radiographic findings- loss of gingival attachment
blunting and apical positioning of margins
what kind of bone loss is seen in radiographic findings of chronic periodontitis?
vertical bone loss
treatment of periodontitis
- eliminate causing factors
- disrupt biofilm
- develop good oral hygiene practices (scaling, root planing, , curretage, plaque control)
- surgical flaps, antibiotic delivery if needed
necrotizing ulcerative periodontitis is similar to
necrotizing ulcerative gingivitis (NUG)
necrotizing ulcerative periodontitis has loss of
clinical attachment and alveolar bone
in order to have periodontitis, you have to have
bone loss
necrotizing ulcerative periodontitis is
destructive
necrotizing ulcerative periodontitis patients are usually
immunosupressed or malnoursheed
necrotizing ulcerative periodontitis are younger than those with
chronic periodontitis
necrotizing ulcerative periodontitis
gingival ulceration and necrosis with rapidly progressing loss of periondontal attachment but deep pockets not seen
necrotizing ulcerative periodontitis
edema or severe pain
what is periodontal abscess
localized purulent infection involving periodontal attachment and alveolar bone-
periodontal abscess seen in adults but rare in
children
periodontal abscess occurs in preexisting periodontal lesion and changes in
subgingival flora
clinical presentation of periodontal abscess
- gingival enlargement along lateral aspect of tooth
- erythematous + edematous
symptoms of periodontal abscess
- throbbing pain
- sensitivity to palpation of involved gingiva
- foul taste
- fever, lymphadenopathy
treatment of periodontal abscess
- drain and or incise affected area
- antibiotics and analgesics if needed
pericoronitis
inflammatory process
pericoronitis
tissue surrounds a partially erupted tooth
predisposing factors of pericoronitis
- food debris and bacteria
- stress
- upper respiratory infection
abccess form of pericoronitis esecially in
mandibular 3rd molars
- extreme pain
- foul taste
- inability to close jaws
- area is erythematous + edematous
treatment of pericoronitis
- antiseptic lavage under flap/removal of excess tissue
- extraction of tooth if needed
