Chronic periodontitis: a case report

U. Rakesh*, Kirthana Rao

Department of Dental and Maxillofacial Surgery, Kauvery Hospital, Chennai, Tamilnadu, India

*Correspondence: drrakeshdorai@gmail.com

Abstract

Periodontitis is an inflammatory condition affecting the gingiva and supporting structures of the teeth. This can affect any age group and is caused by various factors ranging from poor oral hygiene to genetic predisposition. The clinical features range from mild gingivitis to severe necrotizing periodontitis. Unfortunately, most patients do not have acute symptoms and hence report to their dentists only at an advanced stage, which demands extensive dental treatment. In this article, we present the case report of a patient diagnosed with generalized chronic periodontitis with a multifactorial etiology. A specific treatment plan was designed for this patient based on his clinical presentation and investigations, but due to certain challenges a deviation was required in the original plan. The patient was treated with a multidisciplinary approach, prioritizing rehabilitation, to enable him to use his dentition which in turn enhanced his nutritional status and general health.

Keywords: Gingivitis, Periodontitis, Inflammatory disease, Plaque control, Oral prophylaxis

Background

Gingivitis is an inflammatory condition affecting the gingiva around the teeth. Periodontitis is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms. This results in progressive destruction of the periodontal ligament and alveolar bone with increasing probing depth formation, recession or both, ultimately leading to premature loss of teeth. Approximately 10% of the global adult population is highly vulnerable to severe periodontitis, 10–15% appear to be completely resistant to it, while the remainder vary between these two situations [1]. The etiology of periodontitis is most commonly due to accumulation of calculus around the tooth due to poor oral hygiene [2]. The other predisposing factors could be diabetes mellitus, puberty, menstruation, pregnancy, menopause, hyperparathyroidism, hematologic diseases, immune deficiencies, genetic disorders, stress and psychosomatic disorders, nutritional influences, medications, cardiac diseases, smoking, chewing tobacco etc. Periodontitis is seen as the direct consequence of the invasion of gingiva and surrounding structures, predominantly by gram-negative anaerobic bacteria such as A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus, C. rectus, E. nodatum, P. micros, S. intermedius and Treponema sp. Though the etiology is understood as to be bacterial, the pathogenesis is considered inflammatory. Emerging evidence suggests that the host inflammatory response might dictate the composition of the biofilm and the emergence of pathogens, causing the occurrence of periodontitis in the susceptible host [3]. Periodontitis is classified as ‘generalised’ when more than 30% of the dentition is involved and ‘localised’ when less than 30% of the dentition is affected with periodontal damage and the rest of the dentition is affected with gingivitis.

The clinical presentation is gingival inflammation with visible gingival attachment loss, bleeding on probing, periodontal pocket formation with or without associated tooth mobility. A visible clinical presentation of gingival overgrowth is caused by a variety of etiological factors and is exacerbated by local bacterial biofilm accumulation. The periodontopathogen products act on the gingival tissues activating cellular events that induce the alteration of connective tissue homeostasis and the destruction of the alveolar bone. The polymorphonuclear leukocytes and monocytes pass from the subepithelial connective tissue through the junctional epithelium and into the gingival sulcus. The mononuclear cells, together with molecules they secrete and others originating from junctional epithelial cells, blood and tissue fluid represent the first line of defence in the control of the perpetual microbial challenge. This leads to the activation of several key molecular pathways, which ultimately activate host-derived proteinases that enable loss of marginal periodontal ligament fibres, apical migration of the junctional epithelium and allows apical spread of the bacterial biofilm along the root surface leading to periodontal pocket formation and bone loss [4].

Case Presentation

A 60-year-old male patient reported to our Kauvery dental OPD with a chief complaint of sensitivity and mobile teeth in his right upper back tooth region for two weeks with associated difficulty in chewing. He had intermittent pain which subsided on taking medication. He was a Scuba diver and a swimming coach who used to work for the Saudi Royals. The patient gave a history of smoking 20 cigarettes per day for the past 30 years, which he had quit a year back. He was a diabetic and had undergone a coronary artery bypass graft surgery one year back. His medications included Aztor 20 mg, Cardivas 6.25, Clopilet A 150, Cilacar 10 mg, Ondero and Cipla. The intraoral examination revealed severe accumulation of plaque, calculus and stains on his teeth with associated halitosis. On inspection, the gingiva appeared erythematous, swollen and soggy with receded margins involving the entire dentition (Fig. 1). On palpation, tenderness was exhibited with bleeding on probing and increased periodontal pocket depth. Grade 3 mobility was observed in the right upper and lower molars and premolars, few upper and lower incisors and also the left upper premolar and molar teeth. Generalised Grade 1 mobility was seen involving the other teeth. Spacing was seen in the maxillary and mandibular anterior teeth. The radiographic investigations included an Orthopantamograph which revealed horizontal bone loss involving multiple teeth and pathologic migration of maxillary and mandibular anterior teeth (Fig. 2). The bleeding time was 2 mins and the clotting time was 5 min. The final diagnosis was generalised chronic periodontitis as the bone loss involved.

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Fig. 1. Pre-treatment intra-oral photographs showing accumulation of plaque, calculus and associated swollen gums.

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Fig. 2. Orthopantamograph showing horizontal bone loss involving multiple teeth

Treatment plan

The treatment planned for this patient was to perform a gross scaling and extract the teeth with poor prognosis, severe mobility and bone loss after checking a complete blood count and a cardiology opinion. The extraction was to be carried out after modifying the anticoagulant drug dosage under antibiotic prophylaxis. A replacement was to be planned for the edentulous areas after adequate healing.

Treatment rendered and outcome

As per cardiologist’s advice, anticoagulants were stopped for five days before the procedure. INR was checked which was well within normal limits and antibiotic prophylaxis was administered as a preliminary preparation. A gross scaling was done and 2% lignocaine was administered to block the inferior alveolar nerve and the long buccal nerve, following which intra alveolar extraction of the right lower posterior teeth was done. The extraction sockets were curetted well to remove all the granulation tissue and saline irrigation was done. Following the extractions, profuse bleeding with pus discharge from tooth no. 46 region was seen. Digital pressure with gauze was placed over the extraction sockets as usual but with continuous profuse bleeding from the sockets, there was a need for a hemostat – surgispon to be placed in the socket. Suturing was attempted but the fragile mucosa started to bleed, leading to a blood-filled surgical site, and only one simple interrupted suture could be placed successfully. Digital pressure using a gauze soaked in adrenaline was given for 15 to 20 minutes. Once the bleeding was controlled to some extent, 5 to 6 simple interrupted sutures were placed to approximate the tissues and establish wound closure and hemostasis. The patient was given tablet Trapic 500 mg to ensure post-operative hemostasis. Post-operative instructions and emergency contact numbers were shared. The next day, a complete gingival curettage was performed around the other existing teeth to ensure elimination of granulation tissue and removal of sub-gingival calculus. The patient was reviewed after one week and the other extractions were planned after four weeks. A considerable reduction in the gingival swellings were seen. The gingiva looked coral pink in colour with stippling denoting normal colour, contour and consistency. Cardiologist opinion and consent was obtained again. The anticoagulants were stopped again for five days and the other extractions were completed. This time a significant reduction in bleeding was observed with digital pressure with a gauze alone doing the trick. The patient was reviewed subsequently and the wound healing was satisfactory with adequate closure of the extraction sockets (Fig. 3). The patient was asked to maintain a meticulous plaque control regimen which involved regular brushing, use of an antiseptic mouthwash containing chlorhexidine and gingival massage with a topical styptic solution containing Cetrimide, Tannic acid and Zinc chloride. After a healing period of two months, the edentulous areas were replaced with acrylic removable partial dentures as an interim replacement for his lost teeth and he is awaiting fixed partial dentures (Fig. 4).

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Fig. 3. Post extraction photographs showing healed gingival tissue.

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Fig. 4. Post treatment photographs showing replacement of missing teeth with interim partial dentures.

Discussion

The first challenge in treating periodontitis is timely and proper diagnosis. Since this disease is relatively asymptomatic, the patient reports only at a moderate or advanced stage. The second challenge is properly controlling all the factors contributing to the disease which is vital in achieving a good treatment outcome. The third challenge involves long term maintenance of the periodontium. The backbone of periodontal treatment consists of mechanical removal of bacterial deposits and calculus from the subgingival environment either by using hand instruments or ultrasonic devices, performed either surgically or non-surgically, along with a strict regimen for plaque control [5]. The treatment always aims at preserving most of the teeth and extracting only the poor prognosis teeth with severe bone loss or bone loss involving the furcation. It is also important to provide a self-cleansable environment for the patient to maintain the periodontium plaque free.

In this particular case, a phased interventional dental treatment was needed. Though almost every dental treatment should start with an oral prophylaxis like scaling, we tend to overlook that for correcting the chief complaint or for economic reasons. The common belief is that waste of time and money in a prophylaxis is unwarranted as the tooth is going to be extracted, but preparation of inflamed tissue is very important before any invasive dental procedure. We also have to be extremely watchful about the tissue behaviour when patient has multiple co-morbid conditions and parafunctional habits for a long time. As the saying goes, ‘Failing to prepare is preparing to fail., in order to have a good outcome for any treatment modality, it is imperative to get all the inputs local and systemic, analyse and discuss various treatment options and formulate a final plan. In this case, the patient as well as the supporting doctors were informed about the challenges in completing the dental treatment in one sitting and a phased surgical management was agreed with an excellent final result.

Conclusion

Effective management of Periodontitis lies in timely and accurate diagnosis. Elimination of predisposing factors followed by a meticulous plaque control regimen are equally significant to contain disease progression (Fig. 5).

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Fig. 5. Pre-treatment, mid-treatment and post–treatment.

References

  • Muñoz-Carrillo JL, Hernández-Reyes VE, García-Huerta OE, Chávez-Ruvalcaba F, Chávez-Ruvalcaba MI, Chávez-Ruvalcaba KM, et al. Pathogenesis of Periodontal Disease. 2019.
    https://www.intechopen.com/books/periodontal-disease-diagnostic-and-adjunctive-non-surgical-considerations/pathogenesis-of-periodontal-disease.
  • Muna S, Elburki. The Ecology and Pathogenesis of Periodontal Disease. BAOJ Dentistry 2018;4:042.
  • Van Dyke TE. The etiology and pathogenesis of periodontitis revisited. J Appl Oral Sci. 2009;17:51.
  • Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 world workshop on the classification of periodontal and peri-implant diseases and conditions. J Periodontol. 2018;(Suppl. 1): S173-S182.
  • Shaddox LM, Walker CB. Treating chronic periodontitis: current status, challenges, and future directions. Clin Cosmet Investigat Dent 2010;2:79-91.

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