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A. Molar/incisor pattern periodontitis was designated as a separate disease – localized aggressive periodontitis – in the 1999 AAP classification because of the location of lesions and its aggressive nature, characterized by early onset and familial aggregation; affected individuals are otherwise systemically healthy [4,5].

Molar/incisor pattern is defined as interproximal loss of attachment localized to at least two permanent first molars/incisors, one of which is a first molar, and involving no more than two teeth other than first molars and incisors. When the interproximal loss of attachment extends to at least three permanent teeth other than first incisors and molars, then the condition is classified as generalized periodontitis. If left untreated, 35% of originally classified molar/incisor pattern periodontitis may progress to generalized periodontitis [6].

B. Molar/incisor pattern periodontitis was formerly called “periodontosis” [7,8] and later called “early‐onset periodontitis” and “localized prepubertal/juvenile periodontitis” in the 1989 AAP classification because the disease generally affects young patients. Molar/incisor pattern periodontitis was later called “localized aggressive periodontitis” in the 1999 AAP classification, based on clinical, radiographic, historical and/or laboratory findings, rather than the age of the patient.

The current classification grouped “chronic” and “aggressive” under a single category “periodontitis” because the specific etiologic or pathologic elements that account for early onset and molar/incisor pattern clinical presentation are insufficiently defined. Current evident does not support the distinction between chronic and aggressive periodontitis as two separate diseases.

C. The following are primary features [9].

 Rapid attachment loss accompanied with severe bone destruction. The progression rate of molar/incisor pattern periodontitis is about three to four times faster than that of periodontitis with grade A or B. The rapidly progressive vertical bone loss is often half‐moon shaped and symmetric to the contralateral tooth [10].

 Patients will usually be medically healthy children or adolescents.

 Strong familial aggregation.

Secondary features that are frequently but not always present include the following.

 Inconsistency in the relationship between the amount of microbial deposits (i.e. supragingival plaque) and the severity of periodontal destruction.

 Elevated levels of Aggregatibacter actinomycetemcomitans and/or Porphyromonas gingivalis.

 Patients usually exhibit hyperactive polymorphonuclear neutrophils (PMNs) in chemotaxis and superoxide (O2 –) production with hyperresponsive macrophages [11,12].

 Elevated levels of inflammatory cytokines (e.g. PGE2, IL‐1α, IL‐1β) from primed macrophages.

 Progression of attachment loss and bone loss may be self‐arresting and remain stationary for years.

D.

Table 1.5.1 Features distinguishing molar/incisor pattern grade C periodontitis from generalized grade C periodontitis.

Features	Molar/incisor pattern grade C periodontitis	Generalized grade C periodontitis
Age of onset	Circumpubertal	<30 years but may be older
Clinical manifestation	Involves no more than two teeth other than incisors and first molars	Involves at least three teeth other than incisors and first molars
Serum antibody response to infecting agents [13]	Robust response	Poor response

E. The prevalence of molar/incisor pattern periodontitis varies among racial and geographic groups. Molar/incisor pattern periodontitis has a 10‐fold higher prevalence in African Americans, Middle Easterners, and Hispanics [14]. The prevalence is ~0.2% in Caucasian populations and ~2% in those of African descent [15,16]. Molar/incisor pattern periodontitis may also start in the primary dentition [17,18]. The proportion of affected males and females is similar [19,20].

F. Nonmotile Gram‐negative anaerobic rods such as A. actinomycetemcomitans, P. gingivalis [21–24], and red and some orange complex species [25] are the most numerous and prevalent periodontal pathogens in molar/incisor pattern periodontitis and are present in most of the diseased sites compared to healthy sites. The microbiomes of molar/incisor pattern periodontitis may vary among different ethnic groups, but A. actinomycetemcomitans (especially serotype b) was found in higher numbers and frequency, at least in the early stage, when compared with other pathogens [21,26]. Aggregatibacter actinomycetemcomitans produces a leukotoxin that affects the antibacterial function of neutrophils. The heightened antibody responses to A. actinomycetemcomitans may also be responsible for the localized periodontal destruction [27].

The exact reason why the disease is localized to first molars and incisors with such early onset in young adults is still debatable. However, those young patients’ hormonal changes and the fact that the first molars and incisors are the first permanent teeth to erupt may alter the microbial environment in some unique way that causes the periodontal destruction [14].

G. The general treatment methods should be similar to those used for periodontitis, including oral hygiene instruction/reinforcement, plaque control, scaling and root planing, and occlusal adjustment (if necessary).

Additional treatments that may be required in certain patients include the following.

 General medical evaluation to determine the presence of any systemic diseases. Consultation with the physician may be indicated.

 Counseling of family members.

 Adjunctive use of amoxicillin combined with metronidazole [28]. Tetracycline is contraindicated in young patients due to the problem of tooth staining. Systemic administration of amoxicillin 500 mg plus metronidazole 250 mg three times daily for seven days with maintenance every three months resulted in significant clinical improvement and reduced levels of key periodontal pathogens in the long term [29].

 Periodontal maintenance with short interval may be needed.

Teeth with poor prognosis are usually extracted mostly in phase 1 or sometimes phase 2 of periodontal therapy. Most of the intrabony defects that result from molar/incisor pattern periodontitis and that are amenable to regeneration are surgically treated using either guided tissue regeneration (GTR) [30] or enamel matrix derivative (EMD) with xenografts/allografts [31,32] (Figure 1.5.9). See the appropriate chapters in this textbook for more details on these surgical techniques. Limited studies have shown that the adjunctive use of local subgingival antimicrobials does not result in additional improvement of clinical parameters.

H. Scaling and root planing in combination with amoxicillin 375 mg and metronidazole 250 mg (t.i.d. for seven days) in patients with A. actinomycetemcomitans‐associated periodontitis improved clinical parameters and suppressed A. actinomycetemcomitans below cultivable levels in most of the patients for up to two years with supportive periodontal therapy once every three to six months [33,34]. Patients showing compliance with the antibiotic regimen also have better treatment outcome. Long‐term stabilization of periodontal health after amoxicillin 500 mg and metronidazole 250 mg plus periodontal surgeries has been reported, with a small percentage (5–10%) showing recurrence in five years [35,36].

Figure 1.5.9 Classical intrabony defect affecting a mandibular first molar in another patient with localized aggressive periodontitis (top left). Guided tissue regeneration (GTR) was performed to regenerate the periodontal defect using bone grating and membrane (top right). Periapical radiographs depict the vertical bony defect before (lower left) and after (lower right) GTR therapy. Significant radiographic bone fill was obtained after GTR therapy.

Most patients have a relatively good prognosis if kept in a maintenance protocol. It has been shown that 73% of patients undergoing supportive periodontal therapy (SPT) at least every six months would not need further retreatment in over 20 years [37]. Long‐term follow‐up case reports have also shown a low recurrence rate with SPT every three to six months for 30 years [38] or in the absence of consistent maintenance for 15 years [39]. However, 8–30% of patients may progress to a generalized pattern of disease [40,41]. Successful regenerative treatment outcomes have also been shown following GTR [30] or using EMD with xenografts [31,32,42].

The success rate of tooth implants in patients with molar/incisor pattern periodontitis is not conclusive. Overall, molar/incisor pattern stage C periodontitis shows less progression and tooth loss than generalized stage C periodontitis. Considering the defect in host response in these patients, it is reasonable to expect lower survival rates of the teeth and implants in these patients, compared to grade A or B periodontitis patients. Clinicians should be aware that these patients are generally younger than those with grade A or B periodontitis. The implant prosthesis would need to remain esthetic and functional for a longer period of time in these patients. Consultation with other specialists to evaluate the alterative restorative options, such as orthodontic treatment, might also help to determine whether or not to extract.