Читать книгу Clinical Cases in Periodontics - Группа авторов - Страница 25

A. The pathogenesis of periodontal diseases is multifactorial in nature, involving dental plaque, susceptible host, and environmental factors (Figure 1.1.4) [2]. Thus, during medical and dental history‐taking, clinicians should obtain information related to these factors.

Susceptible Host

Patients with diabetes may be at greater risk for developing periodontal diseases compared to healthy counterparts, especially when the diabetic condition is not under control (HbA_1c >7.0%) [1,3]. If necessary, medical consultation with the patient’s physician should be considered. Furthermore, some patients may be susceptible to periodontal diseases genetically. Thus, under family history‐taking, the patient should be asked about the periodontal conditions of his or her family members.

Environmental Factor

Cigarette smoking is a risk factor for developing periodontal diseases [1,4,5]. Under social history‐taking, the patient should be asked about their smoking habit (i.e. never smoked, past smoker, or active smoker). Smoking habit should be recorded as number of cigarettes consumed per day as well as number of years of active smoking.

Figure 1.1.4 Pathogenesis of periodontal diseases.

Source: modified from Kwon and Levin [2].

Dental Plaque

Dental plaque is the etiologic factor for periodontal diseases [6]. Under dental history‐taking, patients should be asked about their routine home oral care or dental plaque control. Their daily frequency of toothbrushing as well as interproximal cleaning (i.e. floss, interdental brush, interdental toothpick) should be recorded. During clinical evaluation, a plaque disclosing tablet may be used to objectively record the patient’s plaque control as well. Furthermore, patients should be asked about their previous periodontal treatment as well as its outcome, all of which should be recorded. If necessary, a consultation with the patient’s previous dental or periodontal provider may be considered.

B.

Furcation Involvement

According to previous studies, furcated molars have a significantly greater chance to be lost than nonfurcated molars [7–9]. Thus clinicians should proactively evaluate molars (or any other multirooted teeth) for furcation involvement, which would ensure their treatment in a timely manner, improving their periodontal prognosis. For easier detection of furcation involvement, a Nabers probe (Figure 1.1.5) may be used instead of a regular periodontal probe.

Figure 1.1.5 Nabers probe (Hu‐Friedy, IL, USA).

Glickman’s Furcation Classification

Grade I	Incipient suprabony lesion. Radiographic changes are rarely found.
Grade II	Furcation bone loss with a horizontal component. Radiographs may not show bone loss in the furcation.
Grade III	A through‐and‐through lesion that is not clinically visible because it is filled. Radiographs show a radiolucency in the furcation.
Grade IV	A through‐and‐through lesion that is clinically visible. The soft tissue has receded apically. Radiolucency is clearly visible in the furcation area.

Figure 1.1.6 Mucogingival anatomy.

Mucogingival Deformity

In general, to maintain gingival health (Figure 1.1.6), the presence of at least 2 mm width of remaining keratinized gingiva is preferred [10]. Mucogingival deformity may be recorded as present for any tooth with less than 2 mm width of remaining keratinized gingiva.

Pathologic Migration

A tooth with a significant periodontal breakdown with severe bone loss may undergo pathologic migration (Figure 1.1.7) [11]. In the case presented above, tooth #3 showed evidence of pathologic migration resulting in supraeruption as well as acquired open interproximal contact between tooth #3 and tooth #4. Clinicians should also evaluate any possible acquired pre‐mature occlusal contact in these teeth with pathologic migration, resulting in occlusal trauma or fremitus.

C. Stage [1] (Tables 1.1.1 and 1.1.2)

The greatest interdental clinical attachment loss of 14 mm (probing depth of 12 mm + gingival recession of 2 mm) was noted on tooth #3 mesiopalatal aspect, with bone loss extending beyond the apical third of the root. Tooth #3, as well as tooth #14 with interdental clinical attachment loss >5 mm, were assigned to stage III. Considering only two of 25 teeth were affected to the same severity, the extent and distribution descriptor “localized” was assigned.

Grade [1]

Figure 1.1.7 Resolution of pathologic migration after successful periodontal treatment, resulting in reduction in acquired diastema between the maxillary central incisors.

Table 1.1.1 Classification of periodontitis based on stages defined by severity (according to the level of interdental clinical attachment loss [CAL], radiographic bone loss and tooth loss), complexity and extent and distribution.

Source: Papapanou et al. [1].

Periodontal stage	Stage I	Stage II	Stage III	Stage IV
Severity	Interdental CAL at site of greatest loss	1–2 mm	3–4 mm	≥5 mm	≥5 mm
	Radiographic bone loss	Coronal third (<15%)	Coronal third (15–33%)	Extending to middle or apical third of root	Extending to middle or apical third of root
	Tooth loss	No tooth loss due to periodontitis	Tooth loss due to periodontitis of ≤4 teeth	Tooth loss due to periodontitis of ≤5 teeth
Complexity	Local	Max. probing depth ≤4 mm Mostly horizontal bone loss	Max. probing depth ≤5 mm Mostly horizontal bone loss	In addition to stage II complexity:Probing depth ≥6 mmVertical bone loss ≥3 mmFurcation involvement Class II or IIIModerate ridge defect	In addition to stage III complexity, need for complete rehabilitation due to:Masticatory dysfunctionSecondary occlusal trauma (tooth mobility degree ≥2)Severe ridge defectBite collapse, drifting, flaringLess than 20 remaining teeth (10 opposing pairs)
Extent and distribution	Add to stage as descriptor	For each stage, describe extent as localized (<30% of teeth involved), generalized, or molar/incisor pattern

Table 1.1.2 Classification of periodontitis based on grades that reflect biologic features of the disease including evidence of, or risk for, rapid progression, and anticipated treatment response, and systemic health.

Source: Papapanou et al. [1].

Periodontitis grade	Grade A: slow rate of progression	Grade B: moderate rate of progression	Grade C: rapid rate of progression
Primary criteria	Direct evidence of progression	Longitudinal data (radiographic bone loss or CAL)	Evidence of no loss over 5 years	<2 mm over 5 years	≥2 mm over 5 years
	Indirect evidence of progression	% bone loss/age	<0.25	0.25–1.0	≥1.0
		Case phenotype	Heavy biofilm deposits with low levels of destruction	Destruction commensurate with biofilm deposits	Destruction exceeds expectation given biofilm deposits; specific clinical patterns suggestive of periods of rapid progression and/or early‐onset disease (e.g. molar/incisor pattern, lack of expected response to standard bacterial control therapies)
Grade modifiers	Risk factors	Smoking	Nonsmoker	Smoker <10 cigarettes/day	Smoker ≥10 cigarettes/day
		Diabetes	Normoglycemic/no diagnosis of diabetes	HbA 1c <7.0% in patients with diabetes	HbA 1c ≥7.0% in patients with diabetes

As direct evidence of progression was not available, indirect evidence was used instead. The percentage bone loss/age was calculated as follows: 80% of alveolar bone loss on #3/44 years old = 1.82. Thus, grade C was assigned.

D. According to the latest 2017 World Workshop on the topic of peri‐implantitis [12,13], there is strong evidence indicating a higher risk of peri‐implantitis development in patients who have a history of periodontitis, poor oral plaque control, and lack of regular periodontal maintenance therapy after implant placement. Furthermore, patients with active periodontal diseases or deep periodontal pockets may be at greater risk of developing peri‐implant diseases than periodontally healthy patients [14,15]. Thus, prior to proceeding with dental implant therapy, clinicians should carefully examine the periodontal conditions carefully and ensure that the patient does not have any active periodontal diseases. Oral hygiene habits need to be developed and meticulous home care abilities should be achieved prior to dental implant planning [16].

E. Clinical signs of occlusal trauma are often overlooked by clinicians; however, the following findings can provide valuable diagnostic information and help formulate the proper treatment plan for patients. According to the 2017 World Workshop on Classification of Periodontal and Peri‐Implant Diseases and Conditions on the topic of occlusal trauma [17], the following list of clinical/radiographic indicators could help identify occlusal trauma: fremitus, progression of mobility, occlusal discrepancies, wear facets, tooth migration, fractured tooth, thermal sensitivity, discomfort/pain on chewing, widening PDL space, root resorption, and cemental tear (Figure 1.1.8). It is important to understand that occlusal trauma by itself does not initiate periodontitis; however, there is evidence suggesting that it alters progression of the disease when combined with dental plaque [18]. It is also important to perform proper occlusal analysis when performing regenerative periodontal surgery, as there evidence to support the view that tooth mobility plays a role in the regenerative outcome [19].

Figure 1.1.8 Cemental tear on tooth #24 resulting in localized alveolar bone loss and increase in mobility. Secondary occlusal trauma was noted during clinical evaluation.

Edentulous alveolar ridge width/height should be recorded during the initial comprehensive examination [20]. This would ensure proper execution of dental implant therapy (implant size selection, depth/angulation of implant fixture, distance between adjacent tooth and implant, prosthetic emergence profile, screw vs. cement retained prosthesis and prosthetic occlusal form).

Esthetic plastic periodontal therapy is also a component of periodontal specialty; therefore, proper documentation of the patient’s smile line (low, average, high) and gingival margin harmony plays a crucial role in treatment planning. When a patient presents with high smile line, it is important to determine the main causative reason (altered passive eruption, vertical maxillary excess, hypermobile lip or combination) [21,22].