The pathogenic mechanism of tonsillar
hypertrophy is unknown and lacks a proper infectious or immunological explanation. Epidemiological studies point to polluted environments as the main cause of tonsillar
hypertrophy in the adaptation of the juvenile organism. Tonsils and adenoids of 67 children aged 2-16 years (mean 5.9 years) were divided into three groups: recurrent
tonsillitis (n = 21), recurrent
tonsillitis with tonsillar
hypertrophy (n = 21) and tonsillar
hypertrophy without history of
tonsillitis (n = 25). The following
biological markers were studied: anti-
streptolysin O antibody and anti-deoxy
ribonuclease B antibody serology, microbiology and cell count of granulocytes in tonsils and adenoids as well as lymphocyte subsets and "ex vivo"
endonuclease activity in tonsils. Anti-
streptolysin O antibody and anti-
deoxyribonuclease B antibody titres were significantly raised in recurrent
tonsillitis. Positive bacterial cultures for Streptococcus pyogenes were rare in cases of tonsillar
hypertrophy. T-lymphocytes counts were lower and the proportion of basophils was higher in hypertrophic tonsils than in recurrent
tonsillitis. Two parameters of apoptosis were studied; the activation of
endonuclease, inducing breakdown of
DNA resulting in cell death, and the sensitivity to
thapsigargin, known to trigger the cleavage of
DNA by apoptotic
endonuclease. In children with tonsillar
hypertrophy both parameters were decreased contrasting with those with recurrent
tonsillitis where apoptosis is increased. It may be speculated that the increase of basophils in children with tonsillar
hypertrophy results in increased release of
interleukin-4, which could prevent lymphoid apoptosis and lead to cell proliferation in tonsillar tissue.
CONCLUSION: Whereas recurrent
tonsillitis is characterised by apoptotic death of lymphoid tissue, tonsillar
hypertrophy is caused by environmental pollution agents that trigger the chronic inflammatory process without apoptotic cell death.