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Deeply infiltrating endometriosis can be defined as endometriosis infiltrating deeper than 5 mm under the peritoneal surface. Type I is a conical lesion suggested to be caused by infiltration; type II is mainly caused by retraction of the bowel over the lesion; type III is the most severe lesion suggested to be caused by adenomyosis externa. Severe cases are clinically apparent by nodularities in the pouch of Douglas, whereas mild and subtle forms of deep endometriosis are easily missed. Clinical examination during menstruation and scrutiny at laparoscopy for indurations, followed, preferably, by CO2-laser-excision are the key features for diagnosis and treatment. It is important to realize that depth of infiltration and lateral spread cannot be evaluated by laparoscopic inspection but only during excision, that CA125 concentration but not ultrasound or nuclear magnetic resonance can be helpful in the diagnosis, and that in the most severe cases medical pretreatment is advocated. Results of excision, as evaluated by disappearance of pain in some 80% of women, by a cumulative pregnancy of some 70% and a low recurrence rate, are excellent. The peritoneal fluid is thought to play a key role in the physiopathology of deep endometriosis which is considered to be endometriosis which has escaped from the influence of the peritoneal fluid. This concept is clinically important for the medical treatment of endometriosis, which is suggested to shrink deep lesions and to bring them back under peritoneal fluid control. A model of endometriosis is proposed and discussed. Subtle lesions are considered a natural condition occurring intermittently in all women, whereas we question whether mild endometriosis is a disease. In some women endometriosis has an aggressive behavior and develops into cystic ovarian endometriosis or into deeply infiltrating endometriosis. In this model subtle and mild forms would be called "endometriosis," whereas deep and cystic ovarian forms could be called "endometriotic disease." It is stressed that deep and cystic ovarian endometriosis are two distinct entities, which is important for our understanding of endometriosis, for classification and for treatment of endometriosis.

PFMC consisted mainly of phagocytic and human leukocyte antigen (HLA)-restricted or HLA unrestricted cytotoxic cells capable of reacting to various antigens entering the cavity from the lower genital tractus. Furthermore, the decreased NK activity reported in PB and PF of women with endometriosis was not likely to be caused by a quantitative defect, since the percentage of NK positive lymphocytes was not different between women with and without endometriosis.

In women with endometriosis, changes in peripheral blood and peritoneal fluid white blood cell (WBC) populations have been reported, but it is known whether these alterations are casually related to or a consequence of endometriosis. The purpose of this study was to test the hypothesis that peripheral blood and peritoneal fluid WBC populations are altered in baboons with spontaneous and induced endometriosis compared to animals without disease. Peripheral blood and peritoneal fluid samples were obtained at laparoscopy from 60 baboons with a normal pelvis (n = 23), spontaneous endometriosis (n = 19) and induced disease (n = 12), luteal phase (n = 20), pregnancy or nursing (n = 11) and in non-cycling animals (n = 8). The WBC concentration was analysed with a Coulter counter and fluorescent antibody cell separation (FACS) analysis was used to measure cluster designation (CD)2, CD4, CD8, interleukin (IL)2R and leucine (Leu) M5 subsets. In peripheral blood, the percentage of CD4+ and IL2R+ cells was increased in baboons with stage II-IV spontaneous or induced endometriosis, suggesting that alterations in peripheral blood WBC populations may be an effect of endometriosis. In peritoneal fluid the WBC concentration and percentages of Leu M5+ macrophages and CD8+ lymphocytes were only increased in baboons with spontaneous endometriosis and not in animals with induced disease, suggesting that alterations in peritoneal fluid WBC populations may lead to the development of endometriosis. In summary, the results of this study suggest that peripheral blood and peritoneal fluid immune cell populations are affected in baboons with endometriosis.

Leucocyte subpopulations localized in endometriotic lesions were analysed using the avidin-biotin immunoperoxidase technique on 15 biopsies obtained by CO2 laser excision. Qualitative assessment of the leucocyte subpopulations was performed with a panel of antihuman monoclonal antibodies for leucocytes (anti-Hle-1), T-lymphocytes (anti-leu-4), T helper/inducer (anti-leu-3a), T suppressor/cytotoxic (anti-leu-2a), B cells (anti-leu-12), HLA-DR (anti-HLA-DR), macrophages (anti-leu-M3) and natural killer cells (anti-leu-7, anti-leu-11; anti-leu-19). Leucocyte common antigen (anti-Hle-1)-positive cells were present in all lesions and were the most frequent stromal leucocytes. Of these, the T lymphocytes are the most frequent subpopulation together with the macrophages. The CD4/CD8 ratio was 0.78. No anti-leu-7 and/or anti-leu-11-positive cells were found although a substantial amount of anti-leu-19-positive cells were found in each lesion. There were very few B cells present in the ectopic endometrial lesions. In conclusion, an important amount of cytotoxic lymphocytes (anti-leu-2a -and anti-leu-19-positive cells) and macrophages (anti-leu-M3) were found in the endometriotic lesions. The possible importance of these intraendometriotic leucocytes for the pathophysiology of endometriosis will be discussed.