SEQUELAE. Most dental pain occurs as a result of caries. Initially, caries presents as a painless white spot (decalcification of the enamel, which may be reversible), followed by cavitation and brownish discoloration. ... Untreated caries can progress through the dentine to the pulp, which becomes inflamed (pulpitis)

1. DENTAL CARIES SEQUELAE
Makerere University
BDSU 3

2. Overview;
 Sequelae; Is a condition that is a consequence of a previous disease
or injury.
 Dental caries is a post-eruptive pathological process involving
demineralisation of the enamel, dentine and cementum by action of
acid produced by acid producing bacteria [ mainly S.mutans,
L.acidophilus and A.viscosus]
 Therefore the following conditions result from dental caries from
enamel enamel caries, dentine caries result , then to pulp[pulpitis] ,
to the perapical area, to bone tissue[ osteomyelitis], sorrounding
soft tissues[cellulitis, Ludwigs angina, parapharyngeal space, deep
neck spaces infection,etc] and even death.
 A fairly systemic approach is given below for a better understanding of
dental caries sequelae beginning with Pulpitis and onwards;

3. PULPITIS
 With invasion of infection from dentine tissue, inflammation of the
pulp i.e. pulpitis results. Pulpitis can either be Acute or Chronic,
depending on prevailing conditions. i.e virulence of bacteria.
 In acute pulpitis, there is a rapid inflammatory changes and rapid
death of pulp tissue. Tooth is hypersensitive, as inflammatory
processes progress pain becomes more persistent. In cases of acute
closed pulpitis, initial hyperemia is limited to the area
immediately beneath the irritant, death of odontoblasts and
adjacent mesenchyme occurs. Minute abscess form. For acute
open pulpitis, occurs when there is an acute exposure with
introduction of infection. More often rapid spread of infection is
followed by death of the pulp. Pain tends to be less than acute
closed pulpitis.

4.  In chronic pulpitis, X-sed by mild hyperemia,
predominance of lymphocytes and plasma cells and a more
abundant connective tissue reaction. In chronic closed
pulpitis, destruction of the pulp tissue at the entry of
infection may cause abscess formation with suppuration at
the centre. Granulation tissue is sometimes laid down.
Calcified material may sometimes be deposited around
damaged area. For chronic open pulpitis, a wide exposed
pulp may survive at a site of chronic open pulpitis.
Sometimes, granulation tissue may proliferate until it
reaches the exposure. i.e chronic hyperplastic pulpitis.
Chronic open pulpitis is painless.

5. APICAL PERIODONTITIS
When pulp necrosis following pulpitis, there is spread of infection to
the apical tissues; Apical periodontitis results, inflammatory changes confined
within a minute area between the root and the bone of the socket. Bone is
relatively resorbed and space is made for proliferative granulation when chronic
infection becomes established. Abscess formation occurs but is soon relieved by
resorption of bone to establish partial drainage.
 In acute periodontitis, typical inflammatory reactions confined to the
periapical area occurs. Pus may form in virulent infection. With resorption of
bone, infection spreads to soft tissues through the periosteum. Swelling ensues
to accommodate exudate.

6. Clinical features of acute periodontitis include; tenderness of tooth, overlying
bone or periosteum may be penetrated by exudate after a day, history of pain
due to previous pulpitis.
 In chronic periodontitis, usually mild infection causing little or no symptoms;
it may follow an acute infection that has been adequately drained and
completely resolved.
Presence of lymphocytes, macrophages and plasma cells, granulation tissue(
granuloma) and osteoclasts resorb the bone to accommodate it. Epithelial
proliferation form irregular strands or loops . Abscess formation
Clinical features; in many cases no symptoms and lesion is accidentally found on
radiograph as an area of radiolucency due to bone resorption around granuloma.
 Inflammatory reactions in the periapical region can trigger formation of a
Periapiacal cyst.
From the periapical region, infection progresses to the bone tissue results. i.e.
Osteomyelitis. Is either Acute or Chronic.

7. OSTEOMYELITIS
 In acute osteomyelitis , oral bacteria such as B.porphyromonas or
Prevotella species are important cause but infection is mixed. Infection of
causes acute inflammation in the medullary soft tissues and inflammatory
exudate spread infection through the marrow. Compression of blood vessels
confined in the rigid boundaries of the vascular canals. Thrombosis and
obstruction then lead to further bone necrosis. When bone has died, healing
is by granulation tissue with formation of coarse fibrous bone.
Clinical features include; severe, throbbing, deep-seated pain and with
external swelling. Later distension of periosteum with pus. Overlying gingiva is
red, swollen and tender. Muscle edema causes difficulty in opening mouth and
swallowing. Regional lymphnodes are enlarged and anesthesia or paraesthesia of
lower lip is x-tic
 In chronic osteomyelitis, arises when there is inadequate management of
the acute phase. Persistent low-grade infection is associated with bone
destruction and granulation tissue formation but little suppurstion. Also can
arise as result of weakly virulent bacteria.

8. FASCIAL SPACE INFECTION[ Cervicofacial
cellulitis]
Bacteria can also spread from pericapical region to perioral tissues
causing Cervicofacial cellulitis. Infection usually arises from lower molar or
third molar.
Ludwig’s angina comprises bilateral involvement of sublingual and
submandibular spaces. Infection can readily spread to lateral pharyngeal and
pterygoid spaces.
Affected tissues are swollen and of board-like hardness. The fascitiis can also
be necrotising. Severe systemic upset associated.
Glottic edema or spread into mediastinum may be fatal.

9. CAVERNOUS SINUS THROMBOSIS
Mostly arises from an upper anterior tooth. Is life
threatening , blindness or death result. Clinically
gross edema of the eyelid is associated with pulsatile
exophthalamos due to venous obstruction.

10. END