Anatomical Description of the Dorsal Capsulo-Scapholunate Septum (DCSS)-Arthroscopic Staging of Scapholunate Instability after DCSS Sectioning.

Background The dorsal capsuloligamentous scapholunate septum (DCSS) is a confluence of the dorsal capsule, the dorsal intercarpal ligament (DIC), and the scapholunate interosseous ligament (SLIOL). It appears to play a role in the stability of the scapholunate articulation. The purpose of this study was to describe the anatomical basis for this structure and to investigate its role in scapholunate instability through sectioning of this structure followed by an arthroscopic and fluoroscopic analysis. Material and Methods In the anatomical part of the study we dissected 3 fresh cadaver wrists to examine the anatomy of the DCSS. In the arthroscopic part of the study we assessed the EWAS grade of SL instability before and after sectioning the DCSS and measured the scapholunate and radiolunate angles fluoroscopically. Results Sectioning the DCSS increased the EWAS grade of SL instability but did not affect the scapholunate gap, the scapholunate angle or radiolunate angle. Conclusion We have demonstrated that there is a distinct structure that is separate from the dorsal capsule, which we have labeled the Dorsal Capsuloligamentous Scapholunate Septum. We believe that the DCSS is a previously unreported secondary stabilizer of the SL joint which may have therapeutic and prognostic implications.

Dorsal wrist capsular tears in association with scapholunate instability: results of an arthroscopic dorsal capsuloplasty.

Purpose The purpose of this study is to report the association of dorsal wrist capsular avulsion with scapholunate ligament instability and to evaluate the results of an arthroscopy-assisted repair. Methods We retrospectively reviewed 10 patients with a mean age of 39.1 years suffering from chronic dorsal wrist pain. They underwent a wrist arthroscopy with an evaluation of the scapholunate ligament complex from the radiocarpal and midcarpal compartments. An avulsion of the dorsal intercarpal ligament (DICL) from the scapholunate interosseous ligament (SLIL) was visible from the radiocarpal compartment in all cases, while the SLIL was intact. The DICL tear was repaired with an arthroscopy-assisted dorsal capsuloplasty. Patients were assessed preoperatively and postoperatively by the QuickDASH (Disabilities of the Arm, Shoulder, and Hand) questionnaire, by the Visual Analog Scale (VAS) for pain, and by a clinical and radiological examination. Results Preoperatively, all patients had reduced flexion and radial deviation of the affected wrist. On the lateral radiograph, 5 of the 10 patients showed an increase of the scapholunate angle (60 to 85°). The scapholunate instability was graded as Messina-European Wrist Arthroscopy Society (EWAS) II in five cases and as grade IIIB in five cases. A tear of the ulnar part of the triangular fibrocartilage complex (TFCC) was found in seven cases. At a mean followup of 16 months, the wrist range of motion (ROM), the grip strength, the QuickDASH, and the VAS of pain improved significatively. The scapholunate angle was normalized in all cases. Discussion Isolated tears of the DICL at its insertion from the dorsal part of the SLIL can be associated with scapholunate instability in the absence of an injury to the SLIL. The diagnosis is made arthroscopically. The arthroscopic dorsal capsuloplasty is a minimally invasive technique that provides short-term satisfactory results. Further studies are needed to determine whether repair of the DICL tear could prevent secondary destabilization of the scapholunate ligament complex. Level of evidence IV (case series) Diagnosis.

MMP- and TIMP-secretion by human cutaneous keratinocytes and fibroblasts--impact of coculture and hydration.

Epithelial-mesenchymal interactions are important in wound healing and scarring, but are difficult to study in vitro. We have previously reported on an in vitro keratinocyte-fibroblast coculture system exploring these interactions and found that coculture modifies the levels of cytokines they secrete. The same coculture model was used to study changes in MMP- and TIMP-activity. We hypothesised that the previously shown decrease of collagen is partly due to increased MMPs. Adult human cutaneous keratinocytes and fibroblasts were cocultured under serum-free conditions. Keratinocytes were either kept at the air-liquid interface or hydrated. The conditioned medium was submitted to a multiplex sandwich enzyme-linked immunosorbent assay including gelatinases, collagenases, stromelysins, and tissue inhibitors of metalloproteinases. Collagen content was determined by western blot. Zymography depicted the gelatinases in conditioned media. For confirmation of the coculture results fibroblasts were treated with conditioned media from keratinocyte monocultures as well. MMP-1, MMP-9, and MMP-10 were mainly secreted by keratinocytes, whereas MMP-2, TIMP-1 and -2 by fibroblasts. MMP-13 was secreted by both cell types at comparable levels. Collagenases, gelatinases, MMP-3, and TIMPs increased significantly in cocultures compared to monocultures. Hydration of keratinocytes revealed a significant increase of MMP-3 and MMP-2, and a decrease of TIMP-2. Paracrine interactions between keratinocytes and fibroblasts modify strongly MMPs and TIMPs, whereas hydration of keratinocytes had a smaller impact in this context. The observed changes may be in part responsible for reduced collagen in coculture-conditioned media. The present coculture experiments reemphasise the role of epidermis in controlling scarring.

The role of the epidermis in the control of scarring: evidence for mechanism of action for silicone gel.

Hypertrophic scars can be reduced by the application of silicone dressing; however, the detailed mechanism of silicone action is still unknown. It is known that silicone gel sheets cause a hydration of the epidermal layer of the skin. An in vitro co-culture experiment has shown that hydration of keratinocytes has a suppressive effect on the metabolism of the underlying fibroblasts resulting in reduced collagen deposition. We tested the hypothesis that silicone sheeting in vivo has a beneficial effect on scarring by reducing keratinocyte stimulation, with a resulting decrease in dermal thickness, hence scar hypertrophy. Silicone adhesive gel sheets were applied to scars in our rabbit ear model of hypertrophic scarring 14 days postwounding for a total of 16 days. Scarring was measured in this model by the scar elevation index (SEI), a ratio of the area of newly formed dermis to the area of the dermis of unwounded skin, and the epidermal thickness index (ETI), a ratio of the averaged epidermal height of the scar to the epidermal thickness of normal epidermis. Specific staining [anti-PCNA (proliferating cell nuclear antigen) and Masson trichrome] was performed to reveal differences in scar morphology. SEIs were significantly reduced after silicone gel sheet application versus untreated scars corresponding to a 70% reduction in scar hypertrophy. Total occlusion reduced scar hypertrophy by 80% compared to semi-occlusion. ETIs of untreated scars were increased by more than 100% compared to uninjured skin. Silicone gel treatment significantly reduced epidermal thickness by more than 30%. Our findings demonstrate that 2 weeks of silicone gel application at a very early onset of scarring reduces dermal and epidermal thickness which appears to be due to a reduction in keratinocyte stimulation. Oxygen can be ruled out as a mechanism of action of silicone occlusive treatment. Hydration of the keratinocytes seems to be the key stimulus.

Hydrated keratinocytes reduce collagen synthesis by fibroblasts via paracrine mechanisms.

Regulating collagen metabolism can control hypertrophic scars in cutaneous wounds. Hypertrophic scars can be reduced by occlusive dressings such as silicone sheeting; however, their mechanism is still unknown. We hypothesized that hydration of keratinocytes reduces the collagen secretion of fibroblasts by modifying the cytokine levels. Stratified human epidermal keratinocytes and confluent human dermal fibroblasts were co-cultured serum free for 72 hours. Keratinocytes were either kept at the air interface or hydrated. Messenger RNA (mRNA) levels of interleukin-1 (IL-1)alpha, IL-1beta, tumor necrosis factor alpha (TNF-alpha), keratinocyte growth factor (KGF), and procollagen-1 were analyzed by real-time reverse transcription-polymerase chain reaction. Secretion of cytokines into conditioned media was quantified by enzyme-linked immunosorbent assay and collagen content by Western blot. The content of collagen-I decreased by 44% in the presence of hydrated keratinocytes. Co-culture with air-treated keratinocytes decreased collagen-I only by 23%. Co-cultured hydrated keratinocytes had significantly higher TNF-alpha mRNA (172%) than hydrated keratinocytes. At the protein level, there was an overall trend toward increased TNF-alpha levels in hydrated cultures. IL-1beta secretion decreased significantly under hydration (42% monoculture, 58% co-culture). Co-culture stimulated a 240% increase of KGF mRNA in fibroblasts compared with monocultured fibroblasts. Fibroblasts secreted 4.5-fold more KGF in hydrated co-cultures and sixfold more KGF in air-treated co-cultures. Hydration of keratinocytes modifies important paracrine interactions between keratinocytes and fibroblasts and reduces collagen-1, which supports the hypothesis that hydration of the epidermis and restoration of water barrier function play an important role in scar formation.

Age effect on HSP70: decreased resistance to ischemic and oxidative stress in HDF.

BACKGROUND: Heat pre-conditioning results in induction of heat shock proteins including HSP70 that gives a cytoprotective effect against further stress. However, HSP70 induction is attenuated in aged cells. The lower HSP70-levels may contribute to the impaired stress response seen in the aged, and to the higher rates of chronic wounds in aged, which arise from repeated ischemia-reperfusion injury. The aim of this study was to investigate a possible connection by comparing the viability of heat pre-conditioned aged versus young human dermal fibroblasts (HDF) after exposure to stress. MATERIALS AND METHODS: Young (15-28) and aged (61-77) HDF were heat pre-conditioned (42 degrees C, 1 h) and after recovery (1, 2, or 20 h) treated with carbonyl-cyanide-m-chlorophenylhydrazone (hypoxic stress) or with hydrogen peroxide (oxidative stress) for 1 h. HSP70 levels were determined by Western blot. Cell damage was assessed by quantifying lactic dehydrogenase (LDH) in conditioned media. Aged HDF were transfected with HSP70-plasmid, consecutively heat pre-conditioned and exposed to oxidative stress. RESULTS: HSP70 increased in heat pre-conditioned young HDF by 96, 189, and 237% after 1, 2, and 20-h recovery, respectively, and in aged HDF by 27, 61, and 26%. LDH-release was only decreased in young HDF 20-h after heat-treatment compared with non-heat treated cells (P < 0.001). HSP70-transfection of aged HDF with plasmid reduced LDH-release by 29%. CONCLUSIONS: Heat pre-conditioning fails to protect aged HDF to oxidative or hypoxic stress due in part to impaired HSP70 induction compared to young.

Oxygen in wound healing--more than a nutrient.

This article provides an overview of the role of oxygen in wound healing. The understanding of this role has undergone a major evolution from its long-recognized importance as an essential factor for oxidative metabolism, to its recognition as an important cell signal interacting with growth factors and other signals to regulate signal transduction pathways. Our laboratory has been engaged in the study of animal models of skin ischemia to explore in vivo the impact of hypoxia as well as the use of oxygen as a therapeutic agent either alone or in combination with other agents such as growth factors. We have demonstrated a synergistic effect of systemic hyperbaric oxygen and growth factors that has been substantiated by Hunt's group. Within the past 10 years research in the field of wound healing has given new insight into the mechanism of action of hypoxia and hyperoxia as modifiers of the normal time-course of wound healing. The article concludes with a discussion of why hypoxia and hyperoxia intercurrently play an important role in wound healing. Hypoxia-inducible factor 1 is crucial in that interplay.