The Latest on Laminitis

Of all the ailments a horse can suffer, laminitis is the one that unfailingly strikes fear into the heart of an owner. Nothing else has as devastating an effect because while laminitis is not always fatal, it promises weeks or months of agony for the horse, endless nursing care for the owner, and multiple veterinary and farrier bills, all with no guarantee that the horse will ever regain useful soundness.

Normal and chronically foundered hoof anatomy

Although we recognize many of the triggers for laminitis -- gorging on grain or lush spring grass, prolonged pounding on a hard road, the after-effects of a severe illness, or a retained placenta in a foaling mare, the hormonal imbalance caused by a condition like Cushing's disease -- there's still much that's mysterious.

In the case of Pokey (a 29-year old gelding of mine who foundered), who was used only for light trail riding and the occasional child's riding lesson, there was nothing I could pinpoint as having set the damage in motion.

Some causes aren't known. This was the case with Pokey, my 29-year old gelding. He was used for light trail riding and occasional lessons, and there was nothing I could pinpoint as the trigger of his laminitis.

This is the case with some 70-80% of laminitis cases, according to Ric Redden, DVM, one of the world's leading laminitis specialists as both a veterinarian and farrier. Pokey had been on the same pasture for the past six months, his diet and work routines hadn't changed, and he hadn't broken into the feed room or gone galloping down a paved road. And while his age made Cushing's disease a possibility, my veterinarian agreed that he didn't demonstrate any of the other symptoms (such as keeping a long winter coat in the summer months or excessive thirst and urination). He sought to reassure me by saying that laminitis often strikes without any obvious cause, which unfortunately wasn't much comfort!

The bad news was that, whatever the cause, the path of destruction was well underway in Pokey's feet by the time I noticed the symptoms. It might have been brewing for days and escaped my notice -- but once in motion, the damage was irreversible. His laminae were already separating from the hoof wall on both front feet, and the coffin bones, loosened from their moorings, had lost their normal position and were pointing downward, putting painful pressure on his soles at the toe.

The good news was that with knowledgeable veterinary and farrier care, we were able to keep the after-effects to a minimum, make him more comfortable with sole support and (later) protective shoeing, and eventually return him to medication-free soundness.

There's more good news: Pokey is not alone in his recovery. Thanks to some considerable advances in our understanding of the mechanism and treatment of laminitis, most horses do survive an attack (the estimate ranges from 60-85%, depending on your source). In fact, Redden says that, "80% of the severe cases I see survive, which is a far cry from what I was doing 10 years ago. It's all about having an understanding of the mechanics -- providing blood flow to the places that need it."

Advancing Our Understanding

The first thing owners and trainers must understand is that laminitis and founder are two separate things. Laminitis, technically speaking, refers to inflammation of the laminae, the blood-saturated inner structures of the hoof that bond the hoof wall to the coffin bone or P3 (for third pedal bone; the first and second pedal bones, P1 and P2, are the long and short pastern bones).

Founder, on the other hand, is a term borrowed from mariners. A foundered ship is one that is sinking. Similarly, founder in a horse refers to the downward movement of P3 within the hoof capsule (relative to the hoof wall). An acute attack of laminitis often (but not always) allows the horse to founder, and a horse which has suffered a laminitis episode and has an altered P3 position is said to be foundered.

Chronic laminitis means the horse must deal with pain and lameness after an initial insult that causes damage. The horse suffered mechanical tearing of the damaged laminae and possibly compression of the sole's tissues by P3. Acute laminitis involves an inflammatory process. (Abscesses are frequent after-effects of the inflammation and pressure, and can cause later pain for the horse.)

To get a better grip on what happens inside the hoof during laminitis, we have to get a visual picture of the internal structures. Let's start with the all-important laminae, the vertically aligned structures that bond the hoof wall to the bone within.

There are two types of laminae -- dermal and epidermal (inner and outer). The dermal laminae are attached to P3 with connective tissues, and as such are stationary. The dermal laminae are also extremely vascular and equipped with a sensitive network of nerves.

The insensitive epidermal laminae, on the other hand, grow downward with the hoof wall from the coronary band. The two types of laminae interlock like laced fingers, bonding the hoof wall to the internal bony structure. The attachment is further strengthened by 150-200 secondary epidermal laminae branching off of each primary epidermal laminae (of which there are 550-600 per hoof). This gives the horse roughly 1.3 square meters of surface area (per hoof) for attaching hoof to bone.

The prevailing understanding of a laminitis attack is as follows: When the laminae become inflamed -- for whatever reason, from carbohydrate overload to stress from a non-weight-bearing lameness on the opposite foot -- the attachment between the laminae fails.

Research by Chris Pollitt, BVSc, PhD, Associate Professor of Equine Medicine at the School of Veterinary Science, University of Queensland, Australia, suggests that all the laminae are affected, but the forces of breakover during locomotion concentrate at the toe and cause more damage there than elsewhere in the hoof. The intricate relationship of the deep flexor tendon, P3, and the laminae -- and the unique characteristics of each foot -- play a major role in the specifics of laminitis development.

During a laminitis attack, the weakened laminae at the toe can no longer successfully balance the opposing pull of the deep digital flexor tendon. They stretch and tear away from the front of the coffin bone and pull away from the inner hoof wall, causing the coffin bone's sharp leading edge to descend toward the sole of the foot. In especially severe laminitis attacks, the laminae tear not only at the front of the hoof, but all the way around, allowing the coffin bone to rotate, or to"sink" (founder). This is generally considered the most catastrophic circumstance, sometimes resulting in the coffin bone punching through the sole of the foot without rotating.

As the coffin bone descends, its leading edge crushes capillaries in the sole below. The evidence of this can be seen when the foot is trimmed in subsequent weeks; there will be a characteristic crescent-shaped bruise in the horn of the sole near the toe called a symmetrical subsolar hematoma. Often there is red bruising along the white line as well. As the laminae die and separate like two sides of a Velcro strip being pulled apart, the resulting cavity or cavities fill with blood, pus, and other debris of the inflammatory process, creating what's called a laminar wedge.

The Influence of Enzymes

This cascade of events helps explain why the damage evolves as it does, but it does less to reveal the reason why the inflammation and edema start in the first place. To better understand the sequence of events that cause a laminitis attack, we have to look at it on a chemical level.

Researchers know that the process of "migration" (whereby the epidermal laminae grow downward while maintaining their connection with the dermal laminae) is regulated by metalloproteinase enzymes (catalysts of biochemical reactions), the activators and inhibitors for which are produced locally within the hoof capsule. In a normal hoof, activators and inhibitors interact to disconnect and re-connect the dermal/epidermal interface during this growth on a cellular level, permitting only limited disconnections in any region at any time so as not to weaken the overall integrity of the bond between the hoof wall and the coffin bone.

Pollitt has done extensive research on these regulating enzymes and how the laminar bond fails in cases of laminitis. He theorizes that an imbalance of specific metalloproteinase enzymes, their activators, or their inhibitors can disrupt the migratory process and set the laminitis cascade in motion. If too much activator is released, for example, it can overwhelm the available inhibitors and create too many "disconnects" in a laminar region, risking the whole bond of hoof wall to bone. When enough of these bonds break, this can cause stretching or tearing of other laminae because of the increased load on them.

It's possible, says Pollitt, that triggers for such enzyme imbalances originate elsewhere in the horse -- in the digestive system, for example, following a carbohydrate overload. Then they are carried to the hooves through the circulatory system, where they proceed to wreak havoc.

Pollitt's research has revealed a possible explanation for this destructive cascade of events. When a horse suffers a carbohydrate overload, such as might occur after gorging on grain or lush spring grass (which is higher in sugars than later-season grass), the gastrointestinal (GI) tract becomes overwhelmed and some of the carbohydrates end up being digested fermentatively in the hindgut rather than in the small intestine (see "From Start to Finish" on page 71 of this issue for more information on equine digestion). Since the digestive microflora in the hindgut are designed to process fiber, not carbohydrates and sugars, they struggle to break down this energy-rich material. This eventually causes a change in the microbial population, with the more sensitive species dying off as the gut pH (a measure of acidity) changes.

Streptococcus bovis, a common environmental bacterium, might then take advantage of the altered environment and take over. In Pollitt's lab, S. bovis has demonstrated the ability to activate metalloproteinase enzymes in the digital laminae, which could initiate the laminar destruction of laminitis. But how does S. bovis in the hindgut affect the laminae of the hooves?

Pollitt hypothesizes that when the population of S. bovis in the hindgut explodes during a carbohydrate overload, the bacteria release large amounts of laminitis trigger factors, which break down the gut wall just enough to allow them access to the horse's bloodstream. Once in the bloodstream, they quickly travel throughout the horse's body and to the laminae. There, they begin degrading the attachment of the secondary laminae to the basement membrane that attaches the outer, insensitive structures of the hoof to the inner ones. This microscopic degradation also affects the capillaries that supply blood and nutrients to the secondary laminae, forcing blood through the larger vessels in the primary laminae, dilating the, and thus allowing delivery of more enzymes to them.

Redden, who emphasizes that his knowledge of laminitis is always evolving, notes, "Dr. Pollitt's work on the enzyme activity is very exciting, too, and may play a major role in our understanding. But there are researchers who disagree with his model...Everyone's got an opinion -- but some of the information that's coming out is for the moment strictly theory, with zero experience behind it. Not everything explored in the lab pans out in the living horse."

One recurring message from virtually every researcher exploring the mysteries of this disease is that laminitis is an extremely individual and variable phenomenon. Steve Adair, DVM, Dipl. ACVS, of the University of Tennessee, says, "It's possible that laminitis is going to turn out to be a syndrome with multiple causes and pathways. The only similarity is the end result."

If this is the case, then laminitis research will likely continue to diverge as scientists explore various aspects of the syndrome with different causes.

Laminitis in the Lab

Adair's research is based on triggering clinical laminitis by administering an extract of black walnut to lab horses. Most horse people are aware that black walnut is toxic to horses; when eaten, black walnut shavings are known to cause laminitis.

"Administering black walnut is an accepted experimental model," he says. "The other method is an intentional carbohydrate overload. Most of the horses that get black walnut return to normal function afterwards. In fact, about 80% are clinically normal within 96 hours. But we don't know yet whether laminitis from black walnut is really the same as laminitis from a carbohydrate overload." Adair hopes to compare the two models in a future study.

Adair feels somewhat conflicted about having to induce laminitis in healthy horses.

"There's really nothing worse than foundering a horse -- but it's almost impossible to use clinical cases of laminitis to study the disease because there's so much variability. Plus there's the moral question of maintaining a placebo group when the horse's owner would clearly prefer that the horse receive some treatment! I try to pool my resources with other researchers to decrease the overall number of animals used, and we use horses that are destined for euthanasia anyway, for other reasons. I also try to keep in mind that what I'm doing is for the good of the horse overall."

Adair is currently exploring microvascular blood flow within the laminitic foot by using laser Doppler flowmetry. This technique involves drilling two to four small holes in the dorsal hoof wall to the white line -- about eight millimeters deep -- and inserting slender probes in the holes. The probes measure the Doppler shift, or frequency change, that light undergoes when reflected by moving objects such as red blood cells flowing through capillaries in the sensitive laminae. Measuring blood flow is important because prolonged decreased blood flow might "starve" the laminae, while increased blood flow might deliver more chemical laminitis trigger factors from the gut. Adair and others are working to clarify the relationship between blood flow, laminitis, and healing.

After administering black walnut extract to the lab horses, Adair begins measuring the microvascular blood flow almost immediately (to establish a baseline, or normal blood flow measurement) and hourly afterward until 12 hours post-insult. Adair has noticed a biphasic cycle of blood flow in induced black walnut laminitis.

"Within two hours of receiving black walnut, I noted a marked decrease in blood flow, which then increased and plateaud at the four- to six-hour mark. Then at 10 to 12 hours, the blood flow decreased again, coinciding with the start of clinical signs of laminitis. This biphasic pattern is a classic sign of ischemic re-perfusion injury; the second decrease is indicative of a secondary insult."

While he has not yet employed the Doppler laser technique with carbohydrate-induced laminitis, Adair suspects that he would see similar results with respect to blood flow. "The difference is that with carbohydrate overload, you'd probably see a slower, more drawn-out process."

Adair's research focuses on prevention. With Louisiana State University's Rustin Moore, DVM, PhD, Dipl. ACVS, Associate Professor of Equine Surgery and Director of the Equine Health Studies Program; Auburn's James Belknap, DVM, MS, PhD, Dipl. ACVS, Assistant Professor of Large Animal Surgery and Medicine; and Doug Allen, DVM, MS, Dipl. ACVS, of the University of Georgia Veterinary School, Adair is hoping to identify a medication or medications that will successfully correct the decrease in microvascular blood flow and perhaps prevent laminitis. This drug therapy could be a godsend when an owner knows a horse has been in a situation that could predispose him to laminitis -- a retained placenta in a mare, for example, or a breaking-into-the-feed-room escapade.

"One burning question we're dealing with is whether increasing the blood flow ought to be our goal," Adair says. "U.S. research says yes, but some of Dr. Pollitt's work indicates the opposite -- that decreasing blood flow in the foot would be beneficial...I don't really know yet which will pan out! In the next few years I suspect we'll have a lot of new information to digest, and it may dramatically change how we treat laminitis."

Assessing the Individual

Over 25 years of treating laminitic horses, Redden has developed a detailed protocol for assessing new cases. This provides him with invaluable data on the progression of the disease.

"The first priority in a treatment regime is to establish a baseline," he said. "Then you can identify the damage. But you need to understand what might have been abnormal about that foot before laminitis became a factor. And that often takes a farrier's eye rather than a veterinarian's.

"I don't think there's one general way to treat laminitis, and there probably never will be," Redden continues. "Laminitis treatment has to be designed for the individual -- every foot and every horse is unique! The way you approach a horse with a thick sole, good concavity to his foot, and an upright conformation will be completely different from the way you deal with a horse with long, sloping pasterns, under-run heels, and a flat sole."

Key to Redden's assessment of a laminitis case is a complete set of radiographs (X rays). While many veterinarians wait to take films until well into the syndrome, Redden doesn't hesitate to get a radiographic record early in the syndrome, preferably at the onset of symptoms.

"You can have significant changes in the first six to eight hours," he says, "so it's vital to get that baseline. In the case of a high degree of insult and a poor quality hoof, the horse can walk out of his foot in the first 24 hours. I recommend taking films immediately. If you wait, you've lost your window of opportunity for that 'before' view."

Radiographs need to be taken to reveal soft tissue details, such as the horn/laminar junction (H/L zone), which shows up as a faint opaque line. "That tells you how much is horn, and how much is laminae," says Redden. "Without that information I can't identify how much damage has been done. The value of positioning the camera (X ray machine) correctly can't be over-stressed. But the more you practice, the easier it is."

Redden uses a special paste designed for human esophagrams (X rays of the esophagus) to outline the hoof wall so that he can accurately measure the H/L zone.

"It's rather like toothpaste with iodine in it," he says. "It shows up white on radiographs. The usual method of laying a metal wire along the hoof wall doesn't accurately reflect all the bumps and valleys that may be present. It simply doesn't accurately represent the face of the wall."

A pivotal baseline measurement is the horn/laminar space, assessed by measuring the distance between the face of the coffin bone just below the extensor process and the radio-opaque line made by the paste on the hoof wall. Different breeds tend to have different widths of this H/L zone. Widening of the H/L zone indicates laminar swelling, and if the H/L zone at the top of the bone is smaller than the same measurement at the apex of the bone, rotation has occurred.

Less useful is the common method of measuring coffin bone rotation. "I never measure degrees of rotation; five different vets will all measure it differently," Redden says. Another concern with this measurement is that previous rotation could have been present before laminitis, which is often misleading. "It is not meaningful data," he adds," because unevenness in the hoof wall and rasping can change the perception of rotation, but not the inside of the foot."

Redden does, however, measure the sole depth and degree of cup (below the apex of P3), as well as the palmar angle between the coffin bone and the ground. (If the horse is not wearing a shoe, the radiograph will need to delineate the ground surface with something that will show up on radiographs as hoof wall and wood are very difficult to distinguish on film.) He also measures digital breakover by dropping a line straight down from the apex of P3 to the ground, then measuring forward to where the toe doesn't touch the ground.

"These measurements are very important for the vet and farrier to set up the mechanics of their treatment," Redden says. "They also give good parameters for measuring treatment success. They can provide valuable comparative data and help tell you whether the bone is stable or still moving," says Redden. "The exam needs to be thorough if your goal is to return this horse to usefulness. A venogram is frequently used to help assess the degree of damage, and evidence shows it to be a therapeutic aid as well." (see "Venograms Offer a Critical Look Inside" on page 38 for more on venograms).

Treatment Options

Once the horse's degree of laminitic insult has been accurately assessed, it's time to recommend a treatment regimen. Here again, experience is vital, as there are almost as many treatment options as there are laminitic horses.

"I've used everything over the years, but there are some methods that I don't use anymore as there are more beneficial methods," says Redden. "I don't do lower hoof wall resections (cutting away the detached hoof wall to reduce pressure on the remaining laminae) anymore for high-scale damage cases, for example, though I sometimes do upper wall resections at the coronary band when the band prolapses over the horn wall, causing pressure ischemia to the coronary plexus and horn growth centers. It needs removing to aid reperfusion (re-established blood supply) to this area. I just take about an inch-wide section below the blowout to help restore circulation."

Heart bar shoes have been the choice of many farriers and veterinarians for laminitic horses. They include a frog-shaped bar to transfer some weight bearing from the hoof wall to the frog.

"Some guys love them, but I think those are the ones who don't really see all that many cases (of laminitis)," Redden says. "They have low mechanical advantages. They work for low-scale cases, but you're not really reducing the load, you're just matching load for load and force for force. You can't make the sole grow with a heart bar shoe, either."

Reducing load on the deep digital flexor tendon is one of the crucial considerations for making a laminitic horse more comfortable, says Redden. When the laminae at the toe are damaged, the pull of the flexor tendon can easily damage them further; every step can worsen the injury. The horse might benefit from a flexor tendon tenotomy, which cuts the tendon to immediately relieve the pressure, but only in mid- to high-scale cases. The tendon will heal within two to four months, with total recovery in eight months to a year, so there's minimal damage from this technique. A tenotomy is only useful, however, when it's preceded by expert therapeutic shoeing to reposition P3 relative to the ground, says Redden.

"It is far more than a salvage procedure when performed in a timely fashion and in conjunction with palmar realignment," he continues. "I have several horses which have returned to athletic performance one to two years post-surgery, a few at top level.

"In terms of drugs, Bute's about all I recommend now, only at a maintenance level," Redden says. "You can't release the pull of the tendon with drugs. The mechanics are far more valuable than the drugs.

"Emergency treatment consists of drastically reducing flexor tendon tension. Three basic things are done: 1) You place the breakover of the shoe or hoof well behind the apex of P3, 2) Raise the heel to create a 20º palmar angle, and 3) Use cushion support to use the entire sole for support. You need radiographs to do these steps properly.

"Discretion must be used with every case," Redden explains. "Supporting a thin sole with extensive internal down load can be disastrous. My modified Ultimates (shoes) put breakover well behind the apex of P3, reducing tendon leverage action. Raising the heel to unload the tendon and using a custom-fit Elastikon cushion distributes support over a large surface area. In all acute cases, I raise the heel and drastically reduce breakover as a means to reduce the pull of the deep flexor tendon. The degree of each is relative to the unique characteristics of the foot. A 45º hoof with no heel must be treated entirely different from the 50º, strong-heeled foot if the same mechanical situation is the goal. You don't just raise them up and expect results with no regard to the individual foot.

"Sole pressure, used in conjunction with attenuating the pull of the tendon by reducing breakover and raising the heels, can work, but it has to be done correctly."

Sandy Loree, farrier and owner of 5S Equine Sole Support Products, believes that it is necessary to load the sole. "We employ a custom-molded insole using insole putty under a rubber pad. Weight bearing can be reduced or eliminated from the wall while loading the sole, bars, frog, and all the depressions as well.

"Laminitis is secondary to a triggering systemic condition," he continues. "The sick, weak laminae are simply overwhelmed by normal mechanical forces. Treat founder as an injury -- minimize weight-bearing forces on the hoof wall, and the foot will heal itself."

Redden's unparalleled field experience with laminitis cases is constantly providing him with more pieces of the puzzle. For example, he recently discovered that a venogram technique developed by himself and Pollitt in 1992, which he has used to assess the degree of damage in the hoof, might offer therapeutic possibilities since it helps open blood vessels (see page 38).

A new shoe Redden designed, nicknamed the "Banana Shoe" because of its continuous curve, also promises to help laminitic horses by allowing the horse to load the foot however he's most comfortable. "Mother Nature takes over the rest," he says.

Prevention Beats a Cure

Farrier Peter Van Dyke notes that so far, "Research into laminitis seems to have done little to reduce the number of horses encountering it." Owners must recognize common laminitis precursors (such as obesity or cresty neck), be able to identify early symptoms, and take early action to minimize damage (put the horse in a stall with deep, soft bedding and no grain, and call the veterinarian and farrier immediately).

Unfortunately, many pivotal structural changes can occur in the foot long before obvious lameness or shortness of stride tips off the owner to the problem. These sub-clinical laminitis cases are hard to identify, but as researchers learn more, they might be able to tune in to some subtle clues.

Regardless of how diverse the various aspects of laminitis research become, there's one common thread almost every veterinarian can agree on: Catching and treating laminitis early is crucial to the horse's successful recovery.

"Once clinical signs are apparent, the damage is largely done," says Adair. "So I'm interested in the first 72 hours, especially the first 12 to 24."

Redden agrees, saying, "We still don't know how to interpret when laminitis begins. We're not treating the disease itself; instead we're still dealing with after-effects."

One of the most important parts of treatment for high-scale cases is the owner's care and dedication -- the owner must be dedicated to the financial, emotional, and physical demands required to treat long-term cases. Also, effective mechanical aids employed early can prevent a large percentage of cases with substantial damage from becoming high-scale, complicated cases.

Although we have not figured out how to prevent laminitis at this time, the better its physiology is understood, the better veterinarians and farriers will be able to facilitate pain relief and recovery. Says Redden, "We know laminitis is a complex syndrome, but it's not as complicated as it once was. We're getting closer."

Venograms Offer a Critical Look Inside

In order to assess the amount of damage a foot has suffered in a laminitis attack, farrier and veterinarian Ric Redden, DVM, who specializes in foot care and treatment, finds performing a venogram an invaluable step. “I used to use this technique on just the really bad cases, but it’s so useful that I do it routinely on every case now,” he says. “We’ve done hundreds and have had no adverse reactions to date.”

A venogram is a procedure whereby contrast media (a liquid which shows up on radiographs) is injected into the digital palmar vein, which feeds into the vascular structures of the hoof.

“We do a nerve block on the horse, sedate him, and put a tourniquet on the fetlock. Then we position him on blocks so we can get the correct views, catheterize the vein, and inject an average of 20 ccs of the contrast media--this will vary a little depending on the size of the hoof.

“As the last drop of media goes in, you’ve got 30 to 40 seconds to take the film; there’s a very small window of opportunity, so we’ve learned to work fast. We take six views in that time, manipulating the foot in different positions to see how loading and unloading the deep flexor affects the circulation to the foot. It becomes a nice quantitative way to find out which areas are compressed, and the degree to which they’re compressed.”

“It’s a very simple procedure once people realize how quickly it has to go--after 30 or 40 seconds the media starts leaking into the interstitial tissue and you get a fuzzy, unclear picture.”

Venograms are even starting to look as if they might have therapeutic as well as diagnostic value, based on Redden’s observation that many horses seem to be in less pain following the procedure.

“Apparently we’re opening vessels which were shut down, and that response seems to last two to three days. We need to do some controlled studies to further explore this,” Redden says.

Redden says venograms also have humane value. For horses with extreme laminitic damage and massive laminar death, “The venogram is a very revealing prognostic tool to help me determine if there’s any point in continuing to treat the horse, or whether he should be euthanized. At a certain level, it’s irreversible and you can’t repair it. A venogram can also reveal the horse who might have had previous rotational damage prior to this attack.”


  • Pollitt, Christopher C. Color Atlas of The Horse's Foot. Barcelona: Mosby-Wolfe, 1995.
  • Redden, Ric. Understanding Laminitis. Lexington: Eclipse Press, 1998.

About the Author

Karen Briggs

Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.

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