Aggressive periodontal diseases were previously known as early-onset diseases,
namely, prepubertal and juvenile periodontitis. A classification system for periodontal
diseases and conditions published in 1999 effectively combined these two diseases
into one⎯aggressive periodontitis (see Further Reading). This classification, which is
used in this chapter, removed the arbitrary age limitations that were previously
inferred by terms such as prepubertal, juvenile, and even adult periodontitis. It is now
recognized that aggressive periodontitis can affect the primary and permanent
dentitions both in localized and generalized forms.
11.11.1 Primary dentition (prepubertal periodontitis)
The disease may present immediately after the teeth have erupted. In the generalized
form the gingiva appear fiery red, swollen, and haemorrhagic. The tissues become
hyperplastic with granular or nodular proliferations that precede gingival clefting and
extensive areas of recession. Gross deposits of plaque are inevitable as the soft tissue
changes make it difficult to maintain oral hygiene. The disease progresses extremely
rapidly, with primary tooth loss occurring as early as 3-4 years of age. The entire
dentition need not be affected, however, as the bone loss may be restricted to one
arch. Children with generalized disease are susceptible to recurrent general infections,
principally otitis media and upper respiratory tract infections.
Localized disease progresses more slowly than the generalized form and bone loss
characteristically affects only incisor-molar teeth. Plaque levels are usually low,
consequently soft tissue changes are minimal with gingivitis and proliferation
involving only the marginal tissues.
The predominant micro-organisms that have been identified are aggressive
periodontopathogens: Actinobacillus actinomycetemcomitans, Porphyromonas
gingivalis, Fusobacterium nucleatum, and Eikenella corrodens. This suggests that
there is an infective component to the disease, although defects in the hosts' response
have also been identified. Profound abnormalities in chemotaxis and phagocytosis of
polymorphonuclear neutrophils and monocytes are frequently reported in these
patients. These immunological defects are heritable risk factors that help to define
phenotypically the disease entity. Conversely, they may also be associated with more
serious and life-threatening conditions, and thus a full medical screen is indicated.
Oral hygiene instruction, scaling, and root planing should be undertaken at frequent
intervals. Bacterial culturing of the pocket flora identifies specific
periodontopathogens. If pathogens persist after oral debridement, an antibiotic such as
metronidazole or amoxycillin (amoxicillin) should be given systemically after
sensitivity testing, as a short course over 1-2 weeks. Generalized disease responds
poorly to treatment. Some improvement has been achieved following a granulocyte
transfusion in a patient with a defect in neutrophil function. Extraction of involved
teeth has also produced an improvement in neutrophil chemotaxis, which suggests
that the defect may be induced by certain organisms in the periodontal flora.
Furthermore, in severe cases of generalized periodontitis, extraction of all primary
teeth (and the provision of a removable prosthesis) can limit the disease to the primary
dentition. Presumably, anaerobic pathogens are unable to thrive in the absence of
teeth. When the permanent teeth erupt, bacterial culturing of the subgingival flora