rel="nofollow" href="#ulink_d016178f-8b07-5a1b-b7b2-a39d009ed1d1">Figure 3.4)
Widened periodontal ligament space
3.5.6 Microscopic Features
Normally bone biopsy is not indicated unless significant pathology (other than condensing osteitis) is suspected
The following microscopic features confirm the diagnosis of condensing osteitis:Replacement of marrow spaces and cancellous bone by dense, sclerotic compact boneBone may show prominent incremental linesMay see fibrosis replacing fatty marrow or scant connective tissueInflammatory changes are absent or minimal
3.5.7 Differential Diagnosis
Differential diagnoses on radiography include:Periapical cemental dysplasiaOsteomaComplex odontomaCementoblastomaOsteoblastomaHypercementosisFigure 3.4 Condensing osteitis. Note the increased radiodensity around the roots of a carious molar (black arrow).(Source: by kind permission of Professor Charles Dunlap, Kansas City, USA.)
3.5.8 Diagnosis
Clinical history is non‐contributory since condensing osteitis is asymptomatic
Most cases of condensing osteitis are incidentally detected on routine radiography
3.5.9 Management
No treatment is required for asymptomatic bony lesions
Tooth that caused the condensing osteitis needs to be identified and treated
Recommended Reading
1 Abbott, P.V. (2004). Classification, diagnosis, and clinical manifestations of apical periodontitis. Endodontic Topics 8: 36–54.
2 Abbott, P.V. and Yu, C. (2007). A clinical classification of the status of the pulp and the root canal system. Australian Dental Journal 52 (1 Suppl): S17–S31.
3 Braz‐Silva, P.H., Bergamini, M.L., Mardegan, A.P. et al. (2019). Inflammatory profile of chronic apical periodontitis: a literature review. Acta Odontologica Scandinavica 77: 173–180.
4 Dabuleanu, M. (2013). Pulpitis (reversible/irreversible). Journal of the Canadian Dental Association 79: d90.
5 Neville, B.W., Damm, D.D., Allen, C.M., and Chi, C.A. (2016). Pulpal and periapical disease. In: Oral and Maxillofacial Pathology, 4ee, 111–136. St Louis, MO: Elsevier.
6 Odell, E.W. (2017). Pulpitis and apical periodontitis. In: Cawson's Essentials of Oral Pathology and Oral Medicine, 9ee, 73–81. Edinburgh: Elsevier.
4 Tooth Wear, Pathological Resorption of Teeth, Hypercementosis and Cracked Tooth Syndrome
CHAPTER MENU
1 4.1 Tooth Wear: Attrition, Abrasion, Erosion, and Abfraction
2 4.2 Pathological Resorption of Teeth
4.1 Tooth wear: Attrition, Abrasion, Erosion, and Abfraction
4.1.1 Definition/Description
Attrition is a normal physiological process characterized by tooth wear caused by tooth‐to‐tooth contact. Usually this affects the tips of cusps of canines and posterior teeth and incisal edges of incisor teeth
Abrasion is tooth wear caused by an abrasive external agent. It affects both enamel and dentin
Erosion is a process characterized by progressive solubilization of tooth substance, usually by exposure to external or gastric acids
Abfraction is the pathological loss of hard tooth substance caused by biomechanical loading forces
4.1.2 Frequency
Prevalence of tooth wear varies from region to region
A universal agreement on prevalence of attrition, abrasion, and erosion does not exist
The most prevalent type of tooth wear is attrition, followed by abrasion and erosion
4.1.3 Aetiology/Risk Factors
Attrition is the physiological wearing of the tooth due to masticatory forces
Bruxism is a known cause of attrition
Abrasion is caused by abrasive dentifrices, cigars, pipes, smokeless tobacco use, improper tooth brushing techniques, and inappropriate use of dental floss or toothpicks
Erosion is caused by dietary acids from soft drinks, fruit juices and wine, chronic regurgitation of gastric contents (as in oesophageal reflux disorder, bulimia, and pregnancy), and chewable vitamin C and aspirin tablets
Abfraction occurs when occlusal forces are eccentrically applied to a tooth
4.1.4 Clinical Features
Attrition:Deciduous and permanent dentitions are affectedIncisal and occlusal surfaces are commonly affected and rarely the entire dentition may be involved (Figure 4.1a)Other teeth may include lingual surfaces of the maxillary anterior teeth and labial surfaces of the lower anterior teethFlat large wear facets corresponding to the pattern of occlusion are commonly seenInterproximal contact points are also affectedUsually asymptomaticAttrition is a slow processDental pulp is usually protected by reactionary dentin and dentinal tubular sclerosisFigure 4.1 (a) Generalized attrition of the incisal and occlusal surfaces. (b) Abrasion of the labial surfaces of maxillary canine and premolars. (c) Erosion of the palatal surfaces in a patient with bulimia(Source: by kind permission of Associate Professor N. Narayana, UNMC Nebraska, USA.)
Abrasion:Incisal and occlusal wear is related to abrasive dietCervical wear of posterior teeth is related to faulty brushing techniquesA horizontal V‐shaped groove is commonly seen at the cervical margin of teeth in those who brush teeth vigorously or use abrasive dentifrice (Figure 4.1b)V‐shaped notches on the incisal edges of anterior teeth are seen in those who use pipes or bobby pins, and in thread bitingAbrasion of the interproximal surfaces is seen in those who use dental floss or toothpicks inappropriately
Erosion:Palatal, occlusal, and labial surfaces of maxillary teeth are commonly affectedCommon among those with bulimia and gastroesophageal reflux disease (Figure 4.1c)Concave facets on palatal and buccal surfaces are seenCusps are dimpledIncisal labial enamel is seen with thin, sharp, and translucent ridgeDentinal hypersensitivity is common
Abfraction:Wedge‐shaped deep defects limited to cervical area like those of abrasionOccasionally subgingival defectsFacial