The senescence-accelerated mouse (SAM) is a murine model of accelerated senescence and consists of the senescence-accelerated prone mouse (SAM-P) and senescence-accelerated resistant mouse (SAM-R), the latter of which shows normal aging characteristics. SAM shows a high incidence of age-associated microscopic amyloid deposition in synovial joints and intervertebral discs and the lesion is histologically quite similar to that of humans. The amyloid fibril protein of these mice is well characterized as a murine systemic senile amyloid (ASSAM). Twenty SAM-P and three SAM-R mice were used for this immunohistological study. Synovial joints and intervertebral discs were stained by immunoperoxidase method (PAP) using anti-ASSAM and anti-mouse AA antibodies and compared with birefringence in a Congo-red-stained section. Positive staining was observed in annulus fibrosus of the intervertebral discs, blood vessels, synovia, and on the surfaces of the meniscus and articular cartilage, exactly at the same site where green birefringence in Congo-red staining was observed. Both ASSAM and AA existed in the articular structures of SAM and the incidence of AA was significantly correlated with systemic signs of inflammation at autopsy. Among blood vessels, synovium and articular cartilage, there was no one tissue where amyloid deposited earlier than others. It was postulated that amyloid is transported via synovial fluid as its fibrillar form or as a precursor and that it deposits on the surface of articular cartilage.