RESUMEN
Stage IV adult acquired flatfoot deformity (AAFD) with secondary chronic deltoid ligament insufficiency is a challenging deformity to treat, with minimal consensus in the literature concerning its surgical management. Many surgical treatment options have been described, including joint-sparing techniques, fusions, osteotomies, and even arthroplasties. However, questions remain as to what, if any, treatment is optimal. This contribution reviews studies on surgical treatments for stage IV AAFD with deltoid ligament failure and provides a critical analysis regarding the quality of outcomes reported for those different treatment options. PubMed and Google Scholar databases were searched between June 1, 2022, and August 15, 2022, for studies published between 1990 and 2022 that describe the treatment of stage IV AAFD with deltoid ligament insufficiency. Articles included in the study focused on subjects with stage IV AAFD and associated deltoid ligament insufficiency undergoing surgical correction. Exclusion criteria included stage I, II, and III AAFD, as well as deltoid ligament repair following acute injury/rupture. Nine studies covering five different treatment options for patients with stage IV AAFD and chronic deltoid insufficiency were included, with minimal overlap in outcome measures used to assess the efficacy of the procedure. Triple arthrodesis with deltoid ligament reconstruction resulted in a 62.5% (5/8) success rate with a residual tibiotalar (TT) angulation of 2° (success defined as <3°). Tibiotalar arthrodesis of four patients resulted in an average post-operative tibiotalar angulation of 4.8° with all patients showing progressive destabilization of the hindfoot complex at 12-18 year follow-ups. Deltoid arthroscopic laminoplasty (Brostrom) resulted in an increased American Orthopaedic Foot and Ankle Society (AOFAS) score from 49.7 pre-op to 91.9 post-op. There was no long-term follow-up of these patients. Deltoid ligament reconstruction using autografts of the peroneus longus resulted in a post-operative valgus of 2.1° in one study and <5° in another. Deltoid ligament reconstruction using an anterior tibial tendon autograft resulted in a gain of 126.4 + 40.2% in stiffness compared to an intact ligament. Twinfix suture anchors resulted in a post-operative hindfoot angle averaging 5.3°. Combined deltoid and spring ligament reconstruction resulted in a 5.1° valgus angulation. There is currently no standard of care or clinical consensus regarding surgical treatment for stage IV AAFD with deltoid insufficiency. Several studies imply that mild valgus malalignment around the tibiotalar joint can result in satisfactory outcomes. A few studies even deemed <5° of valgus tilt post-operatively successful. However, it has been described that any imbalance in tibiotalar tilt is a significant risk factor for progressive arthritis and future ligamentous failure. No treatment option was able to correct valgus tilt to an anatomical standard (i.e., to normal anatomy). These varied findings, along with the lack of consensus on post-surgical measures to assess efficacy, are worrisome and emphasize the need for better surgical options. Moreover, there is a critical need for additional research on the long-term outcomes following stage IV AAFD and deltoid insufficiency repair, particularly, as over five million people in the United States and 10% of the geriatric population are affected by AAFD with a risk of progressing to stage IV.
RESUMEN
BACKGROUND: Intervertebral disc degeneration contributes to low back pain. The avascular intervertebral disc consists of a central hypoxic nucleus pulpous (NP) surrounded by the more oxygenated annulus fibrosus (AF). Lactic acid, an abundant end-product of NP glycolysis, has long been viewed as a harmful waste that acidifies disc tissue and decreases cell viability and function. As lactic acid is readily converted into lactate in disc tissue, the objective of this study was to determine whether lactate could be used by AF cells as a carbon source rather than being removed from disc tissue as a waste byproduct. METHODS: Import and conversion of lactate to tricarboxylic acid (TCA) cycle intermediates and amino acids in rabbit AF cells were measured by heavy-isotope (13C-lactate) tracing experiments using mass spectrometry. Levels of protein expression of lactate converting enzymes, lactate importer and exporter in NP and AF tissues were quantified by Western blots. Effects of lactate on proteoglycan (35S-sulfate) and collagen (3H-proline) matrix protein synthesis and oxidative phosphorylation (Seahorse XFe96 Extracellular Flux Analyzer) in AF cells were assessed. RESULTS: Heavy-isotope tracing experiments revealed that AF cells imported and converted lactate into TCA cycle intermediates and amino acids using in vitro cell culture and in vivo models. Addition of exogenous lactate (4 mM) in culture media induced expression of the lactate importer MCT1 and increased oxygen consumption rate by 50%, mitochondrial ATP-linked respiration by 30%, and collagen synthesis by 50% in AF cell cultures grown under physiologic oxygen (2-5% O2) and glucose concentration (1-5 mM). AF tissue highly expresses MCT1, LDH-H, an enzyme that preferentially converts lactate to pyruvate, and PDH, an enzyme that converts pyruvate to acetyl-coA. In contrast, NP tissue highly expresses MCT4, a lactate exporter, and LDH-M, an enzyme that preferentially converts pyruvate to lactate. CONCLUSIONS: These findings support disc lactate-dependent metabolic symbiosis in which lactate produced by the hypoxic, glycolytic NP cells is utilized by the more oxygenated AF cells via oxidative phosphorylation for energy and matrix production, thus shifting the current research paradigm of viewing disc lactate as a waste product to considering it as an important biofuel. These scientifically impactful results suggest novel therapeutic targets in disc metabolism and degeneration.