The break of the epithelial barrier of gingiva has been a subject of minor interest, albeit
playing a key role in periodontal pathology, transitory bacteraemia, and subsequent systemic lowgrade inflammation (LGI). The significance of mechanically induced bacterial translocation in gingiva
(e.g., via mastication and teeth brushing) has been disregarded despite the accumulated knowledge of
mechanical force effects on tight junctions (TJs) and subsequent pathology in other epithelial tissues.
Transitory bacteraemia is observed as a rule in gingival inflammation, but is rarely observed in
clinically healthy gingiva. This implies that TJs of inflamed gingiva deteriorate, e.g., via a surplus of
lipopolysaccharide (LPS), bacterial proteases, toxins, Oncostatin M (OSM), and neutrophil proteases.
The inflammation-deteriorated gingival TJs rupture when exposed to physiological mechanical forces.
This rupture is characterised by bacteraemia during and briefly after mastication and teeth brushing,
i.e., it appears to be a dynamic process of short duration, endowed with quick repair mechanisms. In
this review, we consider the bacterial, immune, and mechanical factors responsible for the increased
permeability and break of the epithelial barrier of inflamed gingiva and the subsequent translocation
of both viable bacteria and bacterial LPS during physiological mechanical forces, such as mastication
and teeth brushing
