Pulp and Periapical Disease

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PULP AND PERIAPICAL DISEASE : Trauma to a tooth (mechanical, chemical, thermal, infective) often results in pulpal inflammation (pulpitis). (pic E1) Depending on the type of trauma, its severity or duration, the pulpitis may be reversible, but often this is not the case and the inflammation becomes irreversible. The result of untreated irreversible pulpitis is pulp necrosis, followed by the spread of inflammation to affect the apical periodontium (apical periodontitis) and the periapical bone, resulting in bone destruction around the apex of the root (periapical disease). A tooth affected by pulp and periapical diseases should always be treated, it cannot just be ignored. There are two available treatment options, namely to extract the tooth or to perform endodontic treatment and retain the tooth.

Tooth fractures Classification of tooth fractures: Class A1 – involves the enamel only Class A2a – involves the enamel and dentine but has not exposed the pulp chamber Class A2b – involves the enamel and dentine but has also exposed the pulp cavity Fractures may also be classified as crown only, crown-root fractures or root fracture.

Causes of tooth fractures : Chewing hard objects should be avoided. Stones, bones and certain toys are harder than the tooth substance and can result in fracture of the tooth. A slab fracture of the carnassial tooth usually results from dogs chewing, whilst trauma to the anterior teeth (canines and incisors) results from catching a hard object for eg. Stones/Frisbees. Trauma to the front teeth can also result from an anterior collision – with a stationary object or another dog. External head trauma from RTAs or external blows/kicks can also result in tooth fractures.

Tooth abrasion and attrition Wear on tooth surfaces that are in contact with one another or an abrasive surface. This usually results from tooth on tooth contact in certain malocclusions, chewing on fibrous chew toys and balls eg. Tennis balls. (picE2) Occasionally dogs with chronic skin allergies will get abrasion on the incisors from constantly chewing fur/hair. (picE3) Often these conditions result from abnormal excessive behaviour. Dogs should be prevented from cage biting, excessive play with textured balls and chewing stones. Excessive wear will often result in exposure of the pulp cavity. If the wear is gradual, the pulp may respond by laying down more dentine –reparative dentine (also known as tertiary dentine).

Non Vital teeth Teeth can discolour following trauma to the tooth. (picE4). It can be any colour from pink to black, resulting from the haemoglobin breakdown products settling in the dentinal tubules. Studies show that 92% of discoloured teeth have irreversible pulpitis. The pulp may then get secondary infected by anachoresis.

Luxated and Avulsed teeth (picE5) Luxated = partly dislocated from the socket Avulsed = completely removed/pulled out of the socket In these cases of trauma, the blood supply to the tooth is affected, resulting in pulp necrosis.

Caries Caries= tooth decay. (pic E6) Not uncommon in dogs and never really been diagnosed in cats. Caries is an organic demineralization of tooth substance. It is caused initially by acidic metabolites produced during breakdown of simple sugars by specific bacteria (Streptococcus mutans and S.sanguis). Once the enamel has been eroded and the dentine is reached, the destructive process seems to be enhanced. Caries most frequently occurs in the pits and fissures of the molar teeth .

PULPAL REACTIONS - Crown fracture very often involves exposure of the pulp in the young and older animal as the pulp chamber follows the contour of the crown. As the animal gets older there is normally a reduction in the size of the pulp cavity, which is associated with continued deposition of secondary dentine. There are conditions that accelerate the rate of deposition of secondary dentine, thus prematurely reducing the size of the pulp cavity. Attrition and abrasion are two common conditions resulting in a narrow pulp cavity. Injury, orthodontic force and disease can all alter and decrease the pulp chamber and canals. In extreme cases, injury to a tooth will result in the complete obliteration of the pulp chamber and root canals. More unusually, the obliteration is partial, with the pulp chamber retaining the size and shape it had at the time of the injury, and the root canals becoming completely obliterated. On the other hand, injuries that cause inflammation and degeneration/necrosis of the pulp also account for many abnormally large pulp cavities, as dentine production ceases when the pulp is chronically inflamed or necrotic.

PERIAPICAL LESIONS - Pathology in the area surrounding the apex of a root, i.e. periapical pathology, is most commonly a sequel to chronic pulpitis or pulp necrosis. Initially there is inflammation of the apical periodontal ligament. If untreated, the apical periodontitis progresses to involve the surrounding bone, resulting in destruction of the bone, which is replaced by soft tissue. This is evident as an apical rarefaction on a radiograph. The soft tissue may be granulation tissue (periapical granuloma), cyst (periapical or radicular cyst) or abscess (periapical abscess). Pic E7 Treatment for all three entities is the same, i.e. endodontic therapy or if there are complicating factors, e.g. advanced periodontitis, then extraction. An untreated periapical abscess can lead to complications such as osteomyelitis and cellulitis through spread of the infection. ( PicE8) A fistulous tract opening on the skin or oral mucosa may develop. Periapical lesions may be entirely asymptomatic or excruciatingly painful. The clinical signs indicative of periapical pathology are often insidious and not noticed by the owner. It is often only after completion of treatment that the owner reports a dramatic improvement in the animal’s general demeanour. Consequently, periapical lesions confirmed by radiography should be treated even if the animal is not showing obvious signs of pain or discomfort. Similarly, discoloured teeth with a necrotic pulp need to be treated before periapical pathology develops.

Diagnosis of endodontic disease : It is important to determine whether the pulp is exposed or not. If there is an obvious pulp exposure this can be diagnosed clinically by visual inspection of the tooth. Occasionally it may not be obvious and examination under general anaesthesia using a dental explorer probe or path finder needs to be performed. This should NEVER be done in the conscious animal as an exposed pulp will be very sensitive. A red or black spot usually indicates that the pulp is exposed. (pic E9)The red spot indicates a fresh/vital/inflamed pulp, whilst a black spot usually indicates that the pulp has started to become necrotic and the black colour results from degradation of haemoglobin. Whether the pulp is vital or not, the tooth will still require treatment. In cases of caries decay, a brown discolouration is seen on the occlusal surface. Due to the demineralization of the enamel and dentine, this brown discolouration is soft and the explorer probe sticks in the carious dentine. Radiography may help determine whether a root fracture is present, the nature of the fracture (crown-root/vertical fracture) and whether perapical pathology is present. Radiographs also help determine whether teeth with uncomplicated crown fractures need treatment or not. Radiographs do not confirm that the pulp itself is exposed.


COMBINED PERIODONTIC AND ENDODONTIC LESIONS - There are possible pathways of communication between the pulp and the periodontium. These are denuded dentine tubules, lateral and/or accessory pulp canals, and at the apical foramen. Consequently, a periapical lesion may have a periodontal origin and a periodontal type lesion may originate from the pulp. Another possibility is that a lesion is the result of a combination of endodontic and periodontal pathology. The lesions are classified according to aetiology as follows: • A Class I lesion, or endodontic–periodontic lesion, is endodontic in origin, i.e. pathology begins in the pulp and progresses to involve the periodontium. • A Class II lesion, or periodontic–endodontic lesion, is periodontic in origin, i.e. pathology begins in the periodontium and progresses to involve the pulp. (picE10) • A Class III lesion, or true combined lesion, is a fusion of independent periodontic and endodontic lesions.