Arthroscopic Untethering of the Fat Pad of the Knee: Release or Resection of the Infrapatellar Plica (Ligamentum Mucosum) and Related Structures for Anterior Knee Pain.

Anterior knee pain (AKP), a multifactorial symptom complex, can be successfully treated surgically. A specific diagnosis often cannot be made, but the pain is linked to an unrecognized common factor in most patients: the mechanical behavior of the non-isometric contents of the anterior compartment of the knee-the fat pad (FP) and infrapatellar plica (IPP). The objective of this presentation is to describe an effective arthroscopic technique that treats AKP by addressing this common factor. The operation consists of release or resection of the IPP, or ligamentum mucosum, which tethers the FP. These highly innervated tissues act together as a hydraulic shock absorber, filling the anterior compartment. They stretch and deform at the extremes of knee motion because of constraint centrally by the non-isometric IPP. These dynamic changes in shape are eliminated when the plica is released or resected. Pain perception is from perturbed nociceptive nerves: pain relief results from de-tensioning these contained nerves by untethering the fat pad. Ascribing pain causation is problematic because morphologic change, such as inflammation, fibrosis, or contracture of these structures, is only present in a minority of cases. Nonetheless, AKP is both physically linked to these central, pain-sensitive structures and relieved by this operation.

Evaluation of a new staging classification and a Peritoneal Surface Disease Severity Score (PSDSS) in 229 patients with mucinous appendiceal neoplasms with or without peritoneal dissemination.

INTRODUCTION: Most classifications of mucinous appendiceal neoplasms (MAN) do not take into consideration the type of primary tumor or the burden of peritoneal disease. MATERIALS AND METHODS: We conducted a retrospective evaluation of 229 patients with MAN. The severity of their disease was analyzed with the Peritoneal Surface Disease Severity Score (PSDSS) on a five-point scale that included: (1) the primary appendiceal tumor, (2) the type of peritoneal dissemination, and (3) the burden of disease. Overall survival was analyzed according to five tiers of estimated disease severity based on the above parameters. RESULTS: There were 19, 67, 59, 43, and 41 patients with PSDSS 0, I, II, III, and IV, respectively. One hundred seventy-three patients underwent cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC). Overall survival was 80.0 months in this group with 5-year survival of 100%, 79.2%, 23.3%, and 6.9% in patients with PSDSS I, II, III, and IV, respectively (P < 0.001). On multivariate analysis, sex and PSDSS stage were identified as independent predictors of survival. CONCLUSIONS: The PSDSS appears to be an important prognostic indicator in patients with MANs with or without peritoneal dissemination and may improve selection of patients for appropriate therapy from the time of diagnosis.

Multi-institutional retrospective cohort study of spontaneous pneumothorax.

Spontaneous pneumothorax (SP) affects only a subset of patients in a variety of disorders. This multi-institutional study attempted to identify unique clinicopathologic features of spontaneous pneumothorax (SP) in a large cohort. A total of 111 cases from 109 patients were retrieved from 3 institutions over an 11-year period: 27 women, 82 men. 66 were smokers, 16 were non-smokers, 27 unknown. Sixty-six cases (61%) had identifiable disorders (secondary SP). Seven patients had a family history of lung disease: 2 of pneumothorax, 2 of lung cancer, and 1 each of emphysema, COPD, and not further classified. Forty-three cases (32 men, 11 women) were primary. The average age was 28 (men) and 37 (women). 17 smoked, 14 were non-smokers, and 12 unknown. In 26%, a unique recently described entity, pneumothorax-associated fibroblastic lesion (PAFL), was noted. 16% of this subset also had cellular alveolar septae. Abundant intraalveolar macrophages were noted in 12 cases. Five cases of unknown etiology had extensive bullous lung disease not otherwise classified. One patient had unusual cellular areas suggestive of LAM but negative for HMB-45. In conclusion, several distinct morphologic lesions were identified: PAFL, a subset with cellular septae, and a third with numerous intraalveolar macrophages.

A unique, histopathologic lesion in a subset of patients with spontaneous pneumothorax.

CONTEXT: Spontaneous pneumothorax can be idiopathic (primary), or it can occur in association with an underlying predisposing condition (secondary). Spontaneous pneumothorax may be a harbinger of an undiagnosed clinical condition, which may be associated with serious systemic abnormalities, making early recognition and diagnosis important. The pulmonary pathology of some of these disorders has not been fully elucidated. OBJECTIVE: To review cases of pneumothorax in the hope of identifying pathologic features that might correlate to specific clinical syndromes. DESIGN: The pathology computer files at 3 hospitals were searched for all cases of spontaneous pneumothorax, primary and secondary, regardless of etiology during a 11-year period. Ninety-two cases were retrieved. Each of the cases was evaluated for reactive eosinophilic pleuritis, elastosis, pleural fibrosis, emphysema, intra-alveolar macrophages, cholesterol clefts, vasculopathy, and intraparenchymal or intrapleural cysts. Clinical information regarding asthma and smoking history, site of the pneumothorax, family history, radiographic findings, predisposing conditions, recurrence, age, and sex were extracted from the medical records. RESULTS: In 11 patients (12% of all the patients with spontaneous pneumothorax), a distinctive pattern of pleural fibrosis with islands of fibroblastic foci within a myxoid stroma was noted at the pleural-parenchymal interface or leading edge. These lesions correlated with a select subset of patients, consisting predominantly of young men. CONCLUSIONS: Our review identified a distinct pattern of pneumothorax-associated fibroblastic lesions in a subset of cases of spontaneous pneumothorax. Whether this is related to the pathogenesis of the pneumothorax remains to be elucidated.

Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors.

Inflammatory myofibroblastic tumor (IMT) is an indolent spindle cell proliferation that can histologically resemble various malignant mesenchymal neoplasms; however, it generally behaves as a benign or locally recurrent tumor. Most IMTs involve the lung, mesentery, omentum, or retroperitoneum. We report the clinical and pathologic features of six IMTs of the uterus, one of which was included in a previous report, and emphasize the histologic and immunohistochemical features that distinguish IMTs from uterine spindle cell neoplasms that require aggressive treatment. Recently, translocations of the anaplastic lymphoma kinase (ALK) gene and immunohistochemical expression of ALK have been reported in IMTs of various anatomic sites. We compared ALK expression in uterine IMTs with that in uterine mesenchymal neoplasms with which it may be confused. Patients with IMT were between 6 and 46 years of age. None had a history of abdominal surgery; three were multiparous. The IMTs ranged from 1 to 12 cm in maximum dimension. Three grew as polypoid masses that arose in the lower uterine segment, and two of these prolapsed through the cervical os. The three other tumors grew as bulky myometrial masses with focally irregular borders and infiltrated the endometrium, parametrium, or cervical stroma. There were three main microscopic patterns: a hypocellular pattern, a fascicular pattern, and a hyalinized pattern. A lymphoplasmacytic infiltrate was present in all of the tumors, and most had a myxoid background. Mitotic activity ranged from 0 to 2 mitotic figures per 10 high power fields (HPF) except in one tumor that focally had up to 8 mitotic figures per 10 HPF. No nuclear atypia or necrosis was present. Immunohistochemical expression of ALK was present in a cytoplasmic pattern in all IMTs tested. No ALK expression was identified in uterine leiomyoma (n = 7), leiomyosarcoma (n = 6), carcinosarcoma (n = 4), endometrial stromal sarcoma (n = 4), or normal uterine tissues. Follow-up ranging from 1.5 years to 5 years in 4 patients with uterine IMTs revealed no recurrence or metastasis. IMTs should be differentiated from aggressive uterine mesenchymal tumors because they can be treated conservatively and have a more favorable prognosis. ALK expression appears to be of diagnostic value in conjunction with other immunohistochemical stains.

Cell clusters overlying focally disrupted mammary myoepithelial cell layers and adjacent cells within the same duct display different immunohistochemical and genetic features: implications for tumor progression and invasion.

INTRODUCTION: Our previous studies detected focal disruptions in myoepithelial cell layers of several ducts with carcinoma in situ. The cell cluster overlying each of the myoepithelial disruptions showed a marked reduction in or a total loss of immunoreactivity for the estrogen receptor (ER). This is in contrast to the adjacent cells within the same duct, which were strongly immunoreactive for the ER. The current study attempts to confirm and expand previous observations on a larger scale. METHODS: Paraffin sections from 220 patients with ER-positive intraductal breast tumors were double immunostained with the same protocol previously used. Cross-sections of ducts lined by > or = 40 epithelial cells were examined for myoepithelial cell layer disruptions and for ER expression. In five selected cases, ER-negative cells overlying the disrupted myoepithelial cell layer and adjacent ER-positive cells within the same duct were separately microdissected and assessed for loss of heterozygosity and microsatellite instability. RESULTS: Of the 220 cases with 5698 duct cross-sections examined, 94 showed disrupted myoepithelial cell layers with 405 focal disruptions. Of the 94 cases, 79 (84%) contained only ER-negative cell clusters, nine (9.6%) contained both ER-negative and ER-positive cell clusters, and six (6.4%) contained only ER-positive cell clusters overlying disrupted myoepithelial cell layers. Of the 405 disruptions, 350 (86.4%) were overlain by ER-negative cell clusters and 55 (13.6%) were overlain by ER-positive cell clusters (P < 0.01). Microdissected ER-negative and ER-positive cells within the same duct from all five selected cases displayed a different frequency or pattern of loss of heterozygosity and/or microsatellite instability at 10 of the 15 DNA markers. CONCLUSIONS: Cells overlying focally disrupted myoepithelial layers and their adjacent counterparts within the same duct displayed different immunohistochemical and molecular features. These features potentially represent an early sign of the formation of a biologically more aggressive cell clone and the myoepithelial cell layer breakdown possibly associated with tumor progression or invasion.

Osseous involvement in calcific tendinitis: a retrospective review of 50 cases.

OBJECTIVE: The purpose of this study was to describe the spectrum of radiologic and pathologic manifestations of calcific tendinitis involving bone. MATERIALS AND METHODS: We retrospectively reviewed 50 cases of calcific tendinitis involving underlying bone. Clinical data reviewed included patient age and sex and lesion location. Images reviewed included radiographs (n = 44), CT scans (n = 13), MRIs (n = 16), and bone scintigrams (n = 13). Radiologic examinations were evaluated for the presence of cortical erosion, periosteal reaction, and marrow extension. Pathology confirmation was available in 37 cases. RESULTS: The average age of patients was 50 years (range, 16-82 years), with 29 female patients (58%). Calcific tendinitis with associated bone involvement was seen most commonly in the femur (40%) and the humerus (40%). Concretions were most commonly solid-appearing (50%). Cortical erosion was the most common manifestation of osseous involvement (78% of cases). Marrow involvement was shown in 18 (36%) of 50 cases. Marrow extension was most commonly seen in the lesser and greater tuberosities of the humerus, which accounted for 61% (11/18) of cases. Focal increased radionuclide uptake was seen in 13 (100%) of 13 cases. CONCLUSION: Calcific tendinitis presenting with osseous destruction, marrow changes, and soft-tissue calcifications may be confused with neoplasm both radiologically and pathologically. Recognition of the atypical presentation of this common disease may prevent unnecessary biopsy.

Combined E-cadherin and high molecular weight cytokeratin immunoprofile differentiates lobular, ductal, and hybrid mammary intraepithelial neoplasias.

The terminal duct-lobular unit is the origin of 2 distinct variants of intraepithelial neoplasia traditionally separated into ductal and lobular types based on a combination of cytologic and architectural features. In general, distinction of the fully developed or classic lobular intraepithelial neoplasia (LIN) from various grades of ductal intraepithelial neoplasia (DIN) is not a problem. An increasing number of lesions that appear to have intermediate, overlapping ductal and lobular features are being sent to us for consultation because of the distinctly different clinical implication of the 2 diagnoses. We have separated and designated these as MIN (mammary intraepithelial neoplasia, not otherwise specified), whereas others have categorized them into either a definitive ductal or lobular subtype. The recent findings that LIN lacks immunoreaction for E-cadherin coupled with significantly diminished to absent expression of the high molecular weight (HMW) cytokeratins in more than 90% of grade 1b or higher DIN prompted us to evaluate intraepithelial neoplasias for a possibly more precise immunohistochemical categorization. One hundred and ten examples of intraepithelial neoplasias, consisting of 40 classic LIN, 20 unequivocal DIN 1c to DIN 3 (ductal carcinoma in situ), and 50 MIN, were acquired from the files of the Armed Forces Institute of Pathology. These specimens were tested with an antibody to E-cadherin and with antibody 34ssE12 reactive against HMW cytokeratins 1, 5, 10 and 14. All samples of LIN showed complete absence of reactivity with anti-E-cadherin, whereas all cases of DIN displayed a positive immunoreaction. In contrast, the DIN lesions displayed little or no reactivity with 34ssE12, whereas the lobular lesions showed cytoplasmic reactivity, often in a distinct perinuclear pattern. Twenty-three of the morphologically indeterminate cases could be classified as either ductal or lobular based on the immunoprofile, and 27 demonstrated an immunoprofile that differed from either typical DIN or classic LIN. Among the 27 MIN, 11 were negative for both markers (negative hybrids), whereas 16 were positive for both markers (positive hybrids). These 2 antibodies in combination are extremely useful in distinguishing lobular and ductal lesions and clarifying the nature of some of the morphologically intermediate cases. Also, they have confirmed the presence of a group of intraepithelial lesions (MIN) with not only overlapping morphologic features, but also immunoprofiles distinctly different from either DIN or LIN. These MIN lesions may reflect either a transient stage in the development of DIN and LIN (the immediate post-stem cell stage) or a plastic group in transition from one type to the other. This group needs further evaluation for better understanding of its significance, pattern of progression, and behavior.