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A technique is described using the epithelium over a keloid as a graft after excision of the keloid. Advantages of this procedure are availability of skin and avoidance of the danger of keloid formation in a distant donor site. Results in a series of five patients followed for five years were satisfactory in three.
The increased collagen synthesis and deposition, which is characteristic of keloids, may be related to an immune response initiated by wounding. Therefore, we examined various systemic and localized immune parameters in keloid patients to establish if such factors are related to keloid pathogenesis. To determine if there is a systemic immune response, we compared the serum levels of IgG and IgM in keloid patients to those in a closely matched population. In addition, we measured complement levels (Clq, C3, and C4) and receptors for sheep (E), mouse erythrocytes (MRBC), and complement (EAC) on blood lymphocytes. All of these were in the normal range in the keloid patients. However, the extractable IgG from keloid tissue was significantly increased (compared to normal skin and normal scar controls), suggesting a localized immune response. To determine whether keloid formation is associated with a specific histocompatibility locus, human lymphocyte antigen (HLA) profiles of 45 keloid patients were analyzed; no significant differences in the incidence of HLA-A and B antigens were found (compared to 200 controls). These studies suggest that there is a localized immune response involved in keloid pathogenesis, one which is not related to either the HLA-A or B histocompatibility loci.
Cultured fibroblasts isolated from normal and keloid tissue do not differ in their growth characteristics or in the rate of collagen synthesis under routine culture conditions. The addition of hydrocortisone to the culture media results in significant differences in both growth and collagen synthesis between these cell types. Collagen synthesis is inhibited 60% in normal cultures by hydrocortisone (0,5 micrograms/ml) and the population size at which density-dependent growth inhibition is achieved is increased. Keloid-derived fibroblasts grow to a lower maximum density in the presence of hydrocortisone, while their rate of collagen synthesis is not significantly reduced. The rate of non-collagen protein synthesis is increased significantly by hydrocortisone in both cell types. Comparison of normal and keloid-derived cultures obtained from a single individual suggests that the keloid phenotype with respect to both growth and collagen synthesis is restricted to the fibroblasts isolated from the keloid nodule.
Molecular sieve column chromatography was used to determine the amount of type I and III collagen synthesized by normal dermis and keloid biopsies and fibroblasts derived from these tissues. After incubation with radioactive proline, the collagen was extracted and separated into types I and III and then quantitated. There was no significant difference in the percent type III collagen synthesized by fresh keloid biopsies compared to normal dermis. Likewise, there was no significant difference in the percent type III collagen synthesized by keloid fibroblasts compared to normal dermal fibroblasts. However, fibroblasts from both keloid and normal dermis synthesized a lower percentage of type III collagen in cell culture compared to the original biopsies. These findings demonstrate that keloid collagen has the same type distribution as normal dermis and suggest that increased collagen synthesis in these lesions is not related to altered collagen types.
Prevention of postexcisional recurrence of the common earlobe keloid has long been an enigma to the surgeon. The increased realization that pressure aids in diminishing hypertrophic burn scars has stimulated us to develop an effective pressure device to control the collagen overgrowth frequently occurring after initial keloid excision. Our device is a decorative spring-pressure earring that is applied to the earlobe 2 weeks after excision of the keloid. The patient is instructed to wear the earring for 4 to 6 months. An effective evaluation of this device was carried out through its bilateral use in some patients. The earring was used initially on only 1 ear; when early recurrence was detected in the control ear, application of the device diminished and prevented keloid reformation. This innovation promises to be an important adjunct in the prevention of postexcisional recurrence of earlobe keloids, and the preliminary results are reported with a 12 to 15 month follow-up. Constant light pressure is discussed as an effective means of preventing postexcisional recurrence of these lesions.
Low dose superficial x-irradiation to the incisional site after surgical excision of a keloid prevented keloid or hypertrophic scar formation in 31 of 35 patients evaluated (88%). The clinical manifestation of keloids, physiology of wound healing, pathophysiology of keloid formation, and the radiation technique utilized are presented. This study shows that the method is well tolerated, easily administered, and efficient in inhibiting recurrence of keloid or hypertrophic scar formation.
The keloid phenomenon is old and perplexing. Many hypotheses were advanced to account for keloid growth but none of them provided a satisfactory explanation for the clinical manifestations of the disease. To solve the mystery of keloid detailed clinical studies coupled with laboratory tests were undertaken on keloid and non-keloid individuals; these highlighted the determinants of the disease and paved the way to the formulation of the Sebum Auto-immune Theory. The latter provided valid explanations for the clinical manifestations of the disease and indicated a rationale for new trends of management.
Fibroblasts were isolated from keloid, normal skin, and normal scar and maintained in tissue culture for four passages. Growth kinetics were the same for all groups on days 2 through 12. However, the rate of collagen synthesis per fibroblast was greater in keloid derived cells than any controls at all growth phases. Keloid fibroblasts have an autonomous capacity to synthesize collagen at a significantly increased level in vitro, which may explain in part why these lesions are characterized by increased collagen deposition.
Keloids and mandibular unfavorable fractures are reviewed. A case report of a patient with keloid diathesis, who had a mandibular unfavorable fracture, is presented. A grossly carious, abscessed first molar was in the line of fracture. This tooth was the only erupted tooth present in the proximal fragment. Endodontic therapy and restoration of normal contour enabled the surgeons to treat the fractured mandible by means of simple closed reduction. The endodontic treatment pre-empted a major surgical procedure under general anesthesia and also averted a skin incision which would have subsequently formed a disfiguring keloid.
The results obtained for 100 patients by combined surgical and radiation therapy are presented and by means of exemplary cases illustrated. As sson as 24 to 48 hours after excision of the keloid by mostly atraumatic surgical technique, and closing the wound as tension-free as possible, radiation therapy is begun. This takes place under the conditions of surface therapy in single doses of 1.5 Gray two or three times per week up to a total dose of 9 to 12 Gray. Good cosmetic and functional results can be achieved with this technique. The rate of recurrences is extremely low. The radiation load to the patient is so small that it seems justifiable to recommend the combined treatment as the routine method for therapy of keloids. In cases of a known disposition for developing keloids or cicatricial hypertrophies, postoperative radiation therapy is indicated as a prophylactic measure, especially after surgery in the facial region.
Keloids are medically benign, but often psychologically and cosmetically malignant lesions. They are most commonly located on the posterior aspect of the ear lobes. The author's treatment of choice is the combined intralesional steroid and surgical approach. Surgically, the best results are obtained when some of the skin overlying the keloid is used as a split thickness graft after all of the keloidal tissue has been removed. Explicit postoperative wound care instructions are important in insuring complication-free surgery.
There is abundant evidence in the literature that keloids and hypertrophic scars are different stages of the same process. The evidence, clinical and histogenetic, also shows that the hypertrophic scar is the earlier of the two stages. It therefore follows that all keloids do evolve through the hypertrophic scar phase. These conclusions have largely eased the confusion of nomenclature and made a clinicopathologic correlation of the available knowledge on keloid possible.
This study aimed to investigate the potential causal roles of specific circulating microRNAs (miRNAs) and immune cell subsets in the pathogenesis of hypertrophic scars and keloids using a 2-step Mendelian randomization framework. We employed a 2-sample Mendelian randomization approach to evaluate the causal relationships between miRNAs, immune cell genotypes, and scar phenotypes. The analysis integrated miRNA expression quantitative trait loci, immune cell genome-wide association studies, and scar datasets. A 2-step mediation analysis was conducted to assess the indirect effects of miRNAs on scars through immune cell genotypes, using inverse variance weighted methods and complementary sensitivity analyses to ensure robustness. Our analysis identified significant associations between specific miRNAs and scar phenotypes. Notably, miR-6887-5p exhibited a total effect on keloid formation risk (β = 0.324, 95% confidence interval [CI]: 0.073-0.576) and a direct effect (β = 0.283, 95% CI: 0.027, 0.538), with a marginally significant mediation effect through B-cell activating factor receptor on CD20- CD38- B cells (β = 0.042, 95% CI: -0.001, 0.084, P = .047). For hypertrophic scars, miR-345-5p demonstrated a significant total effect (β = -0.501, 95% CI: -0.903, -0.099) and direct effect (β = -0.469, 95% CI: -0.872, -0.066), with a significant mediation effect through CD28+ CD45RA- CD8dim T cell percentage (β = -0.032, 95% CI: -0.062, -0.002, P = .034). miR-4801 showed a significant total effect (β = -0.246, 95% CI: -0.429, -0.064) and direct effect (β = -0.218, 95% CI: -0.402, -0.033), with a marginally significant mediation effect through T cell absolute count (β = -0.028, 95% CI: -0.057, -0.000, P = .043). These findings highlight the interplay between miRNAs and immune cell subsets in scar pathogenesis. This study provides preliminary evidence for the causal roles of specific miRNAs and immune cell subsets in scar formation, emphasizing the potential of miRNA-immune cell axes as therapeutic targets. While the identified associations offer important insights into the molecular mechanisms of scar heterogeneity, further validation through mechanistic studies and clinical trials is necessary to translate these genetic insights into clinical interventions.
Cultured fibroblasts derived from human keloid tissue are presented as a possible model system for studying the genetic regulation of cell growth. Histamine is shown to have a marked effect on the growth of cultured fibroblasts. A small increase in growth rate is seen during the log phase of the culture cycle and a 50% increase in cell number is observed during the plateau phase. Differences in the extent of growth stimulation are observed between strains isolated from different individuals. While most strains showed approximately 50% stimulation, a few were not stimulated and some strains gave a 100% or greater increase in cell number due to histamine. This phenotypic difference in extent of growth stimulation in response to histamine cannot be attributed to the gene or genes for keloid formation. However, elevated levels of histamine in vivo may be a contributing factor to the abnormal cell growth observed in this disorder. The extent of growth stimulation due to histamine decreases with repeated subculturing.
There is a type of keloid that tends to suppuration. The causes and mechanisms, symptomatology, and management of suppurative keloids are discussed briefly.
In a prospective trial, the results of local steroid treatment of keloids have been studied. 52 patients were treated with Kenalog (triamcinolone acetonide) injections alone, whilst in 15 patients, steroid therapy was combined with excision of the keloid. The combined treatment gave no better results than injection therapy alone. The early result of treatment was the complete flattening of the lesions and cessation of itching in the majority of cases. However in one-third of the cases partial recurrence was found after one year, and after 5 years, the recurrence rate was 50%.
We report clinical observations and immunological and laboratory studies whcih suggest that the tendency toward skin malignancies and the keloid diathesis may be two opposing conditions. We conclude that it is quite possible that a keloidal person, armed with a hypersensitive cell-mediated immune response condition and an overactive enzyme system, has a safeguard against acquiring skin malignancies.
The treatment of keloids continues to be an enigma to the surgeon and the patient as well. There is to date no absolute single method that assures success. Generally speaking, we must use all the tools in our armamentarium, including radiation, intra-keloid steroids, surgery and postoperative constant wound pressure in an effort to remold the newly forming collagen. While these do not guarantee satisfactory results, they are the best we have to date and adequately justify our attempts to help patients with this problem. Of great importance is the necessity for the patient to be fully informed of the need for protracted follow-up without guarantees regarding the final outcome.