Professor Yun Fu Zhao Department of Stomatology Changzheng Hospital Second Military Medical University 415 Fengyang Road Shanghai 200003 China Email: firstname.lastname@example.org
Background: Hypercementosis may be idiopathic or secondary to either local factors or systemic disorders. However, periodontitis as an aetiologic factor in the formation of hypercementosis has never been documented in the literature.
Methods: We report a case of periodontitis with hypercementosis, affecting the right mandibular second premolar and first molar teeth.
Results: Our patient’s maxillary was edentulous and the mandibular teeth #47, #43, #42, #41, #31, #32, #33, #36, #37 were missing. The right mandibular second premolar and first molar had first-degree mobility and second-degree mobility respectively. Periodontal pocket depth in the right mandibular second premolar and first molar were 5 mm and 8 mm at buccal pockets, 6 mm and 9 mm at distal pockets, respectively. The radiograph revealed that the roots of both teeth were grossly thickened and blunted. The right mandibular first molar was extracted and sent for histopathological examination. The definitive diagnoses were periodontitis and hypercementosis.
Conclusions: The concomitant occurrence of periodontitis and hypercementosis in our patient suggests that periodontitis is a predisposing factor for hypercementosis development. This condition may be associated with various local stimuli and possible compensative phenomenon.
Hypercementosis was defined by Gardner and Goldstein as ‘an excessive growth of cementum of the tooth’, observed radiographically as circumscribed cementum hyperplasia in 1931.1 This condition is characterized by an excessive, non-neoplastic deposition of radicular cementum and may involve a single tooth, several teeth or the entire dentition (generalized). In many instances, hypercementosis affects the premolar teeth and presents in bilaterally symmetric distribution. Radiographically, hypercementosis is characterized by an overgrowth of cementum contiguous with normal radicular cementum and contained within the boundaries of the periodontal ligament and lamina dura.1,2
Hypercementosis may present secondary to either local factors or systemic disorders, but in most cases represents an idiopathic, age-related phenomenon. Systemic disturbances associated with a more generalized hypercementosis include Paget’s disease of bone, thyroid goiter, rheumatic fever, arthritis, acromegaly, calcinosis, and possibly vitamin A deficiency. A hereditary factor may also be involved, especially in younger patients. Those of local origin usually involve one tooth or a small group of teeth and include periapical pathosis, parafunctional occlusal trauma, and lack of functional opposition (hypercementosis of impacted teeth).1,2 However, periodontitis as an aetiologic factor in the formation of hypercementosis has never been documented in the literature.3 The purpose of this paper is to report a case of periodontitis with hypercementosis, affecting the right mandibular second premolar and first molar teeth in a 76-year-old female patient and to discuss possible aetiologic factors.
A 76-year-old female patient presented with a mild pain of the right mandibular first molar while chewing on some hard substance that had been present for one month. Oral examination revealed that the maxillary was edentulous and the mandibular teeth #47, #43, #42, #41, #31, #32, #33, #36, #37 were missing. There was a full denture sitting on the upper jaw and an eight-unit removable partial denture sitting on teeth #46 and #35. Her right mandibular teeth were free of caries and dental restorations and electric pulp test demonstrated that all of the right mandibular teeth had a vital pulp. The right mandibular second premolar and first molar had first-degree mobility and second-degree mobility respectively. Periodontal pocket depth in the right mandibular second premolar and first molar were 5 mm and 8 mm at buccal pockets, 6 mm and 9 mm at distal pockets, respectively. There was pain on percussion of the first molar. From the radiograph, the roots of the right mandibular second premolar and first molar teeth can be seen to be grossly thickened and blunted due to a fairly symmetrical deposition of a radiopaque material on their surfaces (Fig. 1). Also noted was that both second premolar and first molar had obvious alveolar bone loss with widening of the periodontal ligament, most pronounced at the first molar. The clinical and radiological signs were consistent with periodontitis and hypercementosis.
A review of the patient’s dental history revealed that she had had chronic periodontitis for 26 years. All of the missing teeth had been extracted consecutively since 2007 and these extractions had been less traumatic procedures. Teeth #35 and #46 had served as abutments for two years. All of the remaining teeth had always reacted vitally to pulp testing except for the left mandibular second premolar which was treated endodontically in 2007 and has been asymptomatic ever since.
To establish a definitive diagnosis, the decision was made to remove the right mandibular first molar, leaving the second premolar in situ. The lesion was removed in toto. Granulation tissue present in the alveolar defect was curetted. The tooth specimen and granulation tissue were sent for histopathological examination. Macroscopically, a yellowish hard substance with an irregular surface could be observed in the apical and interradicular area of the extracted tooth (Fig. 2). The thickness of the hyperplastic cementum ranged from 1 to 3 mm. The ground section showed that the bulk of cementum was made up of cellular cementum (Fig. 3). The histopathologic analysis of the soft tissue showed signs of chronic inflammation, resembling granulation tissue. The definitive diagnoses were periodontitis and hypercementosis. The follow-up panoramic radiograph showed normal bone healing six months after and no left mandibular premolars of involvement with hypercementosis (Fig. 4).
Cementum is an adaptable component of the periodontium which may respond to changing functional demands. The formation of cementum is characterized by apposition throughout the functional stage of the tooth life. Sometimes this apposition of cementum is excessive, leading to a very thick cementum layer. This condition is termed hypercementosis.4 Hypercementosis may be idiopathic or associated with a wide variety of conditions that may be either local or systemic in character. Systemic factors tend to lead to a more widespread distribution of hypercementosis (generalized) with symmetrical enlargements of entire roots. Local factors include chronic periapical infection, lack of function due to unopposed teeth and abnormal occlusal trauma. In general, these local factors, especially periapical pathosis, can cause hypercementosis of a single pulpally affected root with formation of a bulbous or nodular enlargement. In spite of the fact that abnormal amounts of cementum are present, the affected roots are separated from periapical bone by both normal appearing periodontal ligament space and intact lamina dura, except Paget hypercementosis which is complete absence of periodontal membrane and lamina dura.1,2,5
Hypercementosis may be completely asymptomatic and found on routine radiographic examination. The diagnosis of hypercementosis is made based on the characteristic radiographic features described. Hypercementosis does not require treatment.6 Once hypercementosis is diagnosed, an effort should be made to identify and remove local causative agents and rule out the presence of systemic disorders such as Paget’s disease in the appropriate clinical context.2 It is interesting to note that hypercementosis augments the total root surface area, which makes the tooth more stable and resistant to occlusal forces as seen in the present patient. Our patient had a long-standing history of chronic periodontitis; three of the four first molar teeth had been extracted due to advanced periodontitis since 2007. The remaining right mandibular first molar with hypercementosis had almost completely lost its bony support due to periodontal disease, but only had second-degree mobility and still served as an abutment for two years. The possible explanation for this condition in our patient is that this excessive apposition of cementum in the apical half of the root may compensate for loss of periodontal tissue due to periodontal disease, thus maintaining the firmness of the tooth.
Cementum is a specialized connective tissue covering the outermost layer of calcified matrix on the root surface, with a primary role to connect the periodontal ligament to the root surface.7 In general, the cemental matrix is porous, allowing only permeation of water and inorganic ions under physiological tissue conditions. Nevertheless, the structure of the diseased root surface is also permeable to saliva organic components and plaque bacterial by-products.7 Invasion of bacteria into cemental matrix has been demonstrated in chronic periodontal pathosis.8,9 Infected cementum has been characterized as a reservoir of periodontopathogenic bacteria. In periodontal involved teeth, plaque bacterial products have been detected in the 10–12 μm deep surface layer.8 Furthermore, Lygre et al.10 found bacterial lipopolysaccharide at a distance of 70 μm from the surface of the periodontal diseased roots. In teeth with heavily infected root canals, bacterial substances have been detected near the dentino-cemental junction.11 Like condensing osteitis, the pathogenesis of hypercementosis in association with periapical pathosis may also be explained by a mild, low grade, chronic infection that exerts a productive phenomenon, but in this case an infection of cementum rather than bone.1 On the other hand, as Suter et al.3 pointed out, the roughness of the root surface because of hypercementosis could have favoured the bacterial contamination leading to localized bone loss with marked gingival recession and overall poor prognosis of the affected teeth. Moreover, intact lamina dura and periodontal membrane space is seen with non-pathologic hypercementosis whereas a definite break in its continuity suggests associated chronic inflammation. In the present case, both related teeth had abnormal periodontal ligament spaces, suggesting that these lesions were associated with chronic inflammation. Because the older radiographs were not obtained and compared, the chronology of periodontitis and hypercementosis development was unknown. Since chronic periapical infection has been implicated in hypercementosis, it might be interesting to speculate that chronic periodontitis may have played a role in the pathogenesis of cementum hyperplasia in our patient.
The pathogenesis of hypercementosis is still uncertain. Many causative factors have been associated with hypercementosis. When associated with local factors, hypercementosis typically involves only the tooth or teeth associated with the inciting agent. At present, it is not possible to draw any conclusions from our patient because it remains unclear why some teeth with periodontitis develop hypercementosis, whereas others are unaffected. For this reason, the search for potential inciting factors is still indispensable. However, we can postulate that hypercementosis induced by periodontitis might contribute to several causative factors, including compensation for loss of periodontal tissue, lack of function due to unopposed teeth or abnormal occlusal trauma and a mild, low grade, chronic inflammation stimulus.
In conclusion, the concomitant occurrence of hypercementosis and periodontitis in our patient suggests that periodontitis also appears to be a predisposing factor for hypercementosis development. This condition may be associated with various local stimuli and possible compensation. However, it is unclear whether one or several factors may have a role in the pathogenesis of cementum hyperplasia in this condition that warrants further investigation.