Sequelae of pulpal disease Flashcards
pulpitis? classifications?
inflammation of the pulpal tissue
Reversible vs irreversible
Acute vs chronic
Symptomatic vs asymptomatic
Tx planning with pulpitis
determine extent with testing and use knowledge/ judgement
MECHANISM OF ACTION:
INFLAMMATION OF THE PULP
Limited blood supply
No collateral support
Destructive, small space
Expansile process due to…
▪ Blood vessel dilation
▪ Leakage of fluid into surrounding tissue
▪ Migration of cells
reversible pulpitis
pulp can recover
reversible pulpitis histo
vasodialtion with lymphocyte infiltration
irrreversible pulpitis, what is happening?
cannot recover, acute inflammation and abcess formation
pulpal necrosis
due to untreated pulpitis
tooth killed with blood supply lost, becomes discolored
acute pulpitis
histology similar to?
must be?
what parts of pulp usually affected?
due to?
commonly in what age group?
similar histology to an abcess, lots of PMN
must be no possible drainage
usually at one pulp horn or all pulp
due to bacterial invasion thru non-sclerosed dentin tubules, adolescents commonly
chronic pulpitis
little to no penentration of virulent bac into the pulp
usually in older teeth with previous restorations, slow caires
dentin tubules have narrowed and reparative dentin formed
is chronic hyperplastic pulpitis symptomatic
no, due to decreased nn fibers
CHRONIC HYPERPLASTIC PULPITIS
primary molars with rampant caries
forms a pulp pollup due to open foramen and ample blood supply
prolif of pulp and granulation tissue form the pollup
CHRONIC HYPERPLASTIC PULPITIS
CHRONIC HYPERPLASTIC PULPITIS histology
fibrotic pulp
POTENTIAL SEQUELLAE OF BACTERIAL PULPITIS flow chart
4 factors of PERIAPICAL LESIONS development
Presence of opened or closed pulpitis
Virulence of involved microorganism
Extent of sclerosis of dentinal tubules
Competency of host immune response
PERIAPICAL GRANULOMA
mass of?
located? what type of teeth?
symptomatic?
mass of chronically inflammed granulation tissue-not true granuloma tissue (granulation tissue)
apex of non-vital teeth ONLY
mostly asymptomatic
PERIAPICAL GRANULOMA radiograph
radiolucency at apex
PERIAPICAL GRANULOMA may develop as?
May develop as the inital periapical pathosis or arise after an initial periapical abscess
PERIAPICAL GRANULOMA could become?
a periapical cyst or abscess
periapical granuloma indication for what Tx?
RCT (or extraction if needed)
periapical granulomas and accessory canals
mostly occur on apex, can possibly occur laterally due to accessory canals
histology of a periapical granuloma
may be deposits of?
granulation tissue present (all inflammatory cells present)
may be cholesterol deposits and RC material
periapical granuloma healing
can be healed with good RCT
cyst, components?
Pathologic cavity located in soft tissue or bone lined by
epithelium
RESTS OF MALASSEZ role in cysts
will proliferate forming the epithelial lining of the cysts
APICAL PERIODONTAL CYST (PERIAPICAL CYST)
inflammatory?
most common in which arch?
symptomatic?
growth rate?
tooth vital?
root resorption?
An inflammatory cyst, most common in mandible
Asymptomatic, slow - growing lesion associated with the root apex of a non - vital tooth
External root resorption possible
PA cyst radiograph
radioluceny at apex
can we know a cyst from radiography?
no we need histo/biopsy
are multiple PA cyst possible
yes, multiple non vital teeth
PA cyst histo/ strucutre
wall made of inflam cells
lining usually hyperplastic epithelium
empty lumen
PERIAPICAL ABSCESS
cells?
tooth vital?
may arise as?
symptomatic? why or why not?
Accumulation of acute inflammatory cells at the apex of a non - vital tooth
May arise as the initial periapical pathosis or as an acute exacerbation of chronic periapical lesion ( P h oenix a b s ces s)
Generally symptomatic , but may be asymptomatic if there is a lack of accumulation of purulent material due to a chronic path of drainage
PA abscess histo
lots of PMN= similar to acute inflamm
PA abscess tx and healing
RCT indicated, removal of pulp may allow bone to heal
POTENTIAL DRAINAGE PATHWAYS OF ACUTE PERIAPICAL INFECTIONS
determined by?
DETERMINED BY LOCATIONS OF APEX
1 . Surface of the gingiva (parulis)
2 .Palate (palatal abscess)
3 . Max sinus
4 . soft tissue spaces (cellulitis)
5 . Floor of mouth (ludwig’s)
palatal abscess
PARULIS (GUM BOIL)
due to?
mechanism of formation?
consists of?
acute PA inflammation
purulent material perforates thru bone, periosteum, soft tissue, epithelium and drains through intraoral sinus
Parilus=intraoral opening of the sinus tract
consists of a mass of inflammed granulation tissue with an epithlialized sinus tract
gum boil/ parulis
abscess
localized collection of pus that has accumulated in a tissue cavity, producing flucutance
cutaneous sinus tract
dental abscesses can drain extraorally to the skin by forming these tracts thru bone
oroantral fistula
usually from?
not from pathology, usually trauma
open communication btwn the sinus and the oral cavity
oroantral fistulas commonly have?
granulation tissue form within them
SINUS TRACT VS. FISTULOUS TRACT
sinus tract: from interior to exterior, parulis is the end of the tract
fistulous tract: connects two anatomic cavities (many types)
types of fistulas
oroantral (mouth to sinus)
oronasal
tracheoesphogeal
cellulitis
diffuse spread of an acute inflammatory process thru fasical planes/soft tissue producing the cardinal signs of inflamm
abscess unable to establish a drainage path into the mouth or onto skin
what occurs with cellulitis often?
trismus= hard to open mouth
Ludwigs angina
agressive, rapidly spreading cellulitis involving multiple anatomic spaces: submental, sublingual and submandibular
produces massive swelling of neck that can extend to the clavicles and block airway=death
medical emergency
canvernous sinus thrombosis
emergency?
how can this happen?
associated with infections in what teeth?
medical emergency
valveless vv of face allow retrograde spread of infectious materials from middle third of face
blood clot may form in the cavernous sinus which is life threatening
associated with spread of infection from maxillary teeth
cavernous sinus contents
osteomyelitis can be caused by?
predispositions?
bacterial infection of bone: odontogenic infections, trauma to bone, NUG, NOMA (developing countries)
Predispositions: chronic systemic disease, immune def, decreased vascularity of bone
acute osteomyelitis
spreads thru what part of bone?
tissue rxn? due to?
spread thru medullary spaces
minimal tissue reaction due to rapid onset/ minimal time to react
chronic osteomyelitis
tissue rxn?
what forms? what occurs?
why would antibiotics be hard to use?
prominent tissue reaction-granulation tissue forms and fibrosis occurs
granulation tissue may wall of site making Antibiotics hard to use
osteomyeltits possible drainage?
can occur via a sinus tract
traumas that can cause osteomyelitis?
extraction, fracture
chronic osteomyelitis radiograph
mixed lucent and opaque lesion, ill defined
acute osteomyelitis histo
lots of PMN in bone
acute osteomyelitis
sequestrum
fragment of necrotic bone separated from adjacent vital bone that usually undergoes spontaneous exfoliation
sequestrum histo with gram stain
would see bone and bacterial debris, lack of cells in lacunae
involucrum
non-vital bone encased by vital bone
PROLIFERATIVE PERIOSTITIS/ GARRE OSTEOMYELITIS
form of?
rxn?
most frequently seen in? where?
form of chronic ostemyelitis, osteomylelitis with proliferative periostitis/garre osteomyelitis
periosteal rxn occur which layers of reactive vital bone are formed producing cortical expansion (onion skin)
seen most frequently in children/young adults in man molar/PM areas involving the lower border/ buccal cortex
proliferative periostitis radiograph
must be occlusal view to see onion skin
proliferative periostitis progression
may need to recontour bone
CHRONIC FOCAL SCLEROSING OSTEOMYELITIS/ CONDENSING OSTEITIS
seen in? where?
localized area of bone sclerosis associated with the apices of teeth with pulpal disease
seen in children/young adults involving the man molars and PM
reaction of bone to inflammation
ACTINOMYCOSIS
spp names
morpholgy
gram/O2
commensual?
means ray fungus but is bacterial infection caused by actinomyces spp
A. israelii and A. vicosus
filamentous bacteria: branching
gram +/ anaerobic
part of normal oral flora
CLASSIFICATION OF ACTINOMYCOSIS
Cervico-facial – 5 5 %
Abdomino-pelvic – 2 5 %
Pulmonary – 1 5 %
entry of actinomycoses?
can extend thru?
can disregard?
area of prior trauma: soft tissue injury, perio pocket, non-vital tooth, extraction site, infected tonsil
direct extension thru soft tissue
disregards fascial planes and lymphatics
presentation of cervico-facial actinomycosis
woody induration and fibrosis= hard
draining sinus tracts
suppuration with sulfur granules
cervicofacial actinomycosis radiograph
Ill defined lucency at the site of entry/ infection
CF actinomycosis, sinus tracts
sulfur granule
what is present in the radiolucency of actinomycosis
bacteria
