Clinical attachment loss
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Clinical attachment loss (CAL) is the predominant clinical manifestation and determinant of periodontal disease.
Anatomy of the attachment
Teeth are attached to the surrounding and supporting alveolar bone by periodontal ligament (PDL) fibers; these fibers run from the bone into the cementum that naturally exists on the entire root surface of teeth. They are also attached to the gingival (gum) tissue that covers the alveolar bone by an attachment apparatus; because this attachment exists superficial to the crest, or height, of the alveolar bone, it is termed the supracrestal attachment apparatus.
The supracrestal attachment apparatus is composed of two layers: the coronal junctional epithelium and the more apical gingival connective tissue fibers. The two layers together form the thickness of the gingival tissue and this dimension is termed the biologic width.
Plaque-induced periodontal diseases are generally classified destructive or non-destructive. Clinical attachment loss is a sign of destructive (physiologically irreversible) periodontal disease.
In gingivitis, inflammation localized to the supracrestal region of the periodontium leads to ulceration of the junctional epithelium. Although this is technically a loss of clinical attachment (because, in health, the epithelium attaches to the surface of the tooth), the term clinical attachment loss is used almost exclusively to refer to connective tissue attachment loss:
Sites with periodontitis exhibit clinical signs of gingival inflammation and loss of connective tissue attachment. Connective
tissue attachment loss refers to the pathological detachment of collagen fibers from cemental surface with the concomitant apical migration of the junctional or pocket epithelium onto the root surface.
- Itoiz, ME; Carranza, FA: The Gingiva. In Newman, MG; Takei, HH; Carranza, FA; editors: Carranza’s Clinical Periodontology, 9th Edition. Philadelphia: W.B. Saunders Company, 2002. pages 26-7.
- Armitage, GC. Clinical evaluation of periodontal disease. Perio 2000 1995;7:39-53