OBJECTIVETo characterize the symptoms of neurogenic intrapelvic syndrome and the pathogenic mechanisms.

METHODSA total of 537 patients with neurogenic intrapelvic syndrome were treated in the Takano Hospital between 2001 and 2005. Clinical data were analyzed retrospectively.

RESULTSThe mean age was 58.5 years old. There were 205 males and 332 females. There were 80 patients(14.9%) who presented with only one symptom with anorectal pain being the most common one (43.8%, 35/80). One hundred and fifty-six(29.1%) patients had two symptoms with anorectal pain and difficult evacuation being the most common combination (26.3%, 41/156). There were 144 patients (26.8%) complained of 3 symptoms and the most common combination was anorectal pain, difficult evacuation, and abdominal discomfort (30.0%, 43/144). A combination of 4 symptoms was reported in 105 patients(19.6%) with the combination of anorectal pain, incontinence, abdominal discomfort, and lumbar discomfort being the most often(65.7%, 69/105). In addition, there were 52 patients(9.7%) who had above 5 symptoms simultaneously. The frequencies of the 5 symptoms were 73.6% for anorectal pain, 27.9% for incontinence, 69.6% for difficult evacuation, 55.3% for abdominal discomfort, and 53.6% for lumbar discomfort.

CONCLUSIONSSymptomatology of neurogenic intrapelvic syndrome is complicated. The pathogenic mechanism may be related to concurrent dysfunction of sacral nerve and pelvic splanchnic nerve.

Encopresis ; etiology ; Female ; Humans ; Male ; Middle Aged ; Pelvic Pain ; etiology ; Retrospective Studies ; Syndrome

The immune-stromal cell interactions play a key role in health and diseases.In periodontitis,the most prevalent infectious disease in humans,immune cells accumulate in the oral mucosa and promote bone destruction by inducing receptor activator of nuclear factor-κB ligand(RANKL)expression in osteogenic cells such as osteoblasts and periodontal ligament cells.However,the detailed mechanism underlying immune-bone cell interactions in periodontitis is not fully understood.Here,we performed single-cell RNA-sequencing analysis on mouse periodontal lesions and showed that neutrophil-osteogenic cell crosstalk is involved in periodontitis-induced bone loss.The periodontal lesions displayed marked infiltration of neutrophils,and in silico analyses suggested that the neutrophils interacted with osteogenic cells through cytokine production.Among the cytokines expressed in the periodontal neutrophils,oncostatin M(OSM)potently induced RANKL expression in the primary osteoblasts,and deletion of the OSM receptor in osteogenic cells significantly ameliorated periodontitis-induced bone loss.Epigenomic data analyses identified the OSM-regulated RANKL enhancer region in osteogenic cells,and mice lacking this enhancer showed decreased periodontal bone loss while maintaining physiological bone metabolism.These findings shed light on the role of neutrophils in bone regulation during bacterial infection,highlighting the novel mechanism underlying osteoimmune crosstalk.