Expert Evaluation and Evidence-Based Management
A hairline that has shifted back an inch since your twenties. A part that is visibly wider than it was two years ago. A crown that the light catches differently now. Androgenetic alopecia develops gradually, which is exactly why so many people underestimate how much ground they have lost until the changes are already substantial. The condition is not sudden, but its progression is relentless without intervention, and the follicles lost to advanced miniaturization do not recover regardless of how effective subsequent treatment becomes.
Androgenetic alopecia, commonly called male pattern hair loss or female pattern hair loss, is the most prevalent form of hair loss in the world. It affects approximately 50 percent of men by age 50, up to 70 percent by age 70, and nearly 40 percent of women by age 70. It is not a disease in the conventional sense. It is a genetically programmed response of certain hair follicles to circulating androgens that progressively miniaturizes them over years and decades, converting thick, pigmented terminal hairs into fine, colorless vellus hairs before the follicle eventually falls silent entirely. The biology is well understood. And critically, there are now multiple evidence-based, FDA-approved treatments that can slow or stop this process and, in many patients, meaningfully restore hair density when initiated early enough.
At Connolly Dermatology, we provide expert evaluation and androgenetic alopecia treatment guided by evidence-based care. Our board-certified dermatologists use trichoscopy, targeted laboratory evaluation, and clinical pattern assessment to confirm the diagnosis and its severity, distinguish androgenetic alopecia from conditions that mimic it, identify hormonal and nutritional contributing factors, and design individualized treatment plans that combine the most effective available therapies. We treat both men and women, and we understand that the presentation, the contributing factors, and the treatment approach differ meaningfully between them.
If you are experiencing hair thinning or recession that concerns you, scheduling a hair loss evaluation with a dermatologist provides the specific diagnosis and treatment direction that over-the-counter products and online research cannot. Have your hair and scalp assessed by the specialists at Connolly Dermatology and get the answers you need to move forward confidently.
Understanding Androgenetic Alopecia
The Biology Behind Pattern Hair Loss and Why Early Treatment Matters
Androgenetic alopecia develops through a genetically programmed interaction between susceptible hair follicles and the androgen hormone dihydrotestosterone, commonly called DHT. The process is not sudden. It unfolds over years through a mechanism called follicular miniaturization, in which progressive cycles of hair growth become incrementally shorter, the hair shaft produced at each cycle becomes finer and less pigmented, and the ratio of active terminal hairs to dormant vellus hairs in susceptible scalp regions gradually shifts toward the latter. Understanding this mechanism explains both why androgenetic alopecia looks and feels the way it does and why the available treatments work.
The Mechanism: DHT and Follicular Miniaturization
Testosterone circulates in the bloodstream and is converted to dihydrotestosterone in peripheral tissues, including the scalp, by the enzyme 5-alpha reductase. DHT is significantly more potent than testosterone at binding androgen receptors. In hair follicles genetically predisposed to androgenetic alopecia, DHT binds androgen receptors in the dermal papilla, the specialized cluster of mesenchymal cells at the base of the follicle that regulates hair growth cycles. This binding triggers a cascade that progressively shortens the anagen growth phase and induces fibrosis of the connective tissue sheath surrounding the follicle. With each successive growth cycle, the anagen phase is a little shorter, the hair shaft produced is a little finer and shorter, and the resting telogen phase occupies a larger proportion of the follicle’s time. Over years of repeated cycles, terminal hairs are replaced by progressively miniaturized vellus hairs that are cosmetically insignificant, and eventually the follicle ceases active cycling entirely.
Critically, this process does not destroy the follicle itself in its early and middle stages. Miniaturized follicles retain their structural architecture and, importantly, their capacity to regenerate if the DHT stimulus is reduced or blocked. This reversibility is what makes pharmacological treatment effective when initiated at the right time. However, in advanced androgenetic alopecia where follicles have been inactive for years, the follicular unit is replaced by fibrous tissue and no longer responds to treatment. This is the most clinically important reason why early evaluation and early treatment produce substantially better outcomes than late intervention.
Male Pattern Hair Loss (MPHL)
In men, androgenetic alopecia follows the well-characterized Hamilton-Norwood classification, which describes seven progressive stages of hair loss beginning with Type I (minimal recession at the temples with a juvenile hairline) and advancing through bitemporal recession, frontal hairline recession, vertex thinning, and eventually confluence of frontal and vertex loss to produce the extensive baldness of Type VI and VII. The initial changes, most commonly noticed as a gradually receding temporal hairline or emerging thinning at the crown, typically begin in the late teens or twenties in men with a strong genetic predisposition. The rate of progression varies considerably between individuals and is influenced by both genetic loading and hormonal factors. Men who begin losing hair earlier in life tend to progress to more extensive baldness. The occipital and temporal fringe remains largely unaffected because these follicles express different androgen receptor profiles and are not susceptible to DHT-mediated miniaturization, which is why these areas serve as the donor zone for hair transplantation.
Female Pattern Hair Loss (FPHL)
In women, androgenetic alopecia presents differently than in men in several important ways. The Ludwig classification describes three stages of progressive central scalp thinning with preservation of the frontal hairline, beginning with visible widening of the central part (Ludwig I), proceeding to more pronounced diffuse thinning over the crown (Ludwig II), and in the most severe cases producing near-complete loss over the crown with the frontal hairline preserved (Ludwig III). Unlike in men, where recession of the hairline and vertex bald spot are prominent, most women maintain their frontal hairline even with advanced crown thinning. Additionally, a significant proportion of women experience a diffuse pattern rather than the classic Ludwig distribution, and some women develop a more male-like pattern with temporal recession.
Female pattern hair loss has the same androgen-dependent mechanism as in men in many women, but the relationship is more complex. Most affected women have normal serum androgen levels, meaning the follicles are more sensitive to androgens at a receptor level due to genetic variation, not elevated hormone levels. In a subset of women, elevated androgens from polycystic ovary syndrome, adrenal dysfunction, or other hormonal disorders drive or significantly accelerate hair loss, making hormonal evaluation an important part of female hair loss assessment. Female pattern hair loss is also commonly exacerbated by hormonal transitions, including menopause-related estrogen withdrawal, postpartum estrogen decline, and the androgenic effects of certain progestin-containing hormonal contraceptives.
Androgenetic Alopecia vs. Conditions That Can Mimic It
Several other hair loss conditions produce thinning that can be confused with androgenetic alopecia, particularly in its earlier stages. An accurate diagnosis is essential because each condition has different treatment priorities.
| Characteristic | Androgenetic Alopecia (Male) | Androgenetic Alopecia (Female) | Telogen Effluvium | Diffuse Alopecia Areata | Frontal Fibrosing Alopecia |
| Primary Cause | DHT-mediated follicular miniaturization in genetically susceptible follicles | Same DHT mechanism; worsened by hormonal transitions and PCOS; often normal androgens | Physiological trigger (illness, stress, nutritional deficiency, hormonal change) causing premature telogen shift | Autoimmune T-cell attack on hair follicles; diffuse or universal form without typical patchy pattern | Lymphocytic scarring inflammation targeting frontal and temporal follicles; variant of lichen planopilaris |
| Pattern of Hair Loss | Bitemporal recession, vertex thinning; follows Hamilton-Norwood stages I through VII | Diffuse crown thinning; widening central part; frontal hairline preserved; Ludwig stages I through III | Diffuse, generalized shedding across entire scalp; no preferential patterned thinning | Diffuse, widespread thinning across entire scalp; may have subtle or no distinct patches | Progressive recession of frontal and temporal hairline as advancing band; often with eyebrow loss |
| Scalp Appearance | Normal scalp skin; increased scalp visibility at crown and temples as hair miniaturizes | Normal scalp skin; widened part; diffuse reduction in hair density over crown | Normal scalp skin; diffuse density reduction; no inflammation or scarring | Normal scalp skin; may have subtle exclamation mark hairs on trichoscopy | Pale, ivory hairline band; perifollicular erythema and scale at advancing active margin; scarring |
| Key Trichoscopy Features | Hair diameter variability >20%; peripilar brown halo sign; miniaturized vellus hairs; empty follicular units at vertex | Same diameter variability; Christmas tree distribution of vellus hairs along central part; follicular units with single hairs | Predominantly telogen (club-shaped) hairs on pull test; normal diameter distribution; no vellus dominance | Exclamation mark hairs; yellow dots; black dots; cadaverous hairs in affected zones | Absent follicular openings at hairline; perifollicular fibrosis scale; lonely single hairs; loss of pigment band |
| Onset and Progression | Gradual; begins in teens to twenties in genetically predisposed individuals; continues across decades without treatment | Gradual; may begin in twenties but often accelerates at menopause; can be exacerbated by postpartum period | Acute or subacute; shedding typically peaks 2 to 3 months after trigger; self-limiting when trigger resolved | Variable; can be rapid; may fluctuate with disease activity; largely reversible with treatment | Slowly progressive; often goes unnoticed for years; permanent once scarring established |
| Reversibility | Partially reversible with sustained medical treatment; follicles that have been inactive for years do not recover | Partially reversible; responds to minoxidil, spironolactone, finasteride/dutasteride; hormonal management if indicated | Fully reversible; shedding resolves within 3 to 6 months of trigger correction; density returns within 12 months | Largely reversible if treated; follicles structurally intact; JAK inhibitors highly effective for severe disease | Permanent in areas where scarring has occurred; treatment slows progression only |
| First-Line Treatment | Topical or oral minoxidil; finasteride 1 mg/day or dutasteride 0.5 mg/day; PRP as adjunct | Topical or oral minoxidil; spironolactone 50 to 200 mg/day; finasteride or dutasteride off-label; hormonal management | Identify and correct trigger; iron/ferritin repletion; thyroid treatment; minoxidil as bridge | Intralesional corticosteroids for patchy disease; JAK inhibitors (baricitinib, ritlecitinib) for severe diffuse disease | Hydroxychloroquine; 5-alpha reductase inhibitors; topical and intralesional corticosteroids; photoprotection |
These patterns represent typical presentations. Features can overlap, and more than one condition can coexist. A board-certified dermatologist using trichoscopy, targeted laboratory testing, and scalp biopsy when indicated makes the definitive diagnosis.
Is Androgenetic Alopecia Dangerous?
Androgenetic alopecia is not dangerous to physical health. It does not become cancerous, does not cause scalp disease, and does not indicate any underlying illness in the vast majority of patients. It is a benign, genetically programmed biological process.
Two dimensions do deserve serious attention, however. First, in women, pattern hair loss that begins suddenly or progresses rapidly, that is accompanied by irregular menstrual cycles, acne, unexplained weight gain, or other features of androgen excess, may be a sign of polycystic ovary syndrome, adrenal dysfunction, or another hormonal disorder that requires diagnosis and treatment beyond hair loss management. Similarly, diffuse hair thinning in women can be the presenting sign of thyroid disease or significant iron deficiency. Professional evaluation identifies these treatable systemic contributors. Second, the psychological impact of androgenetic alopecia is clinically well-documented and should not be dismissed. Published research consistently demonstrates that hair loss, particularly in women and in men who begin losing hair early, produces significant rates of anxiety, reduced self-confidence, social withdrawal, and diminished quality of life. Effective treatment that halts progression and restores density has documented positive effects on psychological well-being. Seeking evaluation is not vanity; it is addressing a condition with real quality-of-life consequences through treatments that work.
Signs and Symptoms of Androgenetic Alopecia
Androgenetic alopecia develops so gradually that many patients struggle to identify exactly when it began. Changes that accumulate over two or three years often become noticeable only at a specific moment, such as when a photograph reveals the difference from years earlier or when a hairstyle that previously covered thinning areas no longer does. Knowing the specific signs to look for at each stage helps you identify the condition earlier and seek evaluation before substantial irreversible miniaturization has occurred.
Signs in Men
Bitemporal Recession: The earliest recognizable change in most men is a gradual recession of the temporal hairline, producing the M-shaped or widow’s peak appearance that distinguishes the mature male hairline from the flat juvenile hairline of adolescence. Minor bitemporal recession is normal in adult men, but progressive deepening of the temporal recessions beyond the anterior hairline is the first signal of androgenetic alopecia in motion.
Vertex Thinning: Concurrent with or following temporal recession, thinning at the crown or vertex of the scalp typically becomes visible. The vertex is often the first area where the scalp becomes visible beneath thinning hair, frequently noticed by others before the affected person observes it in mirrors. The combination of frontal recession and vertex thinning that eventually bridges across the mid-scalp produces the classic horseshoe-shaped residual fringe of the Norwood VI and VII patterns.
Hair Quality Changes: Before significant baldness is visible, the hairs in affected areas become progressively finer, shorter, and lighter in color as they miniaturize. A ponytail, bun, or wet hair observation often reveals that individual hair shafts are considerably thinner than they were several years ago. Styling products that previously provided volume no longer achieve the same effect because the hair shaft caliber has fundamentally reduced.
Increased Shedding: Many men with androgenetic alopecia notice increased hair on their pillow, in the shower drain, and on their hairbrush. This reflects the normal telogen shedding of hairs that have completed shortened anagen cycles. It is often the first symptom that prompts patients to seek evaluation, though the condition has typically been progressing for years before shedding becomes subjectively noticeable.
Signs in Women
Widening of the Central Part: The most common and often earliest noticeable sign in women with female pattern hair loss is a visible widening of the central part line, reflecting diffuse thinning of the crown and vertex hair through which the scalp becomes increasingly visible. A part that has widened progressively over one to two years is a reliable early indicator of androgenetic alopecia rather than a normal aging change.
Reduced Hair Volume and Ponytail Circumference: Women with female pattern hair loss frequently describe their ponytail becoming noticeably thinner, requiring more wraps of a hair tie to secure, and feeling lighter than it previously did. This diffuse reduction in overall hair mass reflects the transition of follicles from terminal to miniaturized vellus status across the crown and vertex.
Increased Scalp Visibility at the Crown: In moderate to advanced female pattern hair loss, the scalp becomes directly visible through the hair over the crown and vertex when the hair is parted or when viewed from above. The frontal hairline is typically preserved, which distinguishes this pattern from frontal fibrosing alopecia and from male-pattern recession.
Increased Shedding: Many women with androgenetic alopecia report increased hair shedding as an early complaint, often before visible thinning is apparent to others. Hair accumulating on clothing, in brushes, and in the shower drain is a consistent early symptom. Importantly, this shedding in androgenetic alopecia is not as dramatic as the acute diffuse shedding of telogen effluvium but rather a chronically elevated baseline rate that slowly reduces hair density over time.
Scalp Sensitivity: Some women with female pattern hair loss report scalp sensitivity, itching, or tingling in areas of active thinning. This likely reflects a low-grade inflammatory component of follicular miniaturization that is documented histologically in early androgenetic alopecia and that may respond to anti-inflammatory adjunctive treatments.
Signs That Indicate You Should Seek Evaluation Now
You should see a dermatologist for androgenetic alopecia evaluation if you notice:
- Temporal recession or crown thinning that was not present one to two years ago
- A visibly wider central part compared to your part from two or more years ago
- A noticeably reduced ponytail circumference or reduced overall hair volume
- Significantly more hair in the shower drain, on your pillow, or on your brush than previously
- Hair that is visibly finer, lighter, and shorter in areas that previously had full terminal hair
- Pattern hair loss beginning before age 30
- Female pattern hair loss accompanied by irregular periods, acne, or unexplained weight gain
- Hair loss that has not responded to 6 months of consistent over-the-counter minoxidil use
- Hair loss causing significant anxiety, self-consciousness, or impact on daily quality of life
The earlier androgenetic alopecia is evaluated and treated, the greater the proportion of follicles that remain responsive to treatment. Delaying evaluation until hair loss is advanced significantly narrows the treatment response window.
Risk Factors for Androgenetic Alopecia
Androgenetic alopecia develops at the intersection of genetic susceptibility and hormonal signaling. Understanding the factors that contribute to its onset and rate of progression helps patients contextualize their hair loss and informs the dermatologic evaluation.
Genetics
Androgenetic alopecia has a strong polygenic genetic basis, meaning multiple genes on multiple chromosomes contribute to susceptibility. The inheritance is not simple, and the popular belief that hair loss is exclusively inherited from the maternal grandfather is a myth. Both maternal and paternal family history are relevant predictors. Among the most important genetic contributions are variants in the androgen receptor gene on the X chromosome, variants in the 5-alpha reductase genes, and multiple autosomal loci identified through genome-wide association studies. Having multiple first-degree relatives with androgenetic alopecia substantially increases personal risk and predicts earlier onset and more extensive progression. Men with a father who developed significant baldness and a maternal grandfather who also showed pattern hair loss face the highest genetic loading.
Age
Androgenetic alopecia is age-progressive in virtually all affected individuals without treatment. Prevalence and severity increase steadily with age in both men and women. In men, approximately 16 percent show signs of androgenetic alopecia by age 18, rising to 53 percent by age 40 and up to 80 percent by age 70. In women, female pattern hair loss affects approximately 6 percent of women under age 50 and 38 percent by age 70, with a notable acceleration in prevalence at menopause. The age of onset strongly predicts ultimate extent; men who begin losing hair in their late teens or early twenties typically experience more extensive baldness over their lifetime than those whose first changes appear in their forties.
Androgen Hormones
Circulating androgen levels are a necessary but not sufficient factor in androgenetic alopecia. DHT, the primary androgen mediating follicular miniaturization, is present in all adults. The key variable is the sensitivity of individual follicles to its effects, which is genetically determined. In men, the post-pubertal rise in testosterone and DHT activates the miniaturization process in genetically susceptible follicles. In women, while most have normal androgen levels, androgens still drive the condition through follicular sensitivity. A subset of women have elevated androgens due to polycystic ovary syndrome, a condition characterized by elevated luteinizing hormone, elevated androgens, and insulin resistance; congenital adrenal hyperplasia; androgen-secreting ovarian or adrenal tumors; or anabolic steroid or testosterone use. These women warrant hormonal evaluation and management of the underlying hormonal disorder as part of their hair loss treatment.
Hormonal Transitions in Women
Several hormonal transitions in women’s lives significantly influence the onset and severity of female pattern hair loss. The postpartum period, during which the sustained high estrogen of pregnancy withdraws abruptly after delivery, is among the most common triggers of clinically significant shedding and visible hair thinning in women. Most postpartum shedding is telogen effluvium that resolves within 6 to 12 months, but in women with underlying androgenetic alopecia, the postpartum hormonal shift can unmask or permanently accelerate previously subclinical pattern loss. Perimenopause and menopause produce a progressive decline in estrogen that removes its protective influence on hair follicles and allows the relative androgenic environment to drive more pronounced follicular miniaturization. Androgenetic alopecia that has been mild or unnoticed often becomes significantly more apparent in the menopausal transition. The androgenic properties of certain progestin-containing hormonal contraceptives can also worsen androgenetic alopecia in susceptible women.
Nutritional and Metabolic Factors
While androgenetic alopecia is primarily genetic and hormonal, several nutritional and metabolic factors can accelerate progression or amplify shedding on top of the underlying pattern loss. Iron deficiency, even in the absence of frank anemia, is associated with increased hair shedding and reduced hair shaft quality in women with androgenetic alopecia. Serum ferritin is the most sensitive indicator; levels below 40 to 70 ng/mL are associated with increased shedding burden in multiple published studies. Vitamin D deficiency has been associated with androgenetic alopecia severity in observational studies. Insulin resistance and metabolic syndrome, which are associated with elevated androgens in women, correlate with more severe female pattern hair loss. Severe caloric restriction and protein deficiency impair follicular cell proliferation and compound the existing miniaturization-related reduction in hair quality.
Medications
Exogenous androgens, including anabolic steroids, testosterone supplementation in men and women, and DHEA, accelerate androgenetic alopecia in genetically susceptible individuals by increasing circulating androgen substrate for DHT production. This is an important counseling point for patients on testosterone replacement therapy who have a personal or strong family history of pattern hair loss. Finasteride and other 5-alpha reductase inhibitors protect against this acceleration and may be initiated proactively in this population.
Can Androgenetic Alopecia Be Prevented?
Androgenetic alopecia cannot be fully prevented when a significant genetic predisposition is present. However, its progression can be meaningfully slowed and, in many patients, substantially reversed with treatment initiated before extensive miniaturization has occurred.
Start Medical Treatment at the First Signs of Progression
The most effective preventive strategy is early treatment. Minoxidil and 5-alpha reductase inhibitors are dramatically more effective at preserving existing hair than at recovering hair from follicles that have been dormant for years. A patient who begins finasteride at Hamilton-Norwood Type II will, on average, retain far more hair over the subsequent decade than a patient who waits until Type IV to begin the same treatment.
Correct Contributing Nutritional Deficiencies
Identifying and correcting iron deficiency, vitamin D deficiency, and significant protein or zinc deficiency reduces the shedding burden superimposed on the underlying androgenetic process and improves the quality of hairs produced by miniaturizing follicles.
Manage Hormonal Triggers in Women
Women approaching menopause who have a family history of female pattern hair loss may benefit from proactive dermatologic evaluation and initiation of appropriate medical therapy before the menopausal estrogen withdrawal accelerates their androgenetic alopecia. Women on androgenic progestins who notice hair changes should discuss contraceptive alternatives with their gynecologist and dermatologist.
Avoid Exogenous Androgens in Genetically Susceptible Individuals
Men and women with a personal history or strong family history of androgenetic alopecia who are considering anabolic steroids, testosterone supplementation, or DHEA should be counseled about the substantial risk of accelerating their hair loss and discuss this risk with their dermatologist before initiating these agents.
Diagnosis and Evaluation of Androgenetic Alopecia
Most androgenetic alopecia is a clinical diagnosis confirmed by pattern recognition, trichoscopy, and, in women, targeted laboratory assessment to identify hormonal and nutritional contributors. In ambiguous cases where the pattern does not fit neatly, where progression is unusually rapid, or where features suggest an alternative or concurrent diagnosis, scalp biopsy provides definitive histopathologic confirmation. The evaluation process at Connolly Dermatology is systematic and comprehensive, addressing both the diagnosis and every modifiable contributing factor.
Clinical History
Your dermatologist documents when hair changes were first noticed, how the pattern and rate of change have evolved over time, and whether shedding has increased subjectively. Personal and family history of hair loss on both sides of the family are recorded. In women, menstrual history, obstetric history, contraceptive history, and perimenopausal status are documented. The complete medication list, including over-the-counter products, vitamins, and supplements, is reviewed with particular attention to testosterone and androgen-related agents. Dietary patterns and recent significant weight changes are explored. Any previously attempted treatments for hair loss and their outcomes are documented.
Clinical Pattern Assessment
In men, the Hamilton-Norwood classification is applied to document current staging and provide a baseline for measuring treatment response over time. In women, the Ludwig classification documents central thinning severity, and the Sinclair scale is sometimes additionally used to capture the global density change across the top of the scalp. Pattern assessment is documented with standardized scalp photography at baseline, providing objective comparison at subsequent follow-up visits.
Trichoscopy
Trichoscopy is dermoscopy applied to the scalp and hair, providing 20 to 100-fold magnification of follicular architecture and hair shaft characteristics that are invisible to the naked eye. It is an essential and highly informative component of androgenetic alopecia evaluation at Connolly Dermatology. The characteristic trichoscopic findings of androgenetic alopecia are hair diameter variability, specifically a proportion of miniaturized thin hairs exceeding 20 percent of follicular units in the affected region, alongside the peripilar sign, a brown perifollicular halo around follicular openings in the affected zone. Empty follicular units where hairs are absent, follicular units producing a single hair instead of the normal two to four, and a reduction in the terminal-to-vellus hair ratio confirm androgenetic alopecia and reflect the stage of miniaturization. The female pattern hair loss Christmas tree distribution, in which vellus hairs decrease in density from the anterior part line toward the occiput, is a characteristic trichoscopic signature of female pattern hair loss. Trichoscopy also identifies features that suggest concurrent or alternative diagnoses, including exclamation mark hairs in alopecia areata or perifollicular scale and absent follicular openings in scarring alopecia.
Hair Pull Test
The hair pull test provides immediate bedside information about active shedding. Approximately 60 hairs are grasped between the thumb and forefinger and smooth traction is applied. A yield of more than 6 telogen hairs per pull is considered positive and indicates active effluvium. In androgenetic alopecia, the pull test is usually negative or weakly positive in the uninvolved occipital scalp but may show slightly elevated telogen yield in actively thinning crown and frontal areas, distinguishing it from telogen effluvium where the pull test is strongly positive across all scalp regions.
Laboratory Studies
Men with a classic pattern of androgenetic alopecia and a positive family history typically do not require laboratory workup. Women with androgenetic alopecia warrant targeted laboratory evaluation to identify hormonal and nutritional contributors that, when corrected, produce meaningful improvement in hair loss outcomes. Standard laboratory evaluation for women includes a complete blood count, serum ferritin (the most sensitive iron status marker for hair loss), thyroid-stimulating hormone, free and total testosterone, DHEA-S (dehydroepiandrosterone sulfate, an adrenal androgen), prolactin, and estradiol in perimenopausal or menopausal patients. Vitamin D 25-OH level is assessed. When polycystic ovary syndrome is suspected, fasting insulin and blood glucose are included. In men with onset before age 25 or unusually rapid progression, or when exogenous androgen use is denied but suspected, testosterone levels may be obtained. Laboratory results guide treatment selection, particularly the decision to include hormonal management with spironolactone or oral contraceptives in women.
Scalp Biopsy
Scalp biopsy is not required for the diagnosis of typical androgenetic alopecia but is indicated when the clinical picture and trichoscopy leave diagnostic uncertainty, when a concurrent scarring alopecia cannot be excluded, when the presentation is atypical for age or sex, or when a patient’s hair loss has not responded to adequate treatment and the accuracy of the original diagnosis needs to be confirmed. Two 4-millimeter punch biopsies, one sectioned horizontally and one vertically, allow histopathologic assessment of the terminal-to-vellus hair ratio, follicular miniaturization track counts, and fibrous stellae from previously active follicles. A terminal-to-vellus ratio below 4:1, compared to the normal 7:1 in non-affected scalp, confirms androgenetic alopecia. The presence of peribulbar lymphocytic inflammation distinguishes alopecia areata. Perifollicular fibrosis and absent follicles in scarred zones identify cicatricial alopecia.
When Should You Get Androgenetic Alopecia Evaluated?
You should see a dermatologist if you notice:
- Progressive temporal recession or crown thinning at any rate of change
- A visibly widening central part or reduced crown density in women
- Hair becoming finer and shorter over successive years in the thinning zone
- Androgenetic alopecia beginning before age 25
- Female pattern hair loss accompanied by menstrual irregularity, acne, or signs of androgen excess
- Hair loss that has not responded to 6 months of consistent over-the-counter minoxidil
- Any hair loss producing significant psychological distress, regardless of its current extent
- Hair loss in a patient considering or currently receiving testosterone replacement therapy
Androgenetic Alopecia Treatment Options
Androgenetic alopecia is one of the most treatable forms of hair loss when intervention begins while a meaningful population of responsive follicles remains. The available treatment armamentarium is broader and more evidence-supported than most patients realize, extending well beyond the single over-the-counter option most patients try first. An individualized treatment plan combining complementary mechanisms, tailored to sex, age, severity, contributing factors, and patient goals, produces substantially better outcomes than any single intervention alone.
Topical Minoxidil
Topical minoxidil is the most widely used pharmacological treatment for androgenetic alopecia and the only topical agent FDA-approved for this indication in both men and women. Minoxidil is a potassium channel opener and vasodilator that increases blood flow to the follicular dermal papilla, prolongs the anagen growth phase, and enlarges the follicle itself, producing a thicker, longer hair shaft. The 2% solution is FDA-approved for women. The 5% solution and 5% foam are FDA-approved for men and are widely used off-label in women at the same dose, with clinical evidence supporting comparable or superior efficacy to the 2% formulation. Applied to the dry scalp in the affected areas once daily (foam) or twice daily (solution), topical minoxidil produces measurable reduction in shedding within the first 2 to 3 months and visible regrowth that reaches its maximum at 6 to 12 months of consistent use. An initial shedding increase in the first 4 to 8 weeks of use, representing premature telogen release as follicles re-enter anagen, is normal and predictable and does not indicate the treatment is worsening hair loss. Benefits are sustained only with continued use; discontinuation produces a return to the untreated loss trajectory within 3 to 6 months.
Oral Minoxidil
Low-dose oral minoxidil has emerged as one of the most significant advances in androgenetic alopecia treatment of the past decade, offering the same follicular benefit as the topical formulation through a systemically delivered, once-daily oral dose that eliminates the application compliance challenges of topical therapy. Used off-label at doses of 0.625 to 2.5 mg daily in women and 2.5 to 5 mg daily in men, oral minoxidil stimulates follicular growth across all scalp regions simultaneously rather than only where applied topically. Multiple randomized controlled trials and large observational studies confirm its superior compliance and its comparable or superior efficacy to topical minoxidil for hair count improvement and patient satisfaction. The most common side effects at these low doses are facial and body hypertrichosis (unwanted hair growth in body areas), particularly relevant for women, and rare peripheral edema or fluid retention. Tachycardia is uncommon at these low doses but warrants monitoring in patients with pre-existing cardiac conditions. Oral minoxidil is particularly valuable for patients with incomplete topical application, for those with scalp sensitivity to the topical vehicle, and for those who prefer a simpler once-daily oral regimen.
Finasteride
Finasteride 1 mg daily is an oral 5-alpha reductase type II inhibitor that is FDA-approved for male androgenetic alopecia. By blocking the enzymatic conversion of testosterone to DHT specifically in the type II enzyme expressed in the scalp, finasteride reduces scalp DHT concentrations by approximately 60 percent. This substantially attenuates the miniaturization stimulus in susceptible follicles, arresting progression in the majority of treated men and producing measurable regrowth that reaches its maximum at 12 to 24 months of treatment. Clinical trial data show that finasteride maintains or improves hair counts compared to baseline in approximately 83 percent of men at two years, compared to progressive loss in the placebo group over the same period. The 5 mg daily dose (dutasteride’s precursor formulation) provides additional efficacy for men with more severe androgenetic alopecia. Finasteride is also used off-label in postmenopausal women with androgenetic alopecia, where it produces meaningful improvements in hair density in clinical trials. It is contraindicated in women who are pregnant or may become pregnant due to the risk of feminization of a male fetus. Sexual side effects including decreased libido, erectile dysfunction, and ejaculatory dysfunction occur in approximately 2 percent of treated men in clinical trials, are reversible in the majority upon discontinuation, and should be discussed in detail during the prescribing consultation.
Dutasteride
Dutasteride 0.5 mg daily inhibits both type I and type II isoforms of 5-alpha reductase, producing a more complete suppression of scalp DHT levels, approximately 90 percent reduction compared to 60 percent with finasteride. In head-to-head clinical trials, dutasteride produces superior hair count outcomes compared to finasteride at the same treatment duration. It is FDA-approved for benign prostatic hyperplasia and is used off-label for androgenetic alopecia in the United States, but is approved specifically for male pattern hair loss in Japan and South Korea, reflecting its robust evidence base for this indication. The more complete DHT suppression makes dutasteride particularly useful for patients with more advanced androgenetic alopecia or for those who have had an inadequate response to finasteride. The side effect profile is similar to finasteride but the effects persist longer after discontinuation due to dutasteride’s substantially longer half-life.
Spironolactone (Women)
Spironolactone is the most commonly prescribed systemic pharmacological treatment for female pattern hair loss in the United States and is used off-label for this indication. At doses of 50 to 200 mg daily, spironolactone competitively blocks androgen receptors in hair follicles and in adrenal tissue, reducing the androgenic signaling that drives miniaturization in susceptible follicles. It produces meaningful improvement in hair density and shedding reduction in the majority of treated women, particularly those with higher androgen levels or clinical signs of hyperandrogenism. It is most effective when combined with topical or oral minoxidil, creating complementary mechanisms that simultaneously address both follicular stimulation and androgen blockade. It requires monitoring for hyperkalemia and blood pressure changes and is contraindicated in pregnancy.
Hormonal Management in Women
Women whose female pattern hair loss is driven or amplified by elevated androgens from polycystic ovary syndrome or adrenal dysfunction benefit from treatment of the underlying hormonal disorder in addition to direct hair loss therapy. Combined oral contraceptives with a low-androgenicity progestin profile, such as those containing norgestimate, desogestrel, or norethindrone acetate, reduce androgenic stimulation of the ovarian axis and complement spironolactone therapy. Women on androgenic progestins should be evaluated for contraceptive alternatives. For perimenopausal and menopausal women with accelerating androgenetic alopecia, hormone replacement therapy discussion with their gynecologist is appropriate, as estrogen-containing preparations attenuate the relative androgenic environment that worsens post-menopausal female pattern hair loss.
Platelet-Rich Plasma (PRP) Therapy
Platelet-rich plasma prepared from the patient’s own blood is injected into the scalp at follicular sites in a series of treatment sessions. The concentrated growth factors released by activated platelets, including platelet-derived growth factor, vascular endothelial growth factor, epidermal growth factor, and insulin-like growth factor-1, stimulate follicular proliferation, increase dermal papilla cell activity, promote angiogenesis around the follicle, and shift follicles from telogen toward anagen. Multiple randomized controlled trials and systematic reviews document statistically significant improvements in hair count, hair shaft diameter, and hair density following PRP treatment in androgenetic alopecia. The standard protocol involves three to four monthly treatment sessions to establish the response, followed by maintenance injections every 3 to 6 months. PRP is most effective as an adjunct that amplifies the response to pharmacological therapy rather than as a standalone treatment, and it is particularly valuable for patients who want to add a biological, drug-free component to their regimen or who have had only partial responses to medications alone.
Low-Level Laser Therapy
Low-level laser therapy devices deliver red or near-infrared light at wavelengths of 650 to 670 nanometers to the scalp. At this wavelength, photons are absorbed by cytochrome c oxidase in mitochondria, stimulating cellular energy production, improving follicular oxygenation, and reducing inflammation in the perifollicular environment. Multiple randomized, double-blind, sham-controlled clinical trials demonstrate significantly greater hair count increases in treated versus sham-device groups with consistent use. FDA-cleared devices in the form of laser combs, bands, caps, and helmets are available for home use, making this an option that can be integrated into a comprehensive treatment plan with minimal visits. Low-level laser therapy is most effective as a component of a multimodal regimen alongside minoxidil and antiandrogen therapy and is particularly well-tolerated, with no systemic side effects.
Hair Transplantation
Hair transplantation is the most definitive treatment for androgenetic alopecia and produces permanent results in transplanted areas through the relocation of DHT-resistant follicles from the occipital donor zone to thinning or bald recipient areas. Two primary techniques are used. Follicular unit transplantation (FUT, or strip technique) harvests a strip of occipital scalp under local anesthesia, from which individual follicular unit grafts are dissected under magnification and transplanted into recipient sites. Follicular unit excision (FUE) uses a small punch device to individually extract follicular units one by one from the donor area, producing smaller scars without a linear strip scar. Both techniques produce natural-appearing results when performed by experienced surgeons with appropriate patient selection. Because transplanted follicles carry the genetic characteristics of the donor zone, they are permanently resistant to DHT-mediated miniaturization and maintain their growth in the transplanted location. Hair transplantation requires careful patient selection. It is most appropriate for patients with stable androgenetic alopecia, adequate donor density, realistic expectations, and ongoing medical management to protect non-transplanted hair from continued miniaturization. It is not appropriate as a standalone approach without medical management, because native non-transplanted follicles continue to miniaturize, eventually leaving transplanted areas as islands surrounded by progressive loss.
Emerging and Adjunctive Therapies
Research into androgenetic alopecia treatment continues to advance. Topical finasteride formulations are under active investigation and clinical development, offering scalp-targeted DHT suppression with substantially reduced systemic absorption compared to oral finasteride, which is particularly relevant for men concerned about systemic sexual side effects. Topical spironolactone 5% cream for women represents a similar locally targeted approach. Clascoterone, a topical androgen receptor antagonist, acts directly on follicular androgen receptors without systemic absorption and is being studied for androgenetic alopecia. Prostaglandin-related pathways, particularly setipiprant as a PTGDR2 antagonist that counters prostaglandin D2-mediated follicular miniaturization, are in clinical trials. Exosome-based therapies delivering growth factor-rich extracellular vesicles to scalp tissue are an emerging area with early promising evidence. Wnt pathway activators and other molecular targets identified through advances in follicular biology research represent the frontier of next-generation androgenetic alopecia treatment.
Why Choose Connolly Dermatology for Androgenetic Alopecia Treatment
Care Guided by Experience and Clinical Judgment
Androgenetic alopecia care that consists of a recommendation to try over-the-counter minoxidil without trichoscopy, without laboratory assessment in women, and without a discussion of the full treatment spectrum is not adequate care for a condition with meaningful, evidence-supported options at every stage. Connolly Dermatology provides the comprehensive, individualized evaluation and treatment that androgenetic alopecia demands, from confirming the diagnosis with trichoscopy to building multimodal treatment plans that combine the most effective available interventions for your specific presentation.
Board-Certified Dermatologists
Our dermatologists are trained in the complete evaluation and management of androgenetic alopecia in both men and women, including the recognition of contributing hormonal and nutritional factors and the management of cases that have been inadequately treated previously. Every recommendation follows current clinical guidelines and reflects the strongest available evidence base.
Trichoscopy at Every Evaluation
We perform trichoscopy at every hair loss evaluation, providing magnified follicular assessment that documents miniaturization ratio, peripilar sign, vellus hair distribution, and any features suggesting an alternative or concurrent diagnosis. Trichoscopic baseline documentation provides objective comparison at subsequent visits to measure treatment response with precision beyond what subjective patient reporting or photographic comparison alone can achieve.
Comprehensive Hormonal and Nutritional Workup in Women
Female pattern hair loss evaluation at Connolly Dermatology includes the complete targeted laboratory assessment needed to identify every hormonal and nutritional contributor to your hair loss. Elevated androgens, thyroid disease, iron deficiency, and vitamin D deficiency each have specific, effective treatments that compound the benefit of direct hair loss therapy. We identify and address every modifiable factor as part of a comprehensive plan.
Full Treatment Spectrum Including Oral Minoxidil and PRP
We offer the complete evidence-based treatment armamentarium for androgenetic alopecia: topical and oral minoxidil, finasteride and dutasteride, spironolactone and hormonal management for women, in-office platelet-rich plasma therapy, low-level laser therapy guidance, and hair transplantation consultation and coordination. Your dermatologist selects the combination best suited to your diagnosis, severity, contributing factors, and treatment preferences rather than defaulting to a single first-line option regardless of whether it is the best fit for your situation.
Honest Communication About Outcomes and Timelines
We tell every patient clearly what to expect from each treatment: what percentage of patients see meaningful response, how long response takes to become visible, what commitment is required to sustain benefit, and what is and is not recoverable given the current stage of their androgenetic alopecia. We do not oversell outcomes. We set accurate expectations from the first visit and track response objectively at follow-up.
Patient Education and Support
Understanding why your hair is changing, how each treatment works mechanistically, why treatment must be sustained continuously, and what combining multiple approaches achieves over a single therapy makes you a far more informed and adherent participant in your own care. We make this education a genuine part of every hair loss consultation.
Compassionate, Patient-Centered Care
Hair loss is personal. It is not trivial. Our team approaches every androgenetic alopecia consultation with the seriousness and sensitivity the condition deserves, and we work to provide the clearest possible picture of your situation and the most effective path forward.
What To Expect During Treatment
Guiding You Through Evaluation and the Next Steps
Many patients who come to Connolly Dermatology for androgenetic alopecia have already tried over-the-counter minoxidil for months with incomplete results, received no specific diagnosis or laboratory workup from a prior provider, or simply been told their hair loss was normal without further evaluation. Our evaluation is structured to fill those gaps, answer the specific diagnostic questions about your hair loss, and build a treatment plan that is genuinely matched to your presentation.
Before Your Appointment
Preparing before your visit significantly improves the quality and efficiency of your evaluation. Take photographs of your current hairline, part line, crown, and temporal areas in good lighting, both as a record and to compare with photographs from two or more years ago if available. Document when you first noticed changes and how your hair loss has progressed since then. Write down every medication, supplement, and vitamin you currently take. For women, note your menstrual history, contraceptive history, obstetric history, and menopausal status, as well as any recent hormonal changes. Document every hair loss treatment you have previously tried and your experience with each. List every family member with hair loss on both your maternal and paternal sides. If you have ever had blood tests related to hair loss, bring the results.
During the Evaluation
Your dermatologist reviews your history in detail, performs a complete scalp examination, and applies trichoscopy to the affected and unaffected scalp regions. The hair pull test is performed. The distribution and severity of your androgenetic alopecia is staged and documented with clinical photographs. Any trichoscopic features suggesting an alternative or concurrent diagnosis are noted.
Your dermatologist explains the diagnosis and its stage, discusses the treatment options appropriate to your severity and sex, and answers your questions about each. For women, laboratory tests are ordered at the first visit, and the treatment plan is confirmed or adjusted once results are reviewed. For men with a clear diagnosis and typical presentation, treatment can be initiated at the first visit. The treatment plan, including every medication’s mechanism, dosing, expected onset of benefit, required duration of use, and potential side effects, is explained in full before any prescription is issued.
After Your First Visit
Most patients begin a combination regimen at the first or second visit, typically pairing a follicular stimulant (topical or oral minoxidil) with an androgen blocker (finasteride, dutasteride, or spironolactone based on sex, preference, and contributing factors), supplemented by PRP if elected or nutritional correction if laboratory results indicate deficiency. An initial shed from minoxidil in the first 4 to 8 weeks is normal and expected, and patients are prepared for this in advance to prevent unnecessary concern or premature discontinuation.
The first treatment response evaluation is typically scheduled 3 to 6 months after initiation. At that visit, trichoscopic comparison to baseline images quantifies the vellus-to-terminal ratio change, and standardized scalp photographs provide objective before-and-after comparison. For patients electing PRP, a series of three to four monthly treatment sessions is scheduled and tracked through the same follow-up structure. Adjustments, such as increasing the dose of oral minoxidil, switching from finasteride to dutasteride, or adding PRP as an adjunct, are made based on the documented response at each visit. Patients who achieve meaningful stabilization or density improvement are transitioned to a maintenance plan with annual or semi-annual visits to monitor the long-term treatment trajectory.
What To Expect During Your Evaluation
Guiding You Through Diagnosis and the Next Steps
Many patients who come to Connolly Dermatology with unexplained rashes have already been to urgent care, a primary care physician, or an emergency room and left without a specific diagnosis or with a treatment that didn’t work. Our evaluation is structured specifically to answer the questions those prior encounters could not. Here is what to expect from the process.
Before Your Appointment
Preparing before your visit significantly improves the quality and efficiency of your evaluation. Photograph your rash if it is not currently active or if its appearance changes day to day. Bring a complete list of every medication you currently take and any you have stopped in the past two to three months, including over-the-counter products, supplements, and vitamins. Document when the rash first appeared, where it started, how it has spread or changed, and every symptom accompanying it. Note any recent illnesses, travel, new product exposures, or dietary changes that preceded or accompanied the rash. Write down every treatment you have already tried and how your skin responded. If you have ever had a similar rash before, note whether it was diagnosed and what treatment was used. This preparation enables your dermatologist to build a clinical picture efficiently from the first minutes of your visit.
During the Evaluation
Your dermatologist conducts a thorough history review followed by a complete skin examination. They assess your rash’s primary lesion type, distribution, secondary features, and any associated findings across your full skin surface including areas you may not have considered relevant. In-office diagnostic tools including dermoscopy, KOH preparation, and Wood lamp examination are applied during the same visit when the clinical picture indicates their use.
Your dermatologist explains their diagnostic assessment clearly, including which diagnoses they are considering, which have been excluded by clinical features, and which require additional testing to confirm. If biopsy is indicated, the procedure is explained in full before it is performed. It is done under local anesthesia and takes less than 15 minutes. Most patients experience minimal discomfort and can drive themselves home afterward. Blood tests and specialized laboratory studies are ordered with an explanation of what each test is looking for and when results are expected.
In many cases, a diagnosis is reached at the first visit. When biopsy or laboratory results are needed, the results consultation is scheduled as soon as results are available, typically within 1 to 2 weeks. No results are sent to patients without a follow-up explanation of what they mean and what action, if any, is required.
After Your Evaluation
Once a diagnosis is established, your treatment plan is explained in full. You receive written instructions for every medication prescribed, including how to apply or take it, for how long, and what results to expect. If the diagnosis identifies a condition requiring referral, the referral is made with a written summary of the dermatologic findings to facilitate a productive specialist visit. If the diagnosis requires medication discontinuation, the appropriate prescribing physician is notified with documentation of the dermatologic assessment.
Follow-up visits are scheduled based on the nature of your diagnosis. Conditions that resolve with treatment are followed to confirmed clearance. Chronic conditions are monitored with regularly scheduled visits to adjust treatment as the disease course evolves. Patients who come to us after months or years of managing an undiagnosed rash without a clear answer frequently describe their first post-diagnosis visit as a significant relief, both the physical relief of effective treatment and the psychological relief of simply knowing what they are dealing with.
Get Clear Answers from Connolly Dermatology
Make Informed Decisions About Your Hair Health
Androgenetic alopecia is progressive, predictable in its mechanism, and genuinely treatable with the right combination of interventions initiated at the right time. The follicles that are actively miniaturizing today will continue to miniaturize without treatment. The follicles that have been dormant for years are not recoverable regardless of how effective future treatment becomes. This is why timing matters more in androgenetic alopecia than almost any other hair loss condition: the window for meaningful treatment response is open now, and it narrows with each passing year.
The treatment armamentarium available today, from oral minoxidil and dual 5-alpha reductase inhibitors through platelet-rich plasma and hair transplantation, offers men and women with androgenetic alopecia a genuinely broad range of effective options. A comprehensive, individualized plan that combines complementary mechanisms, corrects modifiable contributing factors, and is sustained consistently produces results that isolated over-the-counter minoxidil use does not. Professional evaluation confirms the diagnosis, identifies every contributing factor, and matches the most effective combination to your specific presentation and goals.
If you are experiencing pattern hair thinning or recession, a dermatology evaluation provides the trichoscopic diagnosis, targeted laboratory assessment, and individualized treatment plan that produces the best possible outcome. At Connolly Dermatology, our board-certified dermatologists offer expert evaluation, accurate staging, comprehensive treatment from topical and oral medications through PRP therapy, and the honest, detailed communication you deserve when making decisions about your hair.
Schedule a visit with a dermatologist to get clear, informed guidance about your hair loss.
Care You Can Rely On for Skin Changes and Concerns
Supporting You From Evaluation Through Ongoing Care
At Connolly Dermatology, we review every finding based on your skin’s appearance and medical context. Recommendations are made using established dermatologic standards, with treatment options selected to reflect the specific characteristics of the lesion and the patient’s overall skin health.
If you have noticed a changing mole, a new growth, or a skin lesion that raises concern, our team is here to help and guide you through the next steps. Schedule your evaluation at Connolly Dermatology today.
Our Locations
Linwood Commons
2106 New Road Suite D4
Linwood, NJ 08221
(609) 926-8899
(609) 926-6474 (fax)
The Commons
175 Gunning River Road, Bldg. E
Barnegat, New Jersey 08005
(609) 660-8002
(609) 660-8052 (fax)
409 NJ Route 70
Rear of Building
Cherry Hill, NJ 08034
(856) 772-1333
(856) 772-1997 (fax)
2099 New Albany Road
Cinnaminson, New Jersey 08077
(856) 772-1333
(856) 772-1997 (fax)
Eden Hill Medical Center
200 Banning St., Suite 380
Dover, DE 19904
(888) 377-5177
(302) 672-0879 (fax)
Lacey Medical Arts Building
833 Lacey Road
Forked River, NJ 08731
(609) 660-8002
(609) 660-8052 (fax)
Mainland Professional Centre
310 Chris Gaupp Drive, Suite 102
Galloway NJ 08205
(609) 926-8899
(609) 926-6474 (fax)
392 North White Horse Pike
Hammonton, NJ 08037
(609) 926-8899
(609) 926-6474 (fax)
The Bell Works Building – Purple Lot
101 Crawfords Corner Rd., Suite 1116A
Holmdel, NJ 07733
(732) 722-8437
(732) 722-8438 (fax)
1587 The Fairway, Suite C104, Jenkintown, PA 19046
(215) 774-8290
(267) 807-1479 (fax)
108 Roosevelt Blvd
Marmora, NJ 08223
(609) 926-8899
(609) 926-6474 (fax)
MIAMI, FL
Miami Beach
215 Lincoln Road
Miami Beach, Florida 33139
(786) 485-4182
124 Sleepy Hollow Dr., Ste 100
Middletown, DE 19709
(302) 291-9900
305 Jefferson Ave
Milford, DE 19963
(302) 291-9900
(302) 265-2051 (fax)
740 Bethlehem Pike Montgomeryville, PA 18936
(215) 774-8290
(267) 263-4645 (fax)
3532 West Chester Pike
Suite #20
Newtown Square, PA 19073
(888) 377-5177
(267) 807-1479 (fax)
FISHTOWN
2418 E. York St.
Philadelphia, PA 19125
(215) 774-8290
(267) 807-1479 (fax)
Broad Street
701 S. Broad Street Philadelphia, PA 19147
(215) 774-8290
(267) 807-1479 (fax)
18947 John J Williams Hwy
Suite 306
Rehoboth Beach, DE 19971
(888) 377-5177
(302) 291-2651 (fax)
1178 Route 37 West
Toms River, NJ 08755
(732) 722-8437
(732) 350-1363 (fax)
151 Fries Mill Rd. Suite 405
Washington Twp. NJ 08012
(856) 772-1333
(856) 772-1997 (fax)
1667 E. Landis Avenue
Vineland, NJ 08361
(856) 772-1333
(856) 772-1997 (fax)
108 Lacey Road Suite 38 A
Whiting, NJ 08759
(732) 722-8437
(732) 350-1363 (fax)