Pathway 2
Buccal (labial) spread extra-orally
This pathway will occur if the tooth apex is closer to the buccal bone cortex (i.e the anterior aspect of the teeth) and so the swelling will be visible buccally
The swelling will present extra-orally if the root length of the tooth is long
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General steps of the infection:
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Follows the general notes of infection (i.e bacteria gets in and spreads down to the apex of the tooth and then eventually erodes it way through the mandibular bone cortex)
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Then, when the apex of the tooth is closer to the buccal bone cortex, the infection will exit buccally
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But, if the roots of the tooth is long, then the exit point of the infection is below the origin of the buccinator muscle, then this will result in buccal space infection.
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NOTE – That buccal space is common to both maxilla and mandible.
Buccal space
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Borders
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​Medial = buccinator muscle and buccopharyngeal fascia and mucosa
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Lateral = skin of the cheek and subcutaneous tissue
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Anterior = posterior border of zygomaticus major muscle, above, and the depressor anguli oris muscle, below
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Posterior = edge of masseter muscle
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Superior = zygomatic arch
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Inferior = inferior border of the mandible
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Contents of buccal space
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Buccal pad of fat
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Stensen’s duct (aka parotid duct)
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Facia artery
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Important to note that the buccal space is a potential space – so it doesn’t usually exist in normal health
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Signs of buccal space infection:
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Extra-oral/cheek swelling – the swelling will be below the zygomatic arch but above the inferior border of the mandible
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Pain and tenderness
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Obliteration of buccal vestibule
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Swelling of upper/lower lip
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Stages of Infection
​A tooth with long roots such that the apex is positioned below and deep to the buccinator attachment to the bone can cause a facial swelling. This infection starts out in the same way as the short-rooted tooth infection. In this case, however, the root is long and the apex is positioned below the buccinator muscle attachment.
During the initial stages of the tooth infection, the healthy tooth gets invaded by bacteria contained in plaque, which thrive off the carbohydrates in the mouth and produce acid, which slowly destroys the enamel layer.
When the bacteria gain access to the dentine, they invade the dentinal tubules and in this way gain access to the pulp chamber in the middle of the tooth. Within the pulp chamber, the bacteria incite an acute inflammatory reaction which causes an increase in the hydrostatic pressure within the tooth and leads to hypoxia and this leads to destruction of the contents of the pulp and roots canal system, effectively killing the tooth.
It is here, within the pulp chamber, that most of the bacteria will reside, and having destroyed any access for white blood cells normally carried in the blood vessels, makes eradicating the bacteria difficult without either extracting the tooth itself or at least removing the dead contents of the pulp and root canal system and sterilising this area to kill the bacteria. The presence of bacteria means that their by-products/ toxins can leak out of the apex of the tooth, where the nerve would normally exit, and these insight an inflammatory response in the body that causes vasodiltation that in turn causes an increase in hydrostatic pressure within the apical tissues of the periodontal ligament, instigating bone resorption and so a widening the periodontal ligament. The causes the formation of pus (consisting of dead and dying white blood cell and bacteria) which is an abscess.
​Because the apex of the tooth is positioned deep to and below the buccinator muscle, the hydrostatic pressure created due to this bacterial infection triggers an acute inflammatory reaction, erodes through bone and invades the soft tissue below the buccinator, causing an extra oral swelling, also seen as a facial swelling.
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The infection presents as a facial swelling. This infection is treated in a similar way to short rooted tooth infections, through removal of the tooth by extraction, or removal of the dead contents of the root canal and pulp chamber by an endodontic root treatment, and draining the pressure on the soft tissue by incision and drainage of the pus from the facial swelling to create a path of least resistance for the pus to drain.