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Biomedical subjects

Craig Hammerberg

Publications and source records attributed to Craig Hammerberg.

10 recordsLinked to original sources

The effects of laser-mediated hair removal on immunohistochemical staining properties of hair follicles.

BACKGROUND: The mechanisms involved in laser-mediated hair removal remain unclear. One means of reducing hair growth is alteration of follicular stem cells. OBJECTIVE: We sought to examine the effects of laser hair removal on the immunohistochemical staining properties of human hair follicles, including the putative stem cells of the bulge region. METHODS: Treatment of unwanted axillary hair was performed on one side using an 800 nm-wavelength diode laser and on the other side using a 1064 nm-wavelength neodymium:yttrium-aluminum-garnet laser. Serial skin samples were obtained at baseline and various times after treatment and stained using immunohistochemical techniques. RESULTS: Hair shafts were thermally altered, but the immunostaining properties of much of the follicle, including the bulge region, remained generally unchanged. LIMITATIONS: This study only addressed the acute immunohistochemical changes found after a single treatment using specific laser parameters. CONCLUSIONS: Laser-mediated hair removal does not appear to work by frank destruction of follicular stem cells. Other mechanisms including functional alteration of these cells may underlie the clinical efficacy of the procedure.

Adult↗

Microdermabrasion with and without aluminum oxide crystal abrasion: a comparative molecular analysis of dermal remodeling.

BACKGROUND: Microdermabrasion is a popular method of superficial skin resurfacing with effects on dermal remodeling. OBJECTIVE: The purpose of this study was to evaluate the relative importance of the two components of microdermabrasion, negative pressure and abrasion, in stimulating expression of key genes involved in dermal remodeling. METHODS: Ten subjects were treated with a microdermabrasion machine using focal crystal abrasion and negative pressure or negative pressure alone for 3 seconds. Serial biochemical analyses were performed. Reverse transcriptase real-time polymerase chain reaction assays were used to evaluate changes in transcription factor activator protein-1, primary cytokines (interleukin 1beta, tumor necrosis factor-alpha), and matrix metalloproteinases (MMP-1, MMP-3, MMP-9). RESULTS: Significant increases in gene expression of the c-Jun component of activator protein-1, interleukin 1beta, tumor necrosis factor-alpha, MMP-1, MMP-3, and MMP-9 were found with crystal abrasion combined with negative pressure. Negative pressure alone resulted in increased gene expression of MMP-1 and MMP-3 but of a quantitatively reduced magnitude when compared with negative pressure with crystal abrasion. LIMITATIONS: It is unclear that molecular changes seen with these treatments can result in clinical effect. CONCLUSION: The abrasive component of microdermabrasion is necessary for stimulating expression of key genes involved in dermal remodeling.

Adult↗

Dermal matrix remodeling after nonablative laser therapy.

OBJECTIVE: Nonablative laser therapy is widely practiced for cutaneous rejuvenation. We sought to quantify dermal molecular changes after exposure of photodamaged skin to nonablative laser energy. METHODS: Nonablative laser therapy of forearm skin using either a 585-nm wavelength pulsed dye laser or a 1320-nm wavelength neodymium:yttrium-aluminum-garnet laser was performed. Serial biopsy specimens were obtained at baseline and various times after treatment. RESULTS: Statistically significant increases in type I procollagen messenger RNA expression occurred after exposure of photodamaged skin to each laser. Induction was 47% (P < .05) and 84% (P < .05) above baseline levels 1 week after laser therapy among those treated with the pulsed dye and neodymium:yttrium-aluminum-garnet lasers, respectively. Substantial induction of type III procollagen, various matrix metalloproteinases, and primary cytokines was also demonstrated. Responses with respect to all molecules studied were highly variable. LIMITATIONS: This study addresses molecular changes after a single laser exposure whereas clinically, serial treatments are often provided. CONCLUSIONS: Nonablative laser therapy may result in quantifiable alterations in molecules associated with remodeling of the dermal matrix, although responses vary greatly among patients.

Aged↗

Microdermabrasion: a molecular analysis following a single treatment.

BACKGROUND: Microdermabrasion is a popular method of superficial skin resurfacing. It is unclear if dermal remodeling actually occurs. OBJECTIVE: To rigorously investigate the molecular alterations observed following a single microdermabrasion treatment. METHODS: Forty-nine subjects received a single microdermabrasion treatment to buttock skin. Serial in vivo biochemical and immunohistological analyses were performed. Reverse transcriptase real-time polymerase chain reaction and immunohistochemistry assays were used to evaluate changes in transcription factors (AP-1, NF-kappaB), primary cytokines (interleukin-1beta, tumor necrosis factor-alpha), matrix metalloproteinases (MMP-1, MMP-3, MMP-9), barrier repair enzymes (acetyl-coenzyme A carboxylase, 3-hydroxy-3-methylglutaryl coenzyme A reductase), and type I procollagen. Results Elevation of transcription factors, primary cytokines, and matrix metalloproteinases occurs rapidly after a single microdermabrasion treatment. Two of 11 subjects also demonstrated increased type I procollagen messenger RNA and protein levels 14 days after treatment. No alteration in stratum corneum thickness was detected. CONCLUSION: Microdermabrasion activates a dermal remodeling/wound healing cascade with minimal epidermal disruption. Evidence now exists to further study manipulation of variables such as number and timing of microdermabrasion sessions.

Acetyl-CoA Carboxylase↗

Inflammation and extracellular matrix degradation mediated by activated transcription factors nuclear factor-kappaB and activator protein-1 in inflammatory acne lesions in vivo.

Acne is the most common skin disease, causing significant psychosocial problems for those afflicted. Currently available agents for acne treatment, such as oral antibiotics and isotretinoin (Accutane), have limited use. Thus, development of novel agents to treat this disease is needed. However, the pathophysiology of acne inflammation is poorly understood. Before new therapeutic strategies can be devised, knowledge regarding molecular mechanisms of acne inflammation is required. We report here that transcription factors nuclear factor-kappaB and activator protein-1 are activated in acne lesions with consequent elevated expression of their target gene products, inflammatory cytokines and matrix-degrading metalloproteinases, respectively. These elevated gene products are molecular mediators of inflammation and collagen degradation in acne lesions in vivo. This new knowledge enables a rational strategy for development of pharmacological agents that can target the inflammation and matrix remodeling that occurs in severe acne.

Acne Vulgaris↗

Long-term efficacy and safety of tretinoin emollient cream 0.05% in the treatment of photodamaged facial skin: a two-year, randomized, placebo-controlled trial.

BACKGROUND: Long-term (>1 year) placebo-controlled studies of tretinoin in the treatment of photodamaged skin have not been conducted. Recently, we conducted a 2-year placebo-controlled study of tretinoin emollient cream 0.05%, including histopathologic assessment of safety and analysis of markers of collagen deposition. OBJECTIVE: The objective of the study was to determine the long-term safety and efficacy of tretinoin emollient cream 0.05% in the treatment of moderate to severe facial photodamage. METHODS: A total of 204 subjects were treated with tretinoin or placebo (vehicle emollient cream) applied to the entire face once a day for up to 2 years. Clinical and histologic effects were assessed at regularly scheduled clinic visits. RESULTS: Treatment with tretinoin resulted in significantly greater improvement relative to placebo in clinical signs of photodamage (fine and coarse wrinkling, mottled hyperpigmentation, lentigines, and sallowness), overall photodamage severity, and investigator's global assessment of clinical response (p<0.05). Histologic evaluation showed no increase in keratinocytic or melanocytic atypia, dermal elastosis, or untoward effects on stratum corneum following treatment with tretinoin compared with placebo. Immunohistochemistry studies, conducted at three study centers, showed a significant increase relative to placebo in facial procollagen 1C terminal, a marker for procollagen synthesis, at month 12 (p=0.0074). CONCLUSION: Long-term treatment with tretinoin emollient cream 0.05% is safe and effective in subjects with moderate to severe facial photodamage.

Administration, Topical↗

Treatment of acne vulgaris with a pulsed dye laser: a randomized controlled trial.

CONTEXT: The high prevalence of acne vulgaris and its significant morbidity underscore the need for convenient, low-risk, and efficacious therapy. Treatment with various lasers has been reported to improve acne. OBJECTIVE: To evaluate the clinical efficacy of pulsed dye laser therapy in the treatment of acne. DESIGN, SETTING, AND PATIENTS: Randomized, single-blind, controlled, split-face clinical trial of a volunteer sample of 40 patients aged 13 years or older with facial acne conducted at an academic referral center from August 2002 to September 2003. INTERVENTION: One or 2 nonpurpuric pulsed dye laser treatments to half of the face (fluence of 3 J/cm2), serial blinded clinical assessments (lesion counts), and grading of acne severity using standardized bilateral serial photographs. MAIN OUTCOME MEASURES: Comparison of the changes in lesion counts from baseline to 12 weeks between treated and untreated sides of the face and changes in photographic evidence of acne severity as graded by a panel of dermatologists blinded to treatment assignment. RESULTS: After 12 weeks, using intent-to-treat analysis with last observation carried forward, there were no significant differences between laser-treated and untreated skin for changes in mean papule counts (-4.2 vs -2.2; P =.08), mean pustule counts (0 vs -1.0; P =.12), or mean comedone counts (2.9 vs 1.6; P =.63). Grading of serial photographs confirmed the clinical assessments, showing no significant mean (SE) differences in Leeds scores (range, 1-12) for treated skin (3.98 [0.32] at baseline and 3.94 [0.27] at week 12) compared with untreated skin (3.83 [0.32] at baseline and 3.79 [0.28] at week 12) (P>.99). CONCLUSIONS: In this study, the nonpurpuric pulsed dye laser therapy did not result in significant improvement of facial acne. More research is needed before this laser therapy may be recommended as an acne treatment.

Acne Vulgaris↗

Connective tissue remodeling induced by carbon dioxide laser resurfacing of photodamaged human skin.

OBJECTIVE: To quantitatively examine the dynamics of molecular alterations involved in dermal remodeling after carbon dioxide (CO(2)) laser resurfacing of photodamaged human skin. DESIGN: Serial in vivo biochemical analyses after laser therapy. SETTING: Academic referral center, Department of Dermatology, University of Michigan, Ann Arbor. Subjects Volunteer sample of 28 adults, 48 to 76 years old, with clinically evident photodamage of the forearms. Intervention Focal CO(2) laser resurfacing of photodamaged forearms and serial biopsies at baseline and various times after treatment. MAIN OUTCOME MEASURES: Reverse transcriptase real-time polymerase chain reaction technology and immunohistochemistry were used to assess levels of type I and type III procollagens; matrix metalloproteinases (MMPs) 1, 3, 9, and 13; tropoelastin; fibrillin; primary cytokines interleukin 1beta and tumor necrosis factor alpha; and profibrotic cytokine transforming growth factor beta1. RESULTS: Production of type I procollagen and type III procollagen messenger RNA peaked at 7.5 and 8.9 times baseline levels, respectively, 21 days after treatment and remained elevated for at least 6 months. Increases in messenger RNA levels of several cytokines (interleukin 1beta, tumor necrosis factor alpha, and transforming growth factor beta1) preceded and/or accompanied changes in collagen levels. Marked increases in messenger RNA levels of MMP-1 (39 130-fold), MMP-3 (1041-fold), MMP-9 (75-fold), and MMP-13 (767-fold) were noted. Levels of fibrillin and tropoelastin rose in a delayed fashion several weeks after treatment. CONCLUSIONS: The biochemical changes seen after CO(2) laser resurfacing proceed through a well-organized and highly reproducible wound healing response that results in marked alterations in dermal structure. These quantitative changes may serve as a means for comparison as other therapeutic modalities meant to improve the appearance of photodamaged skin are evaluated.

Aged↗

Effect of carbon dioxide laser resurfacing on epidermal p53 immunostaining in photodamaged skin.

OBJECTIVE: To quantitatively examine changes in p53 tumor suppressor gene immunostaining after carbon dioxide (CO(2)) laser resurfacing of photodamaged skin to assess the potential value of this treatment in reducing the risk of progression to cutaneous carcinoma. DESIGN: Serial in vivo immunohistochemical analyses after laser therapy. SETTING: Academic referral center, Department of Dermatology, University of Michigan, Ann Arbor. OTHER PARTICIPANTS: Volunteer sample of 11 adults, 51 to 76 years old, with clinically evident photodamage of the forearms. INTERVENTION: Focal CO(2) laser resurfacing of photodamaged forearms and serial biopsies at baseline, 3 weeks, and 6 months after treatment. MAIN OUTCOME MEASURES: Because keratinocytes with mutations in p53 or altered p53 expression stain via immunohistochemical techniques, image analysis of immunohistochemically stained sections was used to quantify p53 expression. RESULTS: Positive immunostaining for p53 in the interfollicular epidermis was noted in 8 of 11 subjects at baseline, with an average staining density of 250 cells/mm(2). Average staining decreased to 3 cells/mm(2) 3 weeks after treatment. This decrease was sustained at 5 cells/mm(2) 6 months after resurfacing. CONCLUSIONS: There was a consistent decrease in p53 immunostaining in the interfollicular epidermis lasting for at least 6 moths after CO(2) laser resurfacing of photodamaged skin. Since p53 mutation or overexpression is observed in a majority of cases of cutaneous carcinoma, the posttreatment repopulation of the epidermis with p53-negative keratinocytes should theoretically decrease the risk of malignant progression. Further study of laser resurfacing as a prophylactic procedure in patients at high risk for skin cancer development appears warranted.

Administration, Topical↗

Tretinoin treatment before carbon-dioxide laser resurfacing: a clinical and biochemical analysis.

BACKGROUND: Tretinoin is often prescribed before laser resurfacing in an attempt to enhance results. OBJECTIVE: We sought to assess the clinical and biochemical effects of preoperative tretinoin use before laser resurfacing. METHODS: Patients were randomized to apply tretinoin to one forearm and placebo to the other for 3 weeks. Patients' photodamaged forearms were focally treated by carbon-dioxide laser resurfacing. Biopsy specimens were obtained at baseline and various times posttreatment. Real-time polymerase chain reaction technology was used to quantify messenger RNA levels of types I and III procollagen and matrix metalloproteinases-1, 3, and 9. Wounds were assessed for degree of re-epithelialization using a computer graphics-generated template. A colorimeter was used to quantify postoperative erythema. RESULTS: No substantial differences in either biochemical markers or clinical end points were identified between tretinoin and placebo pretreated forearms. CONCLUSIONS: We found no evidence of enhanced collagen formation, accelerated re-epithelialization, or quicker resolution of postoperative erythema with tretinoin pretreatment before laser resurfacing.

Administration, Cutaneous↗