We'll continue about inflammatory lesions, next time there gonna be a discussion CRC of
trauma and inflammation lectures together
Inflammatory lesions are one of the most seen in our field, many diseases that we try to
diagnose and treat are essentially inflammatory, including but not limited to caries,
fractures, periodontal diseases, extraction sockets, compound fractures, hematogenous
spread, or even sterile trauma.
Interesting thing about inflammatory mediators is that they could reset the metabolism of
bone, this tipping may cause bone resorption or further deposition depending on how
acute/chronic the situation is, and depending on the distribution that gives rise to two types,
osteitis and osteomyelitis. A very acute inflammation may not be evident on radiographic
modalities coz it hasn't been there for so long and no apparent effect on bone is evident like
actual bone resorption or deposition, however we have all the clinical signs of 'acute' like
redness, swelling, pain and loss of function. Sometimes u can see subtle widening of PDL
space or changes in bone radio opacity.
If it turns to a chronic inflammation -like when the pt wasn't presented that acutely in ur
clinic, or u didn't provide him with proper tx or didn't administer antibiotics, it can be
observed as a radiolucency or radio opacity or a mixture.
If it was osteomyelitis we see sequestration (floating piece of bone that isn't connected to
the haversian system- basically not vascularized necrotic bone), fistula, or pathological
fracture of the jaw which is a fracture in a background of an existing pathology.
Inflammatory lesions are most common around teeth apices, and could be ill defined or well
defined. In chronic cases the virulence of the pathogen is low and the immunity is high, so
more time for the bone to defend itself, and we get the well defined borders here. The
opposite is the case in ill defined borders which can be seen in acute inflammation and
osteomyelitis, so we see an area of transition between normal and affected bone.
What happens to the periosteum when it undergoes an inflammatory process? It gets
elevated due to all the mediators and edema, and the pluripotential cells within will start the
periosteal rxn that is new bone formation. This is noted in cases of aggressive malignancy
and inflammatory process.
Apical rarefying osteitis is a bone inflammatory process located in perioapical areas, with a
radiolucent appearance, this could be a granuloma, abscess or a cyst, we can easily
distinguish them under the microscope except that it's hard to obtain biopsies from all pts.
And the tooth is nonvital in all the three so how to tell them apart? Size is good if u want to
differentiate granuloma from a cyst, also signs and symptoms helps in telling whether this is
an abscess or granuloma.
Abscess could be acute or chronic, while acute is associated with swelling trismus pain etc,
chronic is always associated with fistula.
So for example if no fistula is there, and the lesion is small in size… It's a granuloma not an
abscess.
Remember that granuloma is smaller than a cyst.
We can use vitality testing to differentiate between these three and PCOD, or other types of
cysts (to be discussed in later lectures)
The difference between apical rarifying oseitis and apical sclerosing osteitis is the sclerosing
part (bone deposition). Remember that the more the sclerosing u see, the more chronic the
inflammation.
Osteitis and osteomyelitis differs in the extension of the lesion, osteitis is a more localized
process while the other is generalized. There're actually predisposing factors like older age
groups and immunocompromised, uncontrolled diabetic, alcoholics and drug addicts,
paget's and petrosis pts, Florid COD .. if we have these factors in a pt who has a badly
carious lower molar for instance, most likely it'll cause osteomyelitis (more extensive lesion).
Also if it's a high virulence pathogen it will add to the problem (Specific chronic infections like
syphilis, actinomycosis, TB). Osteoradionecrosis of the jaws is a part of osteomyelitis too.
Apical periodontitis:
Widening of PDL space at the apex of a non vital tooth, spontaneous throbbing pain coz of
edema and pressure. we can see the halo sign here; where the sinus floor is elevated around
the tooth apex coz of all the remodeling by the inflammatory exudates.
Apical rarefying osteitis:
-Low grade rxn to a low virulence bacteria, and we see the 3 options we talked about
(abscess, granuloma, cyst) depending on the case. It's important here to test the vitality, not
to mix it with the periapical scar that's left after the periapical surgery or an over
instrumentation incidence.
Refer to the book for the pics
-We were shown a radiograph on apical sclerosing osteitis, there's a small black radiolucent
component in a supersclerostic background, so the first thing that catches attention is that
small radiolucency, while the sclerotic component may take years to be noted.
-Hypercementosis and apical sclerosing osteitis: the former has the PDL around the lesion, so
we have cementum along with the hypercementosis then the PDL space then lamina dura,
while the latter's components are cementum, PDL space, and then the radio opaque lesion.
Osteomyelitis:
-Extensive lesion involving bone and bone marrow spaces.
-Malnutrition, diabetes, leukemia, anemia, alcoholism are all predisposing factors.
-Interesting finding in our population is that most osteomyelitis pts doesn't have any of the
factors but were linked to a serious resistance to Lincomycin (that is administered in IV route
in dental clinics), more studies are needed anyway.
-They need to be admitted to hospital with IV antibiotics and painkillers, culture sensitivity
tests,..
-Hypovascularity and abnormal bone are major factors
-More in men.
-More in mandible (for vascularity reasons)
-pain, swelling, purulent discharge, redness and fever
-Now when its acute (less than 10 days) u can see nothing on the radiograph.
In day 10 it starts to show a decrease in density of bone, little bit of a radiolucency.
******Try to look for periosteal rxn coz it's one of the most subtle early features that helps
in early diagnosis and higher chance of successful tx without complications.
In chronic: symptoms are less, bacteria and virulence are less, host response is more
effective, in addition to sinus tract formation.
-So in general u see ill defined moth eaten appearance, fistula and sometimes pathological
fractures.. so it needs far more attention.
-sequestrum is a dead piece of bone, looks like it's floating with no connection to the
surrounding, it needs to be taken out surgically (coz it needs a long time to be degraded by
osteoclasts and it'll just increase the healing period if left).
-ill defined borders and perioosteal rxn.. so every case should be suspected for a malignancy
and vice versa, so it could be malignancy with superimposed infection, even though the
symptoms differ in each case (for example it's more painful in osteomyelitis, loss of function,
redness and swelling too). Orthopedists always biopsy every osteomyelitis, and they take a
culture of every bone malignancy
-DDx: Malignancy, Paget's.
''remember that paget's is hypovascularized bone''
-radiographs aren't enough in making diagnosis, u need to look at the full clinical picture,
history and examination and maybe biopsy.
Diffuse sclerosing osteomyelitis:
-The more chronic form of osteomyelitis.
-older age groups, more in females.
-periosteal rxn
-higher immunity and lower virulence, so we go to a latent chronic stage.
-bone deposition could cause jaw enlargement.
-radio opaque component, usually doesn't cross midline (it's an infection so what are the
odds, except for cases of major trauma or smth).
-Another radiograph, presenting a unilateral swelling in the ramus and body of mandible, so
we can exclude florid as it's usually confined to the body of mandible and is apparent in at
least 3 quadrants. We can put fibrous dysplasia b2a5er el list of ddx coz it strikes younger
age groups as it's a genetic problem, while diffuse sclerosing osteomyelitis happens in older
groups. Paget's is bilateral and happens in more than one bone so this also helps in ddx.
-Another radiographic modality that can be used is bone scan (scintegraphy), it gives us an
idea about the number of active cells in a particular area, can be used in osteomyelitis cases,
bone tumors and condylar hypertrophy as well. Hot areas indicates more active cells, so an
area of inflammation would light up in the scan
proliferative perioostitis (Garre's):
-Subtype of psteomyelitis
- younger, females, mostly mandible, mostly 1st molars
-Onion shell expansion (buccal expansion, in the area of the badly carious tooth), it takes
time so it'll give us this characteristic appearance and the reason is; they're young so
stronger immunity and more vascularized bone, so the effect here is much more organized.
-after a while it'll calcify and become as the level of calcification of the bone itself.
Calcification starts from the inner areas all the way to the whole thing, so it forms good
quality bone later on, remodeling of that area takes too much time which is the case in all
sclerotic bone in inflammatory process
Osteoradionecrosis:
-triggered by Radiotherapy or bisphosphonate use, so these treatments affects vascularity of
bone or osteoclastic activity, and disturb the typical metabolism of bone, increasing the risk
of bone breakdown
-not an infectious process, it's a typical inflammatory process with the exudates and
inflammation
- so the cause isn't related to a certain pathogen, u can't give them antibiotic or antiviral or
antifungal tx, the problem here is in the quality of bone, that's why when it starts there's not
much we can do, we can try hyperbaric oxygen or closing down the wound or keeping the
area aseptic as possible, but really there isn't any documented tx. The best thing in our
control is prevention.. suppose someone has a history of radiotherapy or IV bisphosphonate
(in oral the risk is there too, but to a lesser extent), u do ur best not to have any teeth
extracted in that pt, or not to have any surgeries even if it was crown lengthening.
Subgingival placement of matrix band or rubber dam clamp is contraindicated too! Be less
invasive as possible
-radiographically they look like any other acute osteomyelitis; ill defined lesion, some
sclerotic component, and major radiolucency, In addition to pain and trismus, chronic
sequestration. So all's the same except that the pt has a history of bisphosphonate use or
radiotherapy. Sometimes it get's really extensive so we end up in pathological fractures and
we see all its features (loss of cortex continuity, tip deformity, radiolucent or radio opaque
gap depending on the separation or telescoping there is) these are all the cardinal
radiographic signs of fracture, in a background of an existing pathology
Periodontal disease:
-Is all about clinical signs and symptoms-a dentist with a probe is the one who get to make
the diagnosis not radiographs
-The radiographs only provide you with info like localized/generalized, mild/mod/severe,
horizontal/vertical, it can also help in cases of localized bone loss due to wrong post
placement, perforations and root fractures etc, so in these isolated defects radiographs can
actually help. We may see 'possible' furca involvement when there's no bone in between the
roots, but remember that it could have epithelial attachment clinically so it isn't diagnostic
and we have to use nabers probe. We can't tell whether it's active or not by looking at the
radiographs, although
pericoronitis
-we definitely cannot see it on radiographs, it's a soft tissue problem where the operculum
of wisdoms (especially in mandible) gets infected due to food accumulation, can be
associated with pus discharge and metallic taste, trismus, pain…
-sometimes I can see little bit of an underlying osteitis, or sclerosis of underlying bone
Mucositis:
-Widening of the floor of the sinus with localized thickening of mucosa
-could be allergic, odontogenic, bacterial, viral,…
-don't bother your pt with it, except if it was presented in a set up of pt's complaints, pain,
fluid level present in radiograph, or something that's blocking the wall sinus.. in that case it's
better to refer to ENT