PMID- 18302675
OWN - NLM
STAT- MEDLINE
DCOM- 20080522
LR  - 20220331
IS  - 1354-523X (Print)
IS  - 1354-523X (Linking)
VI  - 14
IP  - 2
DP  - 2008 Mar
TI  - Cellular basis of verruciform xanthoma: immunohistochemical and ultrastructural 
      characterization.
PG  - 150-7
LID - 10.1111/j.1601-0825.2007.01362.x [doi]
AB  - BACKGROUND: Verruciform xanthoma (VX) holds two basic pathogenic interests: (1) 
      Why and how do macrophage foam cells accumulate exclusively in the sub-basal 
      papillae? and (2) What underlies the disease chronicity? Moreover, an unsolved 
      question is which came first - epithelial hyperplasia or foam cell collection? 
      MATERIALS AND METHODS: We analyzed 36 oral mucosal lesions to dissect a series of 
      linked cellular changes in VX using immunohistochemical and ultrastructural 
      techniques. RESULTS: Macrophage scavenger receptor-1 (MSR-1), monocyte 
      chemoattractant protein-1 (MCP-1), CCR2, and oxidized low-density lipoprotein 
      (ox-LDL) were all expressed by foam cells. VX epithelium showed reactivity for 
      MCP-1, HLA-DR and IL8 in varying degrees, and showed a nearly 40% reduction in 
      Langerhans cell density. In sub-epithelial inflammatory infiltrates, CD8+ T cells 
      preponderated (>70%), but only a minority were positive for granzyme B (<1%). 
      Keratinocyte/basal lamina complex exhibited disruption of basal lamina, 
      squamatization and cytolysis of basal cells, fragmentation of desmosomes, and 
      intraepithelial migration of macrophages. In severely inflamed papillae, necrotic 
      foam cells were scavenged by adjacent macrophages. CONCLUSIONS: Under synergistic 
      regulation of T cells, MCP-1/CCR2-mediated macrophage recruitment in the 
      sub-basal papillae and the lysosomal engulfment of epithelial lipids by 
      MSR-1-bearing macrophages may be central in VX formation. Once developed, 
      ox-LDL-induced foam cell necrosis and macrophage-dependent debris disposal may 
      cyclically perpetuate VX.
FAU - Ide, F
AU  - Ide F
AD  - Department of Pathology, Tsurumi University School of Dental Medicine, 2-1-3 
      Tsurumi, Tsurumi-ku, Yokohama 230-8501, Japan. ide-f@tsurumi-u.ac.jp
FAU - Obara, K
AU  - Obara K
FAU - Yamada, H
AU  - Yamada H
FAU - Mishima, K
AU  - Mishima K
FAU - Saito, I
AU  - Saito I
FAU - Kusama, K
AU  - Kusama K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Denmark
TA  - Oral Dis
JT  - Oral diseases
JID - 9508565
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (MSR1 protein, human)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Scavenger Receptors, Class A)
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Basement Membrane/metabolism/pathology/ultrastructure
MH  - Chemokine CCL2/metabolism
MH  - Female
MH  - Foam Cells/pathology/*ultrastructure
MH  - Humans
MH  - Immunohistochemistry
MH  - Keratinocytes/metabolism/pathology/ultrastructure
MH  - Lipoproteins, LDL/metabolism
MH  - Macrophages/*metabolism/pathology/ultrastructure
MH  - Male
MH  - Middle Aged
MH  - Mouth Diseases/metabolism/*pathology
MH  - Mouth Mucosa/metabolism/*pathology/ultrastructure
MH  - Receptors, CCR2/metabolism
MH  - Scavenger Receptors, Class A/metabolism
MH  - T-Lymphocytes/metabolism/ultrastructure
MH  - Warts/metabolism/pathology
MH  - Xanthomatosis/metabolism/*pathology
EDAT- 2008/02/28 09:00
MHDA- 2008/05/23 09:00
CRDT- 2008/02/28 09:00
PHST- 2008/02/28 09:00 [pubmed]
PHST- 2008/05/23 09:00 [medline]
PHST- 2008/02/28 09:00 [entrez]
AID - ODI1362 [pii]
AID - 10.1111/j.1601-0825.2007.01362.x [doi]
PST - ppublish
SO  - Oral Dis. 2008 Mar;14(2):150-7. doi: 10.1111/j.1601-0825.2007.01362.x.