Circuit 4, station 3

Periodontal diseases encompass a spectrum of pathological processes affecting the periodontium, which comprises the supporting structures surrounding the teeth, including the gingival tissue, alveolar bone, cementum, and periodontal ligament. Within this realm of periodontal diseases, gingivitis stands as the mildest form and prevails in up to 90% of the population. Characterised by inflammation of the gingiva due to the accumulation of bacterial plaque and debris at the tooth-gingival interface, gingivitis represents a reversible condition, responsive to improved oral hygiene practices. On the other hand, periodontitis signifies a more advanced stage, wherein the inflammatory process becomes chronic, destructive, and irreversible. Here, bacterial invasion extends deeper into the periodontium, triggering a host immune response aimed at countering the microbial threat. Paradoxically, these host defence mechanisms also contribute to the progressive destruction of the periodontal tissues. Consequently, periodontitis results in the loss of periodontal attachment, potentially leading to alveolar bone resorption and tooth loss.
Periodontitis is categorised into three distinct groups:
1. Necrotising periodontal diseases
2. Periodontitis
3. Periodontitis as a manifestation of systemic diseases
Necrotisiing periodontal diseases represent an aggressive, rapidly progressing condition primarily observed in immunocompromised individuals, such as those with HIV. This form of periodontal disease is characterised by necrosis of the gingival tissue between teeth, accompanied by bleeding and pain.
Etiology
Periodontal diseases originate from a complex interplay of factors, encompassing patient-specific risk elements and suboptimal oral hygiene practices.
Risk factors can be categorised into modifiable and non-modifiable factors. Modifiable risk factors include habits such as tobacco smoking, inadequate oral hygiene, diabetes mellitus, and pregnancy, while non-modifiable factors comprise age and heredity, encompassing genetic predispositions to periodontal diseases.
Inadequate oral hygiene practices play a pivotal role in the initiation and progression of periodontal diseases. Ineffectual oral hygiene techniques foster the accumulation of bacterial plaque on tooth surfaces, inciting gingivitis and potentially advancing to periodontitis. Numerous studies have established a direct correlation between the extent of dental plaque buildup and the severity and prevalence of periodontal diseases.
In instances of insufficient oral hygiene, anaerobic microorganisms, pivotal in the progression of periodontal diseases, colonise the deeper recesses of the periodontium, where they execute destructive actions. Prominent bacteria found in periodontitis include Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. As these organisms infiltrate deeper into the periodontium, they induce inflammation by triggering the release of inflammatory mediators and host defence products.
Of paramount significance among modifiable risk factors is tobacco smoking, which can elevate the risk of developing periodontal diseases by 5-20 times, with an odds ratio of 5.4 between smoking and chronic periodontitis. Furthermore, smokers exhibit more pronounced bone loss, attachment loss, deep periodontal pockets, and tooth loss compared to non-smokers. Smoking also diminishes the efficacy of periodontal treatments, exacerbating the severity of periodontal diseases.
Diabetes mellitus constitutes another substantial contributor to periodontal diseases. This metabolic disorder is associated with pathological processes that exacerbate periodontal breakdown, including impaired wound healing. Complications arising from diabetes further compound the periodontal disease link, with poorly controlled diabetes correlating with heightened disease progression. Individuals with severe periodontal disease and diabetes have an increased mortality risk compared to those without periodontal disease. Diabetes may act as an initiator of insulin resistance, as it is associated with hyperglycemia, impaired glucose tolerance, and poor glycemic control. Additionally, hyperglycemia can enhance the proliferation of bacteria responsible for periodontal disease, intensifying its impact in diabetic individuals.
Pregnancy introduces hormonal fluctuations that incite an inflammatory response associated with gingivitis and periodontitis. While the precise mechanisms remain elusive, maternal hormones have been positively linked to increased levels of Porphyromonas gingivalis, a pivotal microbe in periodontal disease progression. Both hypoestrogenism and hyperestrogenism have been implicated in contributing to gingivitis during pregnancy.
Age, although non-modifiable, occupies a prominent position among risk factors, extensively discussed in the literature. Older individuals tend to manifest a more severe inflammatory response to plaque accumulation, marked by an increased presence of inflammatory cells. This heightened inflammatory response places older individuals at greater risk of experiencing periodontal tissue destruction. Ageing is also associated with diminished dexterity, resulting in less effective oral hygiene practices. Consequently, older individuals often exhibit higher plaque levels, a known risk factor for the development of periodontal diseases. Additionally, research has shown increased clinical attachment loss (CAL) in individuals aged 60 to 90 in comparison to their younger counterparts.
Finally, several genetically linked systemic disorders have been identified to manifest as periodontal diseases. The literature has documented the aetiology of periodontal diseases within these systemic conditions, including Down syndrome, Ehlers-Danlos syndrome (types IV and VIII), and Crohn’s disease.
Epidemiology
Periodontal diseases represent a pervasive oral health concern, affecting up to 90% of the global population, establishing them as the most prevalent oral diseases worldwide. In the United States, cross-sectional studies reveal that approximately 50% of adults exhibit some form of gingivitis, while up to 80% have experienced periodontal diseases at some point in their lives. Specific demographic groups exhibit an elevated incidence of periodontal diseases, with older individuals, males, and African-Americans displaying a heightened susceptibility. Additionally, lower income and education levels are associated with increased severity of periodontitis.
History and Physical Examination
Periodontal diseases encompass a diverse spectrum of manifestations, often characterised by insidious onset and an absence of overt symptoms during their initial stages. Frequently, the earliest clinical indicator of periodontal diseases is gingival bleeding upon brushing or flossing. Patients may also complain of halitosis (bad breath). More advanced presentations include pain and tenderness upon chewing specific substances, tooth sensitivity, gingival recession, the formation of discolored plaque, tooth mobility, and, in severe cases, tooth loss.
Chronic periodontitis, while potentially affecting individuals of any age, predominantly afflicts middle-aged to older adults. Disease severity in chronic periodontitis is determined by the extent of clinical attachment loss (CAL). It is categorised as mild when CAL ranges from 1 to 2 mm, moderate when CAL is between 3 to 4 mm, and severe when CAL exceeds 5 mm.
A more aggressive variant of periodontitis, formerly known as “juvenile periodontitis” or “aggressive periodontitis,” exhibits similar clinical features but predominantly targets younger patients. Unlike chronic periodontitis, this form often affects specific teeth, particularly first molars and incisors, and may occur even in the absence of extensive plaque accumulation typically observed in chronic periodontitis.
Regular dental screenings are pivotal for the early detection of periodontal diseases and for timely intervention. A thorough review of the patient’s medical history, including comorbidities, is essential. Clinical examination may reveal inflamed gingiva, gingival recession, and occasionally, the presence of periodontal pockets containing purulent exudate. Dental probes are employed to measure the depth of dental pockets adjacent to multiple teeth, with probing depths exceeding 3 mm suggesting the presence of periodontal disease. Depths exceeding 6 mm often necessitate more aggressive therapeutic approaches due to the challenges associated with mechanical treatment. Radiographic assessment, through dental X-rays, aids in assessing bone loss corresponding to pocket depth and disease severity.
Evaluation
The diagnosis of periodontal diseases hinges on comparing clinical findings to the characteristics of a healthy periodontium. This assessment involves visual inspection, periodontal probing, and radiographic evaluation of bone levels. A healthy periodontium typically presents with stippled, pale pink gingiva that closely adheres to the underlying bone. The physiological sulcus between the gingiva and the tooth typically measures 1 to 3 mm and exhibits no signs of bleeding. Conversely, signs of periodontal disease encompass active bleeding upon minimal tissue manipulation, pain, unpleasant taste or odour, the presence of periodontal pockets, radiographic evidence of bone loss, clinical attachment loss, and tooth loss. Radiographs of patients with periodontitis reveal alveolar bone loss proximal to deep periodontal pockets, indicating the presence of periodontal pathogens actively triggering the host immune response. Without intervention, bone loss progresses until it compromises tooth support, leading to tooth mobility and eventual loss.
Treatment and Management
Managing periodontal disease involves a systematic approach, commencing with conservative measures. The initial phase of treatment for all types of periodontitis entails professional dental cleaning, encompassing scaling and root planing to remove dental plaque and calculus both above and below the gum line. Integral to this cleaning process is patient education regarding improved at-home oral hygiene practices. Following the completion of the initial cleaning, patients undergo re-evaluation to assess the periodontal status, including an examination of the periodontium and measurements of probing depths to ascertain whether the disease progression has been halted. If resolution is confirmed, patients are scheduled for regular follow-up cleanings since periodontitis is a chronic condition prone to reactivation when conducive conditions prevail.
An essential component of periodontal disease management involves addressing risk factors. Inadequate oral hygiene practices constitute a primary initiator of periodontal disease. Preventing poor oral hygiene habits involves promoting proper daily oral care practices, combined with professional maintenance at intervals tailored to individual patient risk. Recommended self-care involves a three-step daily regimen comprising brushing, flossing, and rinsing. Referral to a dentist for professional cleanings and scheduled follow-up appointments for monitoring disease progression is also advocated.
Tobacco smoking, a major modifiable risk factor, demands focused attention. Smoking significantly elevates the risk of developing periodontal disease, intensifies disease severity, and diminishes the responsiveness to periodontal therapies. The association between smoking and periodontal disease lessens upon smoking cessation.
Diabetes mellitus is well-established as a contributor to periodontal disease, potentially exacerbating periodontitis-related destruction. Moreover, poor glycemic control is linked to heightened disease progression. Uncontrolled glucose levels amplify mortality risk in individuals with severe periodontal disease. Hence, effective management of diabetes mellitus and prediabetes may enhance the outcomes of periodontal therapy.
In cases of persistent periodontal disease refractory to non-pharmacologic interventions, antibiotics may be employed locally or systemically, depending on disease severity. Chlorhexidine gluconate, an antimicrobial compound, is commonly used as an adjunct to mechanical periodontal therapy. It is typically administered as a mouth rinse but can also be employed in gel, varnish, or subgingival chip forms. Chlorhexidine use, in conjunction with regular tooth brushing, reduces dental plaque accumulation and proves beneficial in treating chronic periodontitis. An emerging pharmacotherapeutic advancement involves a chlorhexidine gluconate chip inserted into periodontal pockets post-cleaning, providing sustained release of the compound at the affected site.
Another adjunctive antimicrobial option, consisting of minocycline hydrochloride microspheres placed into pockets following mechanical debridement, is similar in effect to the chlorhexidine chip, effectively reducing dental plaque accumulation.
In rare cases, systemic antibiotics may be warranted, particularly when deep periodontal pockets persist. Commonly prescribed antimicrobial agents include tetracyclines, penicillins, macrolides, quinolones, cephalosporins, and nitroimidazole compounds. These agents vary in their mechanisms of action and may be prescribed singly or in combination to broaden their effectiveness.
For severe cases of periodontal disease, referral to a periodontist may be necessary. Periodontal surgery may be required to effectively address periodontal pockets or attempt to regain lost bone and attachment resulting from the destructive disease process.
Prognosis
The prognosis of periodontal disease hinges upon various factors, including its stage, grade, contributory elements, and the efficacy of its treatment and management. Generally, a higher disease stage and a more rapidly progressive grade portend a poorer prognosis. Additionally, factors like tobacco smoking and uncontrolled diabetes mellitus can significantly impact the disease’s prognosis.
To assess the prognosis of the disease, clinicians utilise McGuire’s developed guide, which aims to predict the survival of individual teeth. This guide assigns each tooth a score, ranging from good to fair, poor, questionable, or hopeless, based on a comprehensive evaluation of multiple factors. It proves invaluable during the initial disease assessment, re-evaluation post-periodontal therapy, and long-term monitoring, taking into consideration patient age, medical status, oral hygiene, socioeconomic factors, extent and pattern of bone loss, and the current state of periodontal health.