Case Report: Resolution of Localized Chronic Periodontitis Associated With Longstanding Calculus Deposits
Case Report: Resolution of Localized Chronic Periodontitis Associated With Longstanding Calculus Deposits
Case Report: Resolution of Localized Chronic Periodontitis Associated With Longstanding Calculus Deposits
Case Report
Resolution of Localized Chronic Periodontitis Associated with
Longstanding Calculus Deposits
Pin-Chuang Lai and John D. Walters
Division of Periodontology, College of Dentistry, The Ohio State University Wexner Medical Center, 305 West 12th Avenue,
Columbus, OH 43210, USA
Correspondence should be addressed to John D. Walters; [email protected]
Received 28 January 2014; Revised 28 March 2014; Accepted 11 April 2014; Published 5 May 2014
Academic Editor: Adrian Kasaj
Copyright 2014 P.-C. Lai and J. D. Walters. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
This report, which is based on nonstandardized serial radiographs obtained over a period of 15 years, documents a case of localized
chronic periodontitis associated with progressive deposition of calculus on the distal aspect of a mandibular second molar. The
site was treated by scaling and root planing, followed by a course of adjunctive systemic azithromycin. Treatment yielded favorable
reductions in probing depth and clinical inflammation, leaving only few isolated sites with pockets no deeper than 4 mm. Two years
after completion of active treatment, there was radiographic evidence of increased bone density distal to the second molar.
1. Introduction
While it is well established that dental plaque is the primary
etiological factor in the pathogenesis of periodontal diseases, epidemiological studies clearly indicate the association
between dental calculus and periodontitis [1, 2]. Dental calculus is calcified bacterial plaque. Supragingival and subgingival
calculus differ in degrees of mineralization, but they are
both typically covered by a layer of bacterial plaque [3, 4].
Although their close relationship with periodontal pathogens
and bacterial by-products makes it somewhat difficult to
investigate the etiological role of dental calculus alone in
periodontitis, it is widely accepted that calculus is a local contributory factor [5]. The rough surface and porous structure
of calculus provide an ideal substrate for bacterial colonization and serve as a reservoir for toxic bacterial components
and antigen [6]. Moreover, studies have identified viable bacteria within supra- and subgingival calculus, including Porphyromonas gingivalis, Treponema denticola, and Aggregatibacter actinomycetemcomitans [79]. Calcifying nanoparticles, the calcified self-propagating entities that are found in
dental calculus may contribute to the formation of calculus
and pathogenic calcification of epithelial cells [10]. If left
untreated, localized periodontal inflammation can persist,
leading to breakdown of supporting tissues. Therefore,
Figure 1: Periapical radiographs of the mandibular right posterior teeth. Radiograph (a) was obtained one month prior to the patients initial
consultation appointment. Arrows indicate the apical and occlusal borders of the calculus deposit. Radiograph (b) was obtained two years
after completion of active periodontal treatment.
2. Case Description
A 59-year-old Caucasian female presented in April 2008 for
a consultation. She had a history of osteopenia and had
been treated with alendronate (Fosamax) for 3 years. Until
recently, her history of dental treatment had been uncomplicated. Her third molars had been extracted and four of
her permanent teeth had been restored with amalgams.
Throughout her life, she had visited her general dentist for
semiannual recall appointments. Her dental hygienist and
dentist had recently detected periodontal pockets around her
maxillary and mandibular right molars. They referred her to
a periodontist, who recommended extraction of teeth 17 and
47 (FDI) and possible surgical treatment of the upper left
molars. Since she had a history of bisphosphonate use, she
was concerned about the potential for development of osteonecrosis of the jaw (ONJ) after the extractions [22]. This
motivated her to seek a second opinion to explore options for
nonsurgical treatment.
The patient brought duplicates of periapical radiographs
that had been obtained one month earlier by her general dentist. The radiographs revealed the presence of moderate periodontal bone loss around teeth 17 and 16 and early to moderate periodontal bone loss around 27 and on the distal aspect of
37 (not shown). There was severe periodontal bone loss on the
distal aspect of 47, which had a pronounced root dilaceration
(Figure 1(a)). In addition, there was a radiopaque mass
associated with the distal aspect of 47, near the level of the
cementoenamel junction. The size and shape of this mass suggested that it was either calculus or a fragment of a third molar
root. The patients oral hygiene was good and clinical signs
of inflammation around the premolars and anterior teeth
were minimal. However, there were probing depths of 5 to
6 mm on the mesial aspect of 17 and the distal aspect of 16
and probing depths of 7 mm on the direct palatal and distopalatal aspects of 27. Tooth 47 had 5 mm depths on its distofacial and direct lingual aspects and a 10 mm depth on the
distolingual. While all of these sites exhibited bleeding on
probing, the distal and direct lingual aspects of 47 were the
Figure 2: Radiographs of the right molars, taken approximately 13 years (a), 11 years (b), 9 years (c), 6 years (d), and 4.5 years (e) prior to
periodontal treatment. The apical and occlusal borders of the calculus are indicated by arrows.
with the distolingual aspect of 27 and the distofacial and distolingual aspect of 47. Given these findings, surgical treatment
was not indicated. The patient was scheduled for periodontal
maintenance therapy every three months after completion of
active treatment. Periodontal probing depths were recorded
at the 12-month and 24-month maintenance appointments.
The patients periodontal probing depths and bleeding upon
probing were essentially unchanged at these visits. A followup radiograph taken at the 24-month recall confirmed that
tooth 47 was free of visible calculus deposits and provided
evidence of increased density of the bone on the distal aspect
of 47 (Figure 1(b)).
3. Discussion
This report documents the progressive deposition of subgingival calculus over a 13-year period, the resorption of the
adjacent bone, and healing following nonsurgical periodontal
therapy. SRP is regarded as the cornerstone of periodontal
therapy. Its effectiveness in the treatment of chronic periodontitis, when accompanied by good oral hygiene, has been
repeatedly shown [23, 24]. Subgingival plaque and calculus
can be substantially removed by SRP [17, 25, 26], creating a
microenvironment that is favorable for tissue healing. In this
case, initial periodontal therapy reduced pocket depths from
a range of 5 to 10 mm to 4 mm. Randomized clinical trials
indicate that SRP of molars leads to a 0.67 to 1.2 mm mean
reduction of pocket depth at sites initially 4 to 6 mm deep
and 0.94 to 2 mm reduction at sites initially deeper than 6 mm
[24]. Isidor and Karring [27] reported a 3.7 mm reduction of
pocket depth at sites with angular defects 12 months after SRP.
4
administration of azithromycin may have also enhanced
the outcome. Although there is currently no standard protocol for antimicrobial chemotherapy in the treatment of
periodontitis, the clinical benefits obtained from adjunctive
systemic antimicrobials can justify their use in patients with
deep pockets and progressive attachment loss [36]. Several
controlled clinical trials have demonstrated that adjunctive
use of systemic azithromycin can significantly enhance the
clinical response to SRP, especially at sites with deep pockets.
At sites with initial depths of 6 mm, adjunctive azithromycin
with SRP resulted in pocket reduction that was approximately
0.7 to 0.9 mm greater than that produced by SRP alone
[37, 38]. In smokers with chronic periodontitis sites initially
deeper than 6 mm, the magnitude of pocket reduction gained
by treatment with azithromycin and SRP was 1.54 mm greater
than that obtained from SRP alone [39]. Azithromycin has a
broad antimicrobial spectrum against a variety of periodontal
pathogens [40]. It typically yields high therapeutic concentrations in gingival tissues and gingival crevicular fluid that are
sustained for at least two weeks after the initial dose [4143].
Its long half-life time allows a once-daily regimen, leading
to better patient compliance. Azithromycin is concentrated
inside host cells including fibroblasts and neutrophils, which
may enhance the clearance of pathogens from diseased sites
[44, 45]. Its anti-inflammatory activity, which is effective in
the treatment of chronic inflammatory pulmonary diseases,
could promote periodontal healing from severe inflammation
[4648]. Consistent with the patients preference to avoid surgical treatment and potential undesirable consequences associated with ONJ, the rationale for utilizing azithromycin was
to enhance the response to SRP. In this specific case, the
potential benefits of azithromycin included suppression of
periodontal pathogens in deep pockets, induction of antiinflammatory activity, and promotion of healing through
persistence at low levels in macrophages and fibroblasts in
periodontal tissues [48]. The observed treatment outcome is
consistent with a previous case series [49], in which bone
regeneration and resolution of gingival inflammation were
observed after a single course of azithromycin in combination
with debridement.
While bisphosphonates are effective in conserving bone
mass and bone trabecular thickness in patients with osteoporosis or osteopenia, their long-term side effects are sources
of concern. In this case, a history of treatment with alendronate and concern about the potential risk of ONJ following extraction of tooth 47 had motivated the patient to
investigate alternative treatment options. Alendronate has an
estimated terminal skeletal half-life of 10.9 years, so its benefits and any side effects are prolonged [50]. While the risk of
developing ONJ in patients who have taken relatively low oral
doses of antiresorptive agents appears to be low, treatment
plans that minimize periosteal and intrabony exposure or
disruption are preferred [22].
It is clear that detection of oral disease at sites that are difficult to access can be challenging. Using tactile exploration
alone, it is difficult to detect calculus on the distal aspect of
a distally inclined second molar. Similarly, radiographic calculus detection can be undermined by the predominance of
radiopacities associated with the bony architecture of the
Conflict of Interests
The authors have no conflict of interests to declare.
Acknowledgment
The authors are grateful for the assistance of Dr. Eric Anderson in editing the radiographs.
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